anti sloβ2  (Alomone Labs)


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    Alomone Labs anti sloβ2
    Distribution of kcnmb2 message and demonstration of β2 (KCNMB2) protein in specific tissues. (A) Quantitative RT-PCR was used to define relative (normalized to β-actin) kcnmb2 message abundance. Each estimate corresponds to mean and standard error for RNA preparations from three mice, each done in triplicate. (B) Total proteins were first immunoprecipitated with the Alomone <t>anti-Sloβ2</t> Ab. Subsequently, aliquots of proteins obtained by IP were then treated with (+) or without (−) N -glycanase, separated by Western blot (WB), and visualized with NeuroMab anti-BKbeta2 N53/32 Ab. All tested tissues reveal β2 protein that is absent in the kcnmb2 −/− mice. Note the apparent diversity of molecular size of glycosylated β2 protein among various tissues. Glycanase-free lanes were omitted for adrenal medulla because of the small size of original tissue samples. Molecular mass is indicated in kilodaltons.
    Anti Sloβ2, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti sloβ2/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti sloβ2 - by Bioz Stars, 2021-12
    94/100 stars

    Images

    1) Product Images from "Knockout of the BK β2 subunit abolishes inactivation of BK currents in mouse adrenal chromaffin cells and results in slow-wave burst activity"

    Article Title: Knockout of the BK β2 subunit abolishes inactivation of BK currents in mouse adrenal chromaffin cells and results in slow-wave burst activity

    Journal: The Journal of General Physiology

    doi: 10.1085/jgp.201411253

    Distribution of kcnmb2 message and demonstration of β2 (KCNMB2) protein in specific tissues. (A) Quantitative RT-PCR was used to define relative (normalized to β-actin) kcnmb2 message abundance. Each estimate corresponds to mean and standard error for RNA preparations from three mice, each done in triplicate. (B) Total proteins were first immunoprecipitated with the Alomone anti-Sloβ2 Ab. Subsequently, aliquots of proteins obtained by IP were then treated with (+) or without (−) N -glycanase, separated by Western blot (WB), and visualized with NeuroMab anti-BKbeta2 N53/32 Ab. All tested tissues reveal β2 protein that is absent in the kcnmb2 −/− mice. Note the apparent diversity of molecular size of glycosylated β2 protein among various tissues. Glycanase-free lanes were omitted for adrenal medulla because of the small size of original tissue samples. Molecular mass is indicated in kilodaltons.
    Figure Legend Snippet: Distribution of kcnmb2 message and demonstration of β2 (KCNMB2) protein in specific tissues. (A) Quantitative RT-PCR was used to define relative (normalized to β-actin) kcnmb2 message abundance. Each estimate corresponds to mean and standard error for RNA preparations from three mice, each done in triplicate. (B) Total proteins were first immunoprecipitated with the Alomone anti-Sloβ2 Ab. Subsequently, aliquots of proteins obtained by IP were then treated with (+) or without (−) N -glycanase, separated by Western blot (WB), and visualized with NeuroMab anti-BKbeta2 N53/32 Ab. All tested tissues reveal β2 protein that is absent in the kcnmb2 −/− mice. Note the apparent diversity of molecular size of glycosylated β2 protein among various tissues. Glycanase-free lanes were omitted for adrenal medulla because of the small size of original tissue samples. Molecular mass is indicated in kilodaltons.

    Techniques Used: Quantitative RT-PCR, Mouse Assay, Immunoprecipitation, Western Blot

    2) Product Images from "Overexpression of Kcnmb2 in Dorsal CA1 of Offspring Mice Rescues Hippocampal Dysfunction Caused by a Methyl Donor-Rich Paternal Diet"

    Article Title: Overexpression of Kcnmb2 in Dorsal CA1 of Offspring Mice Rescues Hippocampal Dysfunction Caused by a Methyl Donor-Rich Paternal Diet

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2018.00360

    Different intrinsic excitability of CA1 pyramidal neurons in the MD F1 mice compared to the CD F1 mice. (A) qRT-PCR showing reduced expression of Kcnmb2 in the hippocampus of MD F1 mice. Unpaired t -test, n = 5 mice for each group. (B) Sample recordings showing action potentials evoked by a depolarizing current injection. Upper : the first spike in response to a current injection (250 pA, 50 ms) into CA1 pyramidal neurons of CD F1 mice (black trace) and MD F1 mice (red trace). Lower: spikes trains evoked by a depolarizing current injection (250 pA, 50 ms) into CA1 pyramidal neurons of MD F1 (red trace) and CD F1 (black trace) mice. (C) Reduced action potential half-width in CA1 pyramidal neurons of MD F1 mice compared to CD F1 controls. Unpaired t -test, n = 27 cells from six CD F1 mice and n = 16 cells from five MD F1 mice. (D) Increased peak fAHP in CA1 pyramidal neurons of MD F1 mice. Unpaired t -test, n = 27 cells from six CD F1 mice and n = 17 cells from five MD F1 mice. (E) Reduced spike number in CA1 pyramidal neurons of MD F1 mice. Unpaired t -test, n = 22 cells from six CD F1 mice and n = 16 cells from five MD F1 mice. In (C–E) , depolarizing current was 250 pA and 50 ms in duration. (F) Prolonged latency to first spike in CA1 pyramidal neurons of MD F1 mice. Depolarizing current was 150 pA and 600 ms in duration. Unpaired t- test, n = 26 cells from six CD F1 mice and n = 16 cells from five MD F1 mice. ∗ P
    Figure Legend Snippet: Different intrinsic excitability of CA1 pyramidal neurons in the MD F1 mice compared to the CD F1 mice. (A) qRT-PCR showing reduced expression of Kcnmb2 in the hippocampus of MD F1 mice. Unpaired t -test, n = 5 mice for each group. (B) Sample recordings showing action potentials evoked by a depolarizing current injection. Upper : the first spike in response to a current injection (250 pA, 50 ms) into CA1 pyramidal neurons of CD F1 mice (black trace) and MD F1 mice (red trace). Lower: spikes trains evoked by a depolarizing current injection (250 pA, 50 ms) into CA1 pyramidal neurons of MD F1 (red trace) and CD F1 (black trace) mice. (C) Reduced action potential half-width in CA1 pyramidal neurons of MD F1 mice compared to CD F1 controls. Unpaired t -test, n = 27 cells from six CD F1 mice and n = 16 cells from five MD F1 mice. (D) Increased peak fAHP in CA1 pyramidal neurons of MD F1 mice. Unpaired t -test, n = 27 cells from six CD F1 mice and n = 17 cells from five MD F1 mice. (E) Reduced spike number in CA1 pyramidal neurons of MD F1 mice. Unpaired t -test, n = 22 cells from six CD F1 mice and n = 16 cells from five MD F1 mice. In (C–E) , depolarizing current was 250 pA and 50 ms in duration. (F) Prolonged latency to first spike in CA1 pyramidal neurons of MD F1 mice. Depolarizing current was 150 pA and 600 ms in duration. Unpaired t- test, n = 26 cells from six CD F1 mice and n = 16 cells from five MD F1 mice. ∗ P

    Techniques Used: Mouse Assay, Quantitative RT-PCR, Expressing, Injection

    Overexpression of Kcnmb2 in the hippocampus masked MD-F1-associated alterations in intrinsic excitability of CA1 pyramidal neurons (A) Representative images showing AAV-associated GFP (right) and Kcnmb2 expression (left) in dorsal hippocampus. Red, green, and blue fluorescence reflects Kcnmb2-, GFP-, and DAPI-associated signal, respectively. Scale bars represent 100 μm. The insets are higher magnification images of the boxed area. (B) Quantification of the relative Kcnmb2 mRNA expression in the hippocampus after delivery of AAV- Kcnmb2 or AAV-control virus into CA1 region of MD and CD F1 mice. Two-way ANOVA followed by Tukey’s multiple comparisons test, n = 4, 4, 6, and 6 samples for CD-control, MD-control, CD- Kcnmb2 , and MD- Kcnmb2 groups, respectively. (C) Sample recordings in virus-infected CA1 pyramidal neurons (GFP + ) showing action potentials evoked by a depolarizing current injection in CD and MD F1 mice. Left : the first spike in response to a current injection (250 pA, 50 ms) into CA1 pyramidal neuron. Right : spikes trains evoked by a depolarizing current injection (250 pA, 50 ms) into CA1 pyramidal neurons. CD F1 neuron (black) and MD F1 neuron (red) infected by AAV-control (solid traces) or AAV- Kcnmb2 (dashed traces) virus. Comparisons of action potential half-width (D) , fAHP (E) , and spike numbers (F) between CD and MD F1 neurons infected by control or Kcnmb2 virus. Two-way ANOVA followed by Sidak’s multiple comparisons test, 5–6 mice per group. AP half-width: n = 21 cells for CD-control, n = 13 cells for MD-control, n = 16 cells for CD- Kcnmb2 and n = 13 cells for MD- Kcnmb2 ; fAHP: n = 14 cells for CD-control, n = 15 cells for MD-control, n = 16 cells for CD- Kcnmb2 and n = 14 cells for MD- Kcnmb2 ; Spike number: n = 20 cells for CD-control, n = 17 cells for MD-control, n = 17 cells for CD- Kcnmb2 and n = 14 cells for MD- Kcnmb2 . ∗ P
    Figure Legend Snippet: Overexpression of Kcnmb2 in the hippocampus masked MD-F1-associated alterations in intrinsic excitability of CA1 pyramidal neurons (A) Representative images showing AAV-associated GFP (right) and Kcnmb2 expression (left) in dorsal hippocampus. Red, green, and blue fluorescence reflects Kcnmb2-, GFP-, and DAPI-associated signal, respectively. Scale bars represent 100 μm. The insets are higher magnification images of the boxed area. (B) Quantification of the relative Kcnmb2 mRNA expression in the hippocampus after delivery of AAV- Kcnmb2 or AAV-control virus into CA1 region of MD and CD F1 mice. Two-way ANOVA followed by Tukey’s multiple comparisons test, n = 4, 4, 6, and 6 samples for CD-control, MD-control, CD- Kcnmb2 , and MD- Kcnmb2 groups, respectively. (C) Sample recordings in virus-infected CA1 pyramidal neurons (GFP + ) showing action potentials evoked by a depolarizing current injection in CD and MD F1 mice. Left : the first spike in response to a current injection (250 pA, 50 ms) into CA1 pyramidal neuron. Right : spikes trains evoked by a depolarizing current injection (250 pA, 50 ms) into CA1 pyramidal neurons. CD F1 neuron (black) and MD F1 neuron (red) infected by AAV-control (solid traces) or AAV- Kcnmb2 (dashed traces) virus. Comparisons of action potential half-width (D) , fAHP (E) , and spike numbers (F) between CD and MD F1 neurons infected by control or Kcnmb2 virus. Two-way ANOVA followed by Sidak’s multiple comparisons test, 5–6 mice per group. AP half-width: n = 21 cells for CD-control, n = 13 cells for MD-control, n = 16 cells for CD- Kcnmb2 and n = 13 cells for MD- Kcnmb2 ; fAHP: n = 14 cells for CD-control, n = 15 cells for MD-control, n = 16 cells for CD- Kcnmb2 and n = 14 cells for MD- Kcnmb2 ; Spike number: n = 20 cells for CD-control, n = 17 cells for MD-control, n = 17 cells for CD- Kcnmb2 and n = 14 cells for MD- Kcnmb2 . ∗ P

    Techniques Used: Over Expression, Expressing, Fluorescence, Mouse Assay, Infection, Injection

    Overexpression of Kcnmb2 in CA1 region of dorsal hippocampus rescued alterations in synaptic transmission onto CA1 pyramidal neurons in MD F1 mice. (A) Sample sIPSCs recorded from virus-infected CA1 pyramidal neurons (GFP + ) in MD and CD F1 mice. Comparisons of sIPSC frequencies (B) and sIPSC amplitudes (C) between CD and MD F1 neurons infected by control or Kcnmb2 virus. Two-way ANOVA followed by Tukey’s multiple comparisons test, CD-control n = 25, MD-control n = 24, CD- Kcnmb2 n = 10, and MD- Kcnmb2 n = 10 neurons from six mice per group. ∗ P
    Figure Legend Snippet: Overexpression of Kcnmb2 in CA1 region of dorsal hippocampus rescued alterations in synaptic transmission onto CA1 pyramidal neurons in MD F1 mice. (A) Sample sIPSCs recorded from virus-infected CA1 pyramidal neurons (GFP + ) in MD and CD F1 mice. Comparisons of sIPSC frequencies (B) and sIPSC amplitudes (C) between CD and MD F1 neurons infected by control or Kcnmb2 virus. Two-way ANOVA followed by Tukey’s multiple comparisons test, CD-control n = 25, MD-control n = 24, CD- Kcnmb2 n = 10, and MD- Kcnmb2 n = 10 neurons from six mice per group. ∗ P

    Techniques Used: Over Expression, Transmission Assay, Mouse Assay, Infection

    Overexpression of Kcnmb2 in CA1 region of dorsal hippocampus rescued LTP deficits in MD F1 mice. (A) LTP induced with a 100 Hz, 1 s tetanus in four groups of mice. Inserts, sample fEPSP traces recorded at 10 min post-tetanus. Three-way ANOVA with the between-subjects factors paternal diet (MD vs. CD) and AAV treatment (AAV-Kcnmb2 vs. AAV-control), and the within-subjects factor time. n = 11 slices from six MD-control mice, n = 23 slices from eight CD-control mice; n = 13 slices from six MD- Kcnmb2 mice and n = 12 slices from seven CD- Kcnmb2 mice. (B) Comparisons of early LTP (left, 0–10 min post-tetanus) and remaining LTP (right, 50–60 min post-tetanus) in SC-CA1 synapses pathway between CD and MD F1 neurons infected by control or Kcnmb2 virus. Two-way ANOVA followed by Tukey’s multiple comparisons test, n = 11 slices from six MD-control mice, n = 23 slices from eight CD-control mice; n = 13 slices from six MD- Kcnmb2 mice and n = 12 slices from seven CD- Kcnmb2 mice. The input–output curve (C) and paired-pulse ratio (PPR) (D) indicating no significant differences in basal synaptic transmission of SC-CA1 pathway between MD and CD F1 mice receiving control or Kcnmb2 virus injection. Three-way ANOVA, n = 23 slices from six MD-control mice, n = 35 slices from eight CD-control mice, n = 25 slices from six MD- Kcnmb2 mice and n = 28 slices from seven CD- Kcnmb2 mice. Inserts in (C) , sample fEPSPs evoked by 40 μA (100 μs) stimulation delivered to SC-CA1 pathway. Inserts in (D) , sample fEPSPs evoked by paired-pulse stimulation (40 μA, 100 μs) with ISI of 50 ms. ∗∗ P
    Figure Legend Snippet: Overexpression of Kcnmb2 in CA1 region of dorsal hippocampus rescued LTP deficits in MD F1 mice. (A) LTP induced with a 100 Hz, 1 s tetanus in four groups of mice. Inserts, sample fEPSP traces recorded at 10 min post-tetanus. Three-way ANOVA with the between-subjects factors paternal diet (MD vs. CD) and AAV treatment (AAV-Kcnmb2 vs. AAV-control), and the within-subjects factor time. n = 11 slices from six MD-control mice, n = 23 slices from eight CD-control mice; n = 13 slices from six MD- Kcnmb2 mice and n = 12 slices from seven CD- Kcnmb2 mice. (B) Comparisons of early LTP (left, 0–10 min post-tetanus) and remaining LTP (right, 50–60 min post-tetanus) in SC-CA1 synapses pathway between CD and MD F1 neurons infected by control or Kcnmb2 virus. Two-way ANOVA followed by Tukey’s multiple comparisons test, n = 11 slices from six MD-control mice, n = 23 slices from eight CD-control mice; n = 13 slices from six MD- Kcnmb2 mice and n = 12 slices from seven CD- Kcnmb2 mice. The input–output curve (C) and paired-pulse ratio (PPR) (D) indicating no significant differences in basal synaptic transmission of SC-CA1 pathway between MD and CD F1 mice receiving control or Kcnmb2 virus injection. Three-way ANOVA, n = 23 slices from six MD-control mice, n = 35 slices from eight CD-control mice, n = 25 slices from six MD- Kcnmb2 mice and n = 28 slices from seven CD- Kcnmb2 mice. Inserts in (C) , sample fEPSPs evoked by 40 μA (100 μs) stimulation delivered to SC-CA1 pathway. Inserts in (D) , sample fEPSPs evoked by paired-pulse stimulation (40 μA, 100 μs) with ISI of 50 ms. ∗∗ P

    Techniques Used: Over Expression, Mouse Assay, Infection, Transmission Assay, Injection

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    Alomone Labs anti sloβ2
    Distribution of kcnmb2 message and demonstration of β2 (KCNMB2) protein in specific tissues. (A) Quantitative RT-PCR was used to define relative (normalized to β-actin) kcnmb2 message abundance. Each estimate corresponds to mean and standard error for RNA preparations from three mice, each done in triplicate. (B) Total proteins were first immunoprecipitated with the Alomone <t>anti-Sloβ2</t> Ab. Subsequently, aliquots of proteins obtained by IP were then treated with (+) or without (−) N -glycanase, separated by Western blot (WB), and visualized with NeuroMab anti-BKbeta2 N53/32 Ab. All tested tissues reveal β2 protein that is absent in the kcnmb2 −/− mice. Note the apparent diversity of molecular size of glycosylated β2 protein among various tissues. Glycanase-free lanes were omitted for adrenal medulla because of the small size of original tissue samples. Molecular mass is indicated in kilodaltons.
    Anti Sloβ2, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti sloβ2/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti sloβ2 - by Bioz Stars, 2021-12
    94/100 stars
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    Distribution of kcnmb2 message and demonstration of β2 (KCNMB2) protein in specific tissues. (A) Quantitative RT-PCR was used to define relative (normalized to β-actin) kcnmb2 message abundance. Each estimate corresponds to mean and standard error for RNA preparations from three mice, each done in triplicate. (B) Total proteins were first immunoprecipitated with the Alomone anti-Sloβ2 Ab. Subsequently, aliquots of proteins obtained by IP were then treated with (+) or without (−) N -glycanase, separated by Western blot (WB), and visualized with NeuroMab anti-BKbeta2 N53/32 Ab. All tested tissues reveal β2 protein that is absent in the kcnmb2 −/− mice. Note the apparent diversity of molecular size of glycosylated β2 protein among various tissues. Glycanase-free lanes were omitted for adrenal medulla because of the small size of original tissue samples. Molecular mass is indicated in kilodaltons.

    Journal: The Journal of General Physiology

    Article Title: Knockout of the BK β2 subunit abolishes inactivation of BK currents in mouse adrenal chromaffin cells and results in slow-wave burst activity

    doi: 10.1085/jgp.201411253

    Figure Lengend Snippet: Distribution of kcnmb2 message and demonstration of β2 (KCNMB2) protein in specific tissues. (A) Quantitative RT-PCR was used to define relative (normalized to β-actin) kcnmb2 message abundance. Each estimate corresponds to mean and standard error for RNA preparations from three mice, each done in triplicate. (B) Total proteins were first immunoprecipitated with the Alomone anti-Sloβ2 Ab. Subsequently, aliquots of proteins obtained by IP were then treated with (+) or without (−) N -glycanase, separated by Western blot (WB), and visualized with NeuroMab anti-BKbeta2 N53/32 Ab. All tested tissues reveal β2 protein that is absent in the kcnmb2 −/− mice. Note the apparent diversity of molecular size of glycosylated β2 protein among various tissues. Glycanase-free lanes were omitted for adrenal medulla because of the small size of original tissue samples. Molecular mass is indicated in kilodaltons.

    Article Snippet: Abs used for IPs were anti-BKCa (1184–1200; Alomone Labs) and anti-Sloβ2 (KCNMB2; Alomone Labs).

    Techniques: Quantitative RT-PCR, Mouse Assay, Immunoprecipitation, Western Blot

    Different intrinsic excitability of CA1 pyramidal neurons in the MD F1 mice compared to the CD F1 mice. (A) qRT-PCR showing reduced expression of Kcnmb2 in the hippocampus of MD F1 mice. Unpaired t -test, n = 5 mice for each group. (B) Sample recordings showing action potentials evoked by a depolarizing current injection. Upper : the first spike in response to a current injection (250 pA, 50 ms) into CA1 pyramidal neurons of CD F1 mice (black trace) and MD F1 mice (red trace). Lower: spikes trains evoked by a depolarizing current injection (250 pA, 50 ms) into CA1 pyramidal neurons of MD F1 (red trace) and CD F1 (black trace) mice. (C) Reduced action potential half-width in CA1 pyramidal neurons of MD F1 mice compared to CD F1 controls. Unpaired t -test, n = 27 cells from six CD F1 mice and n = 16 cells from five MD F1 mice. (D) Increased peak fAHP in CA1 pyramidal neurons of MD F1 mice. Unpaired t -test, n = 27 cells from six CD F1 mice and n = 17 cells from five MD F1 mice. (E) Reduced spike number in CA1 pyramidal neurons of MD F1 mice. Unpaired t -test, n = 22 cells from six CD F1 mice and n = 16 cells from five MD F1 mice. In (C–E) , depolarizing current was 250 pA and 50 ms in duration. (F) Prolonged latency to first spike in CA1 pyramidal neurons of MD F1 mice. Depolarizing current was 150 pA and 600 ms in duration. Unpaired t- test, n = 26 cells from six CD F1 mice and n = 16 cells from five MD F1 mice. ∗ P

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Overexpression of Kcnmb2 in Dorsal CA1 of Offspring Mice Rescues Hippocampal Dysfunction Caused by a Methyl Donor-Rich Paternal Diet

    doi: 10.3389/fncel.2018.00360

    Figure Lengend Snippet: Different intrinsic excitability of CA1 pyramidal neurons in the MD F1 mice compared to the CD F1 mice. (A) qRT-PCR showing reduced expression of Kcnmb2 in the hippocampus of MD F1 mice. Unpaired t -test, n = 5 mice for each group. (B) Sample recordings showing action potentials evoked by a depolarizing current injection. Upper : the first spike in response to a current injection (250 pA, 50 ms) into CA1 pyramidal neurons of CD F1 mice (black trace) and MD F1 mice (red trace). Lower: spikes trains evoked by a depolarizing current injection (250 pA, 50 ms) into CA1 pyramidal neurons of MD F1 (red trace) and CD F1 (black trace) mice. (C) Reduced action potential half-width in CA1 pyramidal neurons of MD F1 mice compared to CD F1 controls. Unpaired t -test, n = 27 cells from six CD F1 mice and n = 16 cells from five MD F1 mice. (D) Increased peak fAHP in CA1 pyramidal neurons of MD F1 mice. Unpaired t -test, n = 27 cells from six CD F1 mice and n = 17 cells from five MD F1 mice. (E) Reduced spike number in CA1 pyramidal neurons of MD F1 mice. Unpaired t -test, n = 22 cells from six CD F1 mice and n = 16 cells from five MD F1 mice. In (C–E) , depolarizing current was 250 pA and 50 ms in duration. (F) Prolonged latency to first spike in CA1 pyramidal neurons of MD F1 mice. Depolarizing current was 150 pA and 600 ms in duration. Unpaired t- test, n = 26 cells from six CD F1 mice and n = 16 cells from five MD F1 mice. ∗ P

    Article Snippet: For immunofluorescence stainings, we used rabbit anti-KCNMB2 polyclonal antibody (1:800; Alomone labs) in conjunction with Alexa-568-conjugated goat anti-rabbit secondary antibody (1:500; Abcam).

    Techniques: Mouse Assay, Quantitative RT-PCR, Expressing, Injection

    Overexpression of Kcnmb2 in the hippocampus masked MD-F1-associated alterations in intrinsic excitability of CA1 pyramidal neurons (A) Representative images showing AAV-associated GFP (right) and Kcnmb2 expression (left) in dorsal hippocampus. Red, green, and blue fluorescence reflects Kcnmb2-, GFP-, and DAPI-associated signal, respectively. Scale bars represent 100 μm. The insets are higher magnification images of the boxed area. (B) Quantification of the relative Kcnmb2 mRNA expression in the hippocampus after delivery of AAV- Kcnmb2 or AAV-control virus into CA1 region of MD and CD F1 mice. Two-way ANOVA followed by Tukey’s multiple comparisons test, n = 4, 4, 6, and 6 samples for CD-control, MD-control, CD- Kcnmb2 , and MD- Kcnmb2 groups, respectively. (C) Sample recordings in virus-infected CA1 pyramidal neurons (GFP + ) showing action potentials evoked by a depolarizing current injection in CD and MD F1 mice. Left : the first spike in response to a current injection (250 pA, 50 ms) into CA1 pyramidal neuron. Right : spikes trains evoked by a depolarizing current injection (250 pA, 50 ms) into CA1 pyramidal neurons. CD F1 neuron (black) and MD F1 neuron (red) infected by AAV-control (solid traces) or AAV- Kcnmb2 (dashed traces) virus. Comparisons of action potential half-width (D) , fAHP (E) , and spike numbers (F) between CD and MD F1 neurons infected by control or Kcnmb2 virus. Two-way ANOVA followed by Sidak’s multiple comparisons test, 5–6 mice per group. AP half-width: n = 21 cells for CD-control, n = 13 cells for MD-control, n = 16 cells for CD- Kcnmb2 and n = 13 cells for MD- Kcnmb2 ; fAHP: n = 14 cells for CD-control, n = 15 cells for MD-control, n = 16 cells for CD- Kcnmb2 and n = 14 cells for MD- Kcnmb2 ; Spike number: n = 20 cells for CD-control, n = 17 cells for MD-control, n = 17 cells for CD- Kcnmb2 and n = 14 cells for MD- Kcnmb2 . ∗ P

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Overexpression of Kcnmb2 in Dorsal CA1 of Offspring Mice Rescues Hippocampal Dysfunction Caused by a Methyl Donor-Rich Paternal Diet

    doi: 10.3389/fncel.2018.00360

    Figure Lengend Snippet: Overexpression of Kcnmb2 in the hippocampus masked MD-F1-associated alterations in intrinsic excitability of CA1 pyramidal neurons (A) Representative images showing AAV-associated GFP (right) and Kcnmb2 expression (left) in dorsal hippocampus. Red, green, and blue fluorescence reflects Kcnmb2-, GFP-, and DAPI-associated signal, respectively. Scale bars represent 100 μm. The insets are higher magnification images of the boxed area. (B) Quantification of the relative Kcnmb2 mRNA expression in the hippocampus after delivery of AAV- Kcnmb2 or AAV-control virus into CA1 region of MD and CD F1 mice. Two-way ANOVA followed by Tukey’s multiple comparisons test, n = 4, 4, 6, and 6 samples for CD-control, MD-control, CD- Kcnmb2 , and MD- Kcnmb2 groups, respectively. (C) Sample recordings in virus-infected CA1 pyramidal neurons (GFP + ) showing action potentials evoked by a depolarizing current injection in CD and MD F1 mice. Left : the first spike in response to a current injection (250 pA, 50 ms) into CA1 pyramidal neuron. Right : spikes trains evoked by a depolarizing current injection (250 pA, 50 ms) into CA1 pyramidal neurons. CD F1 neuron (black) and MD F1 neuron (red) infected by AAV-control (solid traces) or AAV- Kcnmb2 (dashed traces) virus. Comparisons of action potential half-width (D) , fAHP (E) , and spike numbers (F) between CD and MD F1 neurons infected by control or Kcnmb2 virus. Two-way ANOVA followed by Sidak’s multiple comparisons test, 5–6 mice per group. AP half-width: n = 21 cells for CD-control, n = 13 cells for MD-control, n = 16 cells for CD- Kcnmb2 and n = 13 cells for MD- Kcnmb2 ; fAHP: n = 14 cells for CD-control, n = 15 cells for MD-control, n = 16 cells for CD- Kcnmb2 and n = 14 cells for MD- Kcnmb2 ; Spike number: n = 20 cells for CD-control, n = 17 cells for MD-control, n = 17 cells for CD- Kcnmb2 and n = 14 cells for MD- Kcnmb2 . ∗ P

    Article Snippet: For immunofluorescence stainings, we used rabbit anti-KCNMB2 polyclonal antibody (1:800; Alomone labs) in conjunction with Alexa-568-conjugated goat anti-rabbit secondary antibody (1:500; Abcam).

    Techniques: Over Expression, Expressing, Fluorescence, Mouse Assay, Infection, Injection

    Overexpression of Kcnmb2 in CA1 region of dorsal hippocampus rescued alterations in synaptic transmission onto CA1 pyramidal neurons in MD F1 mice. (A) Sample sIPSCs recorded from virus-infected CA1 pyramidal neurons (GFP + ) in MD and CD F1 mice. Comparisons of sIPSC frequencies (B) and sIPSC amplitudes (C) between CD and MD F1 neurons infected by control or Kcnmb2 virus. Two-way ANOVA followed by Tukey’s multiple comparisons test, CD-control n = 25, MD-control n = 24, CD- Kcnmb2 n = 10, and MD- Kcnmb2 n = 10 neurons from six mice per group. ∗ P

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Overexpression of Kcnmb2 in Dorsal CA1 of Offspring Mice Rescues Hippocampal Dysfunction Caused by a Methyl Donor-Rich Paternal Diet

    doi: 10.3389/fncel.2018.00360

    Figure Lengend Snippet: Overexpression of Kcnmb2 in CA1 region of dorsal hippocampus rescued alterations in synaptic transmission onto CA1 pyramidal neurons in MD F1 mice. (A) Sample sIPSCs recorded from virus-infected CA1 pyramidal neurons (GFP + ) in MD and CD F1 mice. Comparisons of sIPSC frequencies (B) and sIPSC amplitudes (C) between CD and MD F1 neurons infected by control or Kcnmb2 virus. Two-way ANOVA followed by Tukey’s multiple comparisons test, CD-control n = 25, MD-control n = 24, CD- Kcnmb2 n = 10, and MD- Kcnmb2 n = 10 neurons from six mice per group. ∗ P

    Article Snippet: For immunofluorescence stainings, we used rabbit anti-KCNMB2 polyclonal antibody (1:800; Alomone labs) in conjunction with Alexa-568-conjugated goat anti-rabbit secondary antibody (1:500; Abcam).

    Techniques: Over Expression, Transmission Assay, Mouse Assay, Infection

    Overexpression of Kcnmb2 in CA1 region of dorsal hippocampus rescued LTP deficits in MD F1 mice. (A) LTP induced with a 100 Hz, 1 s tetanus in four groups of mice. Inserts, sample fEPSP traces recorded at 10 min post-tetanus. Three-way ANOVA with the between-subjects factors paternal diet (MD vs. CD) and AAV treatment (AAV-Kcnmb2 vs. AAV-control), and the within-subjects factor time. n = 11 slices from six MD-control mice, n = 23 slices from eight CD-control mice; n = 13 slices from six MD- Kcnmb2 mice and n = 12 slices from seven CD- Kcnmb2 mice. (B) Comparisons of early LTP (left, 0–10 min post-tetanus) and remaining LTP (right, 50–60 min post-tetanus) in SC-CA1 synapses pathway between CD and MD F1 neurons infected by control or Kcnmb2 virus. Two-way ANOVA followed by Tukey’s multiple comparisons test, n = 11 slices from six MD-control mice, n = 23 slices from eight CD-control mice; n = 13 slices from six MD- Kcnmb2 mice and n = 12 slices from seven CD- Kcnmb2 mice. The input–output curve (C) and paired-pulse ratio (PPR) (D) indicating no significant differences in basal synaptic transmission of SC-CA1 pathway between MD and CD F1 mice receiving control or Kcnmb2 virus injection. Three-way ANOVA, n = 23 slices from six MD-control mice, n = 35 slices from eight CD-control mice, n = 25 slices from six MD- Kcnmb2 mice and n = 28 slices from seven CD- Kcnmb2 mice. Inserts in (C) , sample fEPSPs evoked by 40 μA (100 μs) stimulation delivered to SC-CA1 pathway. Inserts in (D) , sample fEPSPs evoked by paired-pulse stimulation (40 μA, 100 μs) with ISI of 50 ms. ∗∗ P

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Overexpression of Kcnmb2 in Dorsal CA1 of Offspring Mice Rescues Hippocampal Dysfunction Caused by a Methyl Donor-Rich Paternal Diet

    doi: 10.3389/fncel.2018.00360

    Figure Lengend Snippet: Overexpression of Kcnmb2 in CA1 region of dorsal hippocampus rescued LTP deficits in MD F1 mice. (A) LTP induced with a 100 Hz, 1 s tetanus in four groups of mice. Inserts, sample fEPSP traces recorded at 10 min post-tetanus. Three-way ANOVA with the between-subjects factors paternal diet (MD vs. CD) and AAV treatment (AAV-Kcnmb2 vs. AAV-control), and the within-subjects factor time. n = 11 slices from six MD-control mice, n = 23 slices from eight CD-control mice; n = 13 slices from six MD- Kcnmb2 mice and n = 12 slices from seven CD- Kcnmb2 mice. (B) Comparisons of early LTP (left, 0–10 min post-tetanus) and remaining LTP (right, 50–60 min post-tetanus) in SC-CA1 synapses pathway between CD and MD F1 neurons infected by control or Kcnmb2 virus. Two-way ANOVA followed by Tukey’s multiple comparisons test, n = 11 slices from six MD-control mice, n = 23 slices from eight CD-control mice; n = 13 slices from six MD- Kcnmb2 mice and n = 12 slices from seven CD- Kcnmb2 mice. The input–output curve (C) and paired-pulse ratio (PPR) (D) indicating no significant differences in basal synaptic transmission of SC-CA1 pathway between MD and CD F1 mice receiving control or Kcnmb2 virus injection. Three-way ANOVA, n = 23 slices from six MD-control mice, n = 35 slices from eight CD-control mice, n = 25 slices from six MD- Kcnmb2 mice and n = 28 slices from seven CD- Kcnmb2 mice. Inserts in (C) , sample fEPSPs evoked by 40 μA (100 μs) stimulation delivered to SC-CA1 pathway. Inserts in (D) , sample fEPSPs evoked by paired-pulse stimulation (40 μA, 100 μs) with ISI of 50 ms. ∗∗ P

    Article Snippet: For immunofluorescence stainings, we used rabbit anti-KCNMB2 polyclonal antibody (1:800; Alomone labs) in conjunction with Alexa-568-conjugated goat anti-rabbit secondary antibody (1:500; Abcam).

    Techniques: Over Expression, Mouse Assay, Infection, Transmission Assay, Injection