cav2 3  (Synaptic Systems)


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  • 99
    Name:
    Ca2 channel R type alpha 1E
    Description:
    Synonyms Cav2 3 Cacna1e channel alpha 1E Cacna1E Price 325 00 Host rabbit Immunogen Recombinant protein corresponding to AA 1921 to 2222 from rat Ca2 channel R type alpha 1E Cav2 3 UniProt Id Q07652 Reactivity rat mouse Quantity 50 µg
    Catalog Number:
    152 403
    Product Aliases:
    Cav2.3, Cacna1e, channel alpha-1E, Cacna1E
    Price:
    325.00
    Host:
    rabbit
    Immunogen:
    Recombinant protein corresponding to AA 1921 to 2222 from rat Ca2+ channel R-type alpha-1E (Cav2.3) (UniProt Id: Q07652)
    Reactivity:
    rat mouse
    Quantity:
    50 µg
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    Structured Review

    Synaptic Systems cav2 3
    Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and <t>Cav2.3-KO</t> mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p
    Synonyms Cav2 3 Cacna1e channel alpha 1E Cacna1E Price 325 00 Host rabbit Immunogen Recombinant protein corresponding to AA 1921 to 2222 from rat Ca2 channel R type alpha 1E Cav2 3 UniProt Id Q07652 Reactivity rat mouse Quantity 50 µg
    https://www.bioz.com/result/cav2 3/product/Synaptic Systems
    Average 99 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    cav2 3 - by Bioz Stars, 2020-11
    99/100 stars

    Images

    1) Product Images from "Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus"

    Article Title: Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2019.00027

    Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p
    Figure Legend Snippet: Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p

    Techniques Used: Western Blot, Expressing, Mouse Assay

    AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Injection

    Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Mass Spectrometry

    Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p
    Figure Legend Snippet: Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p

    Techniques Used: Knock-Out, Injection

    2) Product Images from "Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus"

    Article Title: Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2019.00027

    Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p
    Figure Legend Snippet: Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p

    Techniques Used: Western Blot, Expressing, Mouse Assay

    AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Injection

    Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Mass Spectrometry

    Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p
    Figure Legend Snippet: Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p

    Techniques Used: Knock-Out, Injection

    3) Product Images from "Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus"

    Article Title: Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2019.00027

    Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p
    Figure Legend Snippet: Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p

    Techniques Used: Western Blot, Expressing, Mouse Assay

    AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Injection

    Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Mass Spectrometry

    Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p
    Figure Legend Snippet: Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p

    Techniques Used: Knock-Out, Injection

    4) Product Images from "Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus"

    Article Title: Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2019.00027

    Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p
    Figure Legend Snippet: Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p

    Techniques Used: Western Blot, Expressing, Mouse Assay

    AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Injection

    Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Mass Spectrometry

    Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p
    Figure Legend Snippet: Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p

    Techniques Used: Knock-Out, Injection

    5) Product Images from "Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus"

    Article Title: Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2019.00027

    Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p
    Figure Legend Snippet: Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p

    Techniques Used: Western Blot, Expressing, Mouse Assay

    AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Injection

    Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Mass Spectrometry

    Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p
    Figure Legend Snippet: Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p

    Techniques Used: Knock-Out, Injection

    6) Product Images from "Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus"

    Article Title: Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2019.00027

    Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p
    Figure Legend Snippet: Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p

    Techniques Used: Western Blot, Expressing, Mouse Assay

    AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Injection

    Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Mass Spectrometry

    Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p
    Figure Legend Snippet: Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p

    Techniques Used: Knock-Out, Injection

    7) Product Images from "Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus"

    Article Title: Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2019.00027

    Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p
    Figure Legend Snippet: Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p

    Techniques Used: Western Blot, Expressing, Mouse Assay

    AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Injection

    Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Mass Spectrometry

    Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p
    Figure Legend Snippet: Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p

    Techniques Used: Knock-Out, Injection

    8) Product Images from "Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus"

    Article Title: Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2019.00027

    Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p
    Figure Legend Snippet: Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p

    Techniques Used: Western Blot, Expressing, Mouse Assay

    AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Injection

    Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Mass Spectrometry

    Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p
    Figure Legend Snippet: Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p

    Techniques Used: Knock-Out, Injection

    9) Product Images from "Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus"

    Article Title: Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2019.00027

    Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p
    Figure Legend Snippet: Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p

    Techniques Used: Western Blot, Expressing, Mouse Assay

    AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Injection

    Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Mass Spectrometry

    Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p
    Figure Legend Snippet: Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p

    Techniques Used: Knock-Out, Injection

    10) Product Images from "Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus"

    Article Title: Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2019.00027

    Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p
    Figure Legend Snippet: Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p

    Techniques Used: Western Blot, Expressing, Mouse Assay

    AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Injection

    Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Mass Spectrometry

    Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p
    Figure Legend Snippet: Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p

    Techniques Used: Knock-Out, Injection

    11) Product Images from "Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus"

    Article Title: Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2019.00027

    Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p
    Figure Legend Snippet: Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p

    Techniques Used: Western Blot, Expressing, Mouse Assay

    AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Injection

    Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Mass Spectrometry

    Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p
    Figure Legend Snippet: Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p

    Techniques Used: Knock-Out, Injection

    12) Product Images from "Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus"

    Article Title: Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2019.00027

    Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p
    Figure Legend Snippet: Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p

    Techniques Used: Western Blot, Expressing, Mouse Assay

    AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Injection

    Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Mass Spectrometry

    Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p
    Figure Legend Snippet: Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p

    Techniques Used: Knock-Out, Injection

    13) Product Images from "Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus"

    Article Title: Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2019.00027

    Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p
    Figure Legend Snippet: Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p

    Techniques Used: Western Blot, Expressing, Mouse Assay

    AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Injection

    Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Mass Spectrometry

    Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p
    Figure Legend Snippet: Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p

    Techniques Used: Knock-Out, Injection

    14) Product Images from "Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus"

    Article Title: Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2019.00027

    Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p
    Figure Legend Snippet: Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p

    Techniques Used: Western Blot, Expressing, Mouse Assay

    AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Injection

    Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Mass Spectrometry

    Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p
    Figure Legend Snippet: Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p

    Techniques Used: Knock-Out, Injection

    15) Product Images from "Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus"

    Article Title: Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2019.00027

    Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p
    Figure Legend Snippet: Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p

    Techniques Used: Western Blot, Expressing, Mouse Assay

    AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Injection

    Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Mass Spectrometry

    Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p
    Figure Legend Snippet: Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p

    Techniques Used: Knock-Out, Injection

    16) Product Images from "Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus"

    Article Title: Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2019.00027

    Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p
    Figure Legend Snippet: Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p

    Techniques Used: Western Blot, Expressing, Mouse Assay

    AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Injection

    Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Mass Spectrometry

    Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p
    Figure Legend Snippet: Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p

    Techniques Used: Knock-Out, Injection

    17) Product Images from "Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus"

    Article Title: Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2019.00027

    Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p
    Figure Legend Snippet: Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p

    Techniques Used: Western Blot, Expressing, Mouse Assay

    AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Injection

    Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Mass Spectrometry

    Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p
    Figure Legend Snippet: Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p

    Techniques Used: Knock-Out, Injection

    18) Product Images from "Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus"

    Article Title: Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2019.00027

    Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p
    Figure Legend Snippet: Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p

    Techniques Used: Western Blot, Expressing, Mouse Assay

    AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Injection

    Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Mass Spectrometry

    Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p
    Figure Legend Snippet: Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p

    Techniques Used: Knock-Out, Injection

    19) Product Images from "Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus"

    Article Title: Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2019.00027

    Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p
    Figure Legend Snippet: Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p

    Techniques Used: Western Blot, Expressing, Mouse Assay

    AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Injection

    Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Mass Spectrometry

    Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p
    Figure Legend Snippet: Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p

    Techniques Used: Knock-Out, Injection

    20) Product Images from "Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus"

    Article Title: Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2019.00027

    Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p
    Figure Legend Snippet: Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p

    Techniques Used: Western Blot, Expressing, Mouse Assay

    AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Injection

    Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Mass Spectrometry

    Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p
    Figure Legend Snippet: Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p

    Techniques Used: Knock-Out, Injection

    21) Product Images from "Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus"

    Article Title: Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2019.00027

    Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p
    Figure Legend Snippet: Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p

    Techniques Used: Western Blot, Expressing, Mouse Assay

    AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Injection

    Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Mass Spectrometry

    Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p
    Figure Legend Snippet: Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p

    Techniques Used: Knock-Out, Injection

    22) Product Images from "Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus"

    Article Title: Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2019.00027

    Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p
    Figure Legend Snippet: Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p

    Techniques Used: Western Blot, Expressing, Mouse Assay

    AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Injection

    Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Mass Spectrometry

    Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p
    Figure Legend Snippet: Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p

    Techniques Used: Knock-Out, Injection

    23) Product Images from "Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus"

    Article Title: Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2019.00027

    Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p
    Figure Legend Snippet: Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p

    Techniques Used: Western Blot, Expressing, Mouse Assay

    AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Injection

    Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Mass Spectrometry

    Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p
    Figure Legend Snippet: Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p

    Techniques Used: Knock-Out, Injection

    24) Product Images from "Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus"

    Article Title: Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2019.00027

    Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p
    Figure Legend Snippet: Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p

    Techniques Used: Western Blot, Expressing, Mouse Assay

    AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Injection

    Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Mass Spectrometry

    Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p
    Figure Legend Snippet: Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p

    Techniques Used: Knock-Out, Injection

    25) Product Images from "Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus"

    Article Title: Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2019.00027

    Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p
    Figure Legend Snippet: Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p

    Techniques Used: Western Blot, Expressing, Mouse Assay

    AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Injection

    Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Mass Spectrometry

    Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p
    Figure Legend Snippet: Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p

    Techniques Used: Knock-Out, Injection

    26) Product Images from "Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus"

    Article Title: Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2019.00027

    Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p
    Figure Legend Snippet: Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p

    Techniques Used: Western Blot, Expressing, Mouse Assay

    AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Injection

    Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Mass Spectrometry

    Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p
    Figure Legend Snippet: Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p

    Techniques Used: Knock-Out, Injection

    27) Product Images from "Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus"

    Article Title: Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2019.00027

    Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p
    Figure Legend Snippet: Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p

    Techniques Used: Western Blot, Expressing, Mouse Assay

    AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Injection

    Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Mass Spectrometry

    Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p
    Figure Legend Snippet: Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p

    Techniques Used: Knock-Out, Injection

    28) Product Images from "Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus"

    Article Title: Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2019.00027

    Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p
    Figure Legend Snippet: Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p

    Techniques Used: Western Blot, Expressing, Mouse Assay

    AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Injection

    Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Mass Spectrometry

    Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p
    Figure Legend Snippet: Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p

    Techniques Used: Knock-Out, Injection

    29) Product Images from "Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus"

    Article Title: Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2019.00027

    Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p
    Figure Legend Snippet: Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p

    Techniques Used: Western Blot, Expressing, Mouse Assay

    AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Injection

    Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Mass Spectrometry

    Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p
    Figure Legend Snippet: Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p

    Techniques Used: Knock-Out, Injection

    30) Product Images from "Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus"

    Article Title: Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2019.00027

    Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p
    Figure Legend Snippet: Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p

    Techniques Used: Western Blot, Expressing, Mouse Assay

    AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Injection

    Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Mass Spectrometry

    Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p
    Figure Legend Snippet: Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p

    Techniques Used: Knock-Out, Injection

    31) Product Images from "Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus"

    Article Title: Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2019.00027

    Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p
    Figure Legend Snippet: Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p

    Techniques Used: Western Blot, Expressing, Mouse Assay

    AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Injection

    Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Mass Spectrometry

    Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p
    Figure Legend Snippet: Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p

    Techniques Used: Knock-Out, Injection

    32) Product Images from "Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus"

    Article Title: Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2019.00027

    Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p
    Figure Legend Snippet: Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p

    Techniques Used: Western Blot, Expressing, Mouse Assay

    AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Injection

    Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Mass Spectrometry

    Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p
    Figure Legend Snippet: Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p

    Techniques Used: Knock-Out, Injection

    33) Product Images from "Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus"

    Article Title: Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2019.00027

    Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p
    Figure Legend Snippet: Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p

    Techniques Used: Western Blot, Expressing, Mouse Assay

    AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Injection

    Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Mass Spectrometry

    Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p
    Figure Legend Snippet: Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p

    Techniques Used: Knock-Out, Injection

    34) Product Images from "Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus"

    Article Title: Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2019.00027

    Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p
    Figure Legend Snippet: Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p

    Techniques Used: Western Blot, Expressing, Mouse Assay

    AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Injection

    Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Mass Spectrometry

    Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p
    Figure Legend Snippet: Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p

    Techniques Used: Knock-Out, Injection

    35) Product Images from "Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus"

    Article Title: Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2019.00027

    Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p
    Figure Legend Snippet: Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p

    Techniques Used: Western Blot, Expressing, Mouse Assay

    AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Injection

    Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Mass Spectrometry

    Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p
    Figure Legend Snippet: Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p

    Techniques Used: Knock-Out, Injection

    Related Articles

    Isolation:

    Article Title: Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus
    Article Snippet: .. In agreement with this data we show that Cav2.3 and BK alpha co-immunoprecipitate from freshly isolated mouse hippocampal tissue, demonstrating that BK and Cav2.3 reside in a complex in the hippocampus. ..

    other:

    Article Title: Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus
    Article Snippet: The result shown in shows that in mouse hippocampus, Cav2.3 and BK channels form a macromolecular complex.

    Article Title: Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus
    Article Snippet: Discussion In this study, we show that a genetic deletion of Cav2.3 leads to altered AP waveform in CA1 pyramidal cells, and that this alteration leads to increased synaptic efficacy at the CA1-subiculum synapse.

    Article Title: Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus
    Article Snippet: This adds to the known functions of Cav2.3 as a calcium source for potassium channels in spines, to regulate incoming synaptic signals, and establishes Cav2.3 as a central regulator of calcium-dependent potassium channels to shape both incoming and outgoing signals in CA1 pyramidal neurons and may explain why Cav2.3 has been implicated in neurological diseases like epilepsy and Fragile X syndrome.

    Expressing:

    Article Title: Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus
    Article Snippet: .. Additionally our data builds on the finding that FMRP regulates expression of Kv4.2 by Gross et al. , by providing an additional pathway for Kv4.2 regulation in FXS through Cav2.3. ..

    Mouse Assay:

    Article Title: Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus
    Article Snippet: .. Cav2.3−/− CA1 Pyramidal Cells Have Altered Action Potential Waveforms To investigate the effect of chronic loss of the voltage gated calcium-channel Cav2.3 on the intrinsic firing properties of hippocampal pyramidal neurons in the CA1 area, we performed whole-cell current-clamp recordings of these neurons in acute hippocampal slices of 6–8-week-old mice lacking Cav2.3. ..

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    Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and <t>Cav2.3-KO</t> mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p
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    Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus

    doi: 10.3389/fncel.2019.00027

    Figure Lengend Snippet: Representative images and quantification of western blot analysis of calcium- and voltage-gated potassium channels. (A) Total expression of BK and SK2 potassium channels in mouse hippocampus showed no significant differences between WT and Cav2.3-KO mice (WT = 8, KO = 6; p > 0.05). In contrast, in the Cav2.3-KO, the total level of Kv4.2 was significantly increased compared to the WT (WT = 8, KO = 6; p

    Article Snippet: The separated proteins were immuonoblotted using Cav2.3 (1:1,000, Synaptic Systems, Germany) or BK antibody (1:2,000, Alomone Labs, Israel) and visualized by Alexa Fluor 680 secondary antibody (1:10,000, Invitrogen, Carlsbad, CA, USA) and Alexa Fluor 800 secondary antibody (1:5,000, Rockland, Knox County, MA, USA).

    Techniques: Western Blot, Expressing, Mouse Assay

    AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus

    doi: 10.3389/fncel.2019.00027

    Figure Lengend Snippet: AP waveform properties from CA1 pyramidal neurons. (A) Average first AP elicited by a +150 pA current injection for WT (black traces) and Cav2.3 KO (red traces) ± SEM. (B–G) Quantification of (A) . Firing threshold = first derivative of voltage > 0.2, and AP onset = time between current step onset and firing threshold. After-hyperpolarization (AHP) is calculated relative to firing threshold. (H) Example traces showing the first six APs elicited by a +200 pA current injection for WT (black traces) and Cav2.3 KO (red traces). (I–N) Quantification of (H) . Instead of AP onset, this analysis shows the inter-spike interval (time between peak voltages) and AHP was calculated as the minimum voltage between two APs. n = 17 for WT, and 19 for KO, all data shown as mean ± SEM, with Student’s T -Test to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Article Snippet: The separated proteins were immuonoblotted using Cav2.3 (1:1,000, Synaptic Systems, Germany) or BK antibody (1:2,000, Alomone Labs, Israel) and visualized by Alexa Fluor 680 secondary antibody (1:10,000, Invitrogen, Carlsbad, CA, USA) and Alexa Fluor 800 secondary antibody (1:5,000, Rockland, Knox County, MA, USA).

    Techniques: Injection

    Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus

    doi: 10.3389/fncel.2019.00027

    Figure Lengend Snippet: Altered synaptic connectivity between CA1 and subiculum. (A–D) Analysis of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from subicular pyramidal neurons in the presence of Gabazine. (A) Representative traces from WT (black traces) and Cav2.3 KO (red traces) and cumulative probability of sEPSC amplitudes for all recorded events ( n > 5,000). Insets represent the average traces over all sEPSCs. (B) Quantification of amplitude and frequency for the average event recorded from each cell per genotype ( n = 20). (C) Cumulative distribution and quantification for the rise- and decay-times for the average sEPSCs. (D) Quantification for the charge conveyed with each sEPSC (area under the current trace). (E–H) Experimental setup (E) and analysis (F–H) of paired-pulse facilitation between CA1 and subiculum. (F,G) EPSP amplitude and decay time are not significantly different between WT and KO [analyzed from the first elicited EPSP of the 1,000 ms inter-stimulus intervals (ISIs) pulse]. Insets in (H) represent average traces for WT (black) and Cav2.3 KO (red) for two representative ISI. All data shown as mean ± SEM, with student’s T -Test or two-way ANOVA where appropriate, to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Article Snippet: The separated proteins were immuonoblotted using Cav2.3 (1:1,000, Synaptic Systems, Germany) or BK antibody (1:2,000, Alomone Labs, Israel) and visualized by Alexa Fluor 680 secondary antibody (1:10,000, Invitrogen, Carlsbad, CA, USA) and Alexa Fluor 800 secondary antibody (1:5,000, Rockland, Knox County, MA, USA).

    Techniques: Mass Spectrometry

    Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus

    doi: 10.3389/fncel.2019.00027

    Figure Lengend Snippet: Cav2.3 knockout (KO) CA1 pyramidal cells are hyperexcitable. (A) Resting membrane potential (Vrest; A1 ) and cell capacitance (A2) , measured after break-in. (B) Input resistance quantified as the slope of an IV-curve for hyperpolarizing current steps from −160 to −20 pA. Insets represent averaged voltage traces for wildtype (WT; black) and KO (red) recordings during current injection. (C) Hyperpolarization activated current I H , measured as sag-percentage from maximum voltage deflection (C1) and as the slope of the rebound potential after the end of a series of hyperpolarizing current injections plotted against the steady-state voltage during the current injection (C2) . (D) Firing frequency of action potentials (APs) in CA1 pyramidal neurons of Cav2.3 KO and WT animals, elicited by current steps from Vrest, by injection of positive or negative current in steps of 20 pA. Inset shows example recordings for injections of +200 pA WT (black traces) or Cav2.3 KO (red traces). n = 17 for WT, and 21 for KO. All data shown as mean ± SEM, with Student’s T -Test to probe for significance (n.s. = not significant, * p

    Article Snippet: The separated proteins were immuonoblotted using Cav2.3 (1:1,000, Synaptic Systems, Germany) or BK antibody (1:2,000, Alomone Labs, Israel) and visualized by Alexa Fluor 680 secondary antibody (1:10,000, Invitrogen, Carlsbad, CA, USA) and Alexa Fluor 800 secondary antibody (1:5,000, Rockland, Knox County, MA, USA).

    Techniques: Knock-Out, Injection