ω conotoxin gvia  (Alomone Labs)


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    Structured Review

    Alomone Labs ω conotoxin gvia
    Isosaponarin inhibits the [Ca 2+ ] C and the N- and P/Q-type Ca 2+ channel-mediated glutamate release. ( A ) [Ca 2+ ] C was monitored using Fura-2. Synaptosomes were stimulated with 4-AP (1 mM) in the absence (control) or presence of isosaponarin that was added 10 min before stimulation. ( B ) Effect of isosaponarin on 4-AP-evoked glutamate release in the presence of the Ca 2+ channel toxins <t>ω-conotoxin</t> <t>GVIA</t> or ω-agatoxin IVA, which was added either alone or in combination. Data are presented as mean ± SEM (n = 5 per group). *** p
    ω Conotoxin Gvia, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "The Effect of Isosaponarin Derived from Wasabi Leaves on Glutamate Release in Rat Synaptosomes and Its Underlying Mechanism"

    Article Title: The Effect of Isosaponarin Derived from Wasabi Leaves on Glutamate Release in Rat Synaptosomes and Its Underlying Mechanism

    Journal: International Journal of Molecular Sciences

    doi: 10.3390/ijms23158752

    Isosaponarin inhibits the [Ca 2+ ] C and the N- and P/Q-type Ca 2+ channel-mediated glutamate release. ( A ) [Ca 2+ ] C was monitored using Fura-2. Synaptosomes were stimulated with 4-AP (1 mM) in the absence (control) or presence of isosaponarin that was added 10 min before stimulation. ( B ) Effect of isosaponarin on 4-AP-evoked glutamate release in the presence of the Ca 2+ channel toxins ω-conotoxin GVIA or ω-agatoxin IVA, which was added either alone or in combination. Data are presented as mean ± SEM (n = 5 per group). *** p
    Figure Legend Snippet: Isosaponarin inhibits the [Ca 2+ ] C and the N- and P/Q-type Ca 2+ channel-mediated glutamate release. ( A ) [Ca 2+ ] C was monitored using Fura-2. Synaptosomes were stimulated with 4-AP (1 mM) in the absence (control) or presence of isosaponarin that was added 10 min before stimulation. ( B ) Effect of isosaponarin on 4-AP-evoked glutamate release in the presence of the Ca 2+ channel toxins ω-conotoxin GVIA or ω-agatoxin IVA, which was added either alone or in combination. Data are presented as mean ± SEM (n = 5 per group). *** p

    Techniques Used:

    2) Product Images from "Distinct mechanisms of CB1 and GABAB receptor presynaptic modulation of striatal indirect pathway projections to mouse Globus Pallidus"

    Article Title: Distinct mechanisms of CB1 and GABAB receptor presynaptic modulation of striatal indirect pathway projections to mouse Globus Pallidus

    Journal: bioRxiv

    doi: 10.1101/2022.07.21.500979

    P/Q-type are the predominant VGCC controlling presynaptic Ca 2+ and GABAergic transmission at the indirect pathway projections to the GPe. A: Timecourse of VGCC blocker application effects on PreCaTs and raw photometry traces. B: Summary of drug effects: baseline, last 2 minutes of drug, last 2 minutes of washout. Blockade of P/Q -type VGGCs (Agatoxin, n = 6 slices) significantly decreased PreCaTs from baseline, whereas no significant effect on PreCaTs was observed by blocking N-type VGCCs (Conotoxin, n= 8 slices) or L-type VGCCs (Nifedipine, n = 5 slices). C: Timecourse of VGCC blocker application effects on oIPSCs and raw electrophysiological traces. D: Comparison of drug effects: baseline, last 2 minutes of drug, last 2 minutes of washout. Blockade of P/Q -type VGGCs (Agatoxin, n = 5 cells) significantly decreased PreCaTs from baseline, and smaller but significant effects were induced by blocking N-type VGCCs (Conotoxin, n = 5 cells) or L-type VGCCs (Nifedipine, n = 5 cells). * p
    Figure Legend Snippet: P/Q-type are the predominant VGCC controlling presynaptic Ca 2+ and GABAergic transmission at the indirect pathway projections to the GPe. A: Timecourse of VGCC blocker application effects on PreCaTs and raw photometry traces. B: Summary of drug effects: baseline, last 2 minutes of drug, last 2 minutes of washout. Blockade of P/Q -type VGGCs (Agatoxin, n = 6 slices) significantly decreased PreCaTs from baseline, whereas no significant effect on PreCaTs was observed by blocking N-type VGCCs (Conotoxin, n= 8 slices) or L-type VGCCs (Nifedipine, n = 5 slices). C: Timecourse of VGCC blocker application effects on oIPSCs and raw electrophysiological traces. D: Comparison of drug effects: baseline, last 2 minutes of drug, last 2 minutes of washout. Blockade of P/Q -type VGGCs (Agatoxin, n = 5 cells) significantly decreased PreCaTs from baseline, and smaller but significant effects were induced by blocking N-type VGCCs (Conotoxin, n = 5 cells) or L-type VGCCs (Nifedipine, n = 5 cells). * p

    Techniques Used: Transmission Assay, Blocking Assay

    3) Product Images from "Hydrogen Peroxide Scavenging Restores N-Type Calcium Channels in Cardiac Vagal Postganglionic Neurons and Mitigates Myocardial Infarction-Evoked Ventricular Arrhythmias in Type 2 Diabetes Mellitus"

    Article Title: Hydrogen Peroxide Scavenging Restores N-Type Calcium Channels in Cardiac Vagal Postganglionic Neurons and Mitigates Myocardial Infarction-Evoked Ventricular Arrhythmias in Type 2 Diabetes Mellitus

    Journal: Frontiers in Cardiovascular Medicine

    doi: 10.3389/fcvm.2022.871852

    Reduction of the H 2 O 2 levels through transfection of Ad.CAT gene increased T2DM-reduced N-type Ca 2+ currents in CVP neurons in T2DM rats. BaCl 2 replaced CaCl 2 in the extracellular solution for Ca 2+ current recording. (A) Original whole-cell patch-clamp recording of Ca 2+ currents from sham, T2DM, and T2DM+Ad.CAT rats. (B) Current-voltage (I–V) curve of N-type Ca 2+ currents in CVP neurons from all groups of rats. (C) Quantitative data of total Ca 2+ currents, other types of Ca 2+ currents, and N-type Ca 2+ currents elicited by 500-ms test pulse at 0 mV from holding potential of −80 mV in CVP neurons from all groups. ω-conotoxin GVIA, a specific N-type Ca 2+ channel blocker, was used to block the N-type Ca 2+ channel. N-type Ca 2+ currents were obtained by subtracting Ca 2+ currents under treatment of ω-conotoxin GVIA from total Ca 2+ currents. N = 8 neurons from 6 rats per group; data are means ± SEM. Statistical significance was determined by two-way repeated measures ANOVA with post-hoc Bonferroni test for data presented in (B) . Statistical significance was determined by one-way ANOVA with post-hoc Bonferroni test for data presented in (C) . * P
    Figure Legend Snippet: Reduction of the H 2 O 2 levels through transfection of Ad.CAT gene increased T2DM-reduced N-type Ca 2+ currents in CVP neurons in T2DM rats. BaCl 2 replaced CaCl 2 in the extracellular solution for Ca 2+ current recording. (A) Original whole-cell patch-clamp recording of Ca 2+ currents from sham, T2DM, and T2DM+Ad.CAT rats. (B) Current-voltage (I–V) curve of N-type Ca 2+ currents in CVP neurons from all groups of rats. (C) Quantitative data of total Ca 2+ currents, other types of Ca 2+ currents, and N-type Ca 2+ currents elicited by 500-ms test pulse at 0 mV from holding potential of −80 mV in CVP neurons from all groups. ω-conotoxin GVIA, a specific N-type Ca 2+ channel blocker, was used to block the N-type Ca 2+ channel. N-type Ca 2+ currents were obtained by subtracting Ca 2+ currents under treatment of ω-conotoxin GVIA from total Ca 2+ currents. N = 8 neurons from 6 rats per group; data are means ± SEM. Statistical significance was determined by two-way repeated measures ANOVA with post-hoc Bonferroni test for data presented in (B) . Statistical significance was determined by one-way ANOVA with post-hoc Bonferroni test for data presented in (C) . * P

    Techniques Used: Transfection, Patch Clamp, Blocking Assay

    4) Product Images from "Presynaptic HCN channels constrain GABAergic synaptic transmission in pyramidal cells of the medial prefrontal cortex"

    Article Title: Presynaptic HCN channels constrain GABAergic synaptic transmission in pyramidal cells of the medial prefrontal cortex

    Journal: Biology Open

    doi: 10.1242/bio.058840

    T-type Ca2+ channel blockers occlude the increment in mIPSC frequency induced by blocking HCN channels. (A) Representative traces of mIPSCs recorded in pyramidal cell. Holding potential: −70 mV. (B) The cumulative fraction distribution of inter-event intervals (left) and amplitude (right) of mIPSCs before (Control), during (ZD7288, 30 µM), and after co-application of ZD7288 with T-type Ca 2+ channel selective blocker mibefradil (Mib; 10 µM) ( ZD+Mib ). (C,D) Bar graph demonstrating the effects of co-application of ZD7288 and Ca 2+ channel blockers for T-type (pimozide, 1 µM; mibefradil, 10 µM), P/Q-type (ω-agatoxin IVA, 500 nM), N-type (ω-Conotoxin GVIA, 500 nM), and L-type (nifedipine, 2 mM) Ca 2+ channels on the frequency (C) and amplitude (D) of mIPSCs. Open circles for individual cells and bar for grouped data. ** P
    Figure Legend Snippet: T-type Ca2+ channel blockers occlude the increment in mIPSC frequency induced by blocking HCN channels. (A) Representative traces of mIPSCs recorded in pyramidal cell. Holding potential: −70 mV. (B) The cumulative fraction distribution of inter-event intervals (left) and amplitude (right) of mIPSCs before (Control), during (ZD7288, 30 µM), and after co-application of ZD7288 with T-type Ca 2+ channel selective blocker mibefradil (Mib; 10 µM) ( ZD+Mib ). (C,D) Bar graph demonstrating the effects of co-application of ZD7288 and Ca 2+ channel blockers for T-type (pimozide, 1 µM; mibefradil, 10 µM), P/Q-type (ω-agatoxin IVA, 500 nM), N-type (ω-Conotoxin GVIA, 500 nM), and L-type (nifedipine, 2 mM) Ca 2+ channels on the frequency (C) and amplitude (D) of mIPSCs. Open circles for individual cells and bar for grouped data. ** P

    Techniques Used: Blocking Assay

    5) Product Images from "Natural Product Isoliquiritigenin Activates GABAB Receptors to Decrease Voltage-Gate Ca2+ Channels and Glutamate Release in Rat Cerebrocortical Nerve Terminals"

    Article Title: Natural Product Isoliquiritigenin Activates GABAB Receptors to Decrease Voltage-Gate Ca2+ Channels and Glutamate Release in Rat Cerebrocortical Nerve Terminals

    Journal: Biomolecules

    doi: 10.3390/biom11101537

    ISL-mediated inhibition of 4-AP-evoked glutamate release in the presence of N-, P/Q-, or L-type VGCC blockade. ( A ) 4-AP-evoked glutamate release from synaptosomes incubated in the presence of 1.2 mM CaCl 2 , and in the absence (control) or presence of 10 µM ISL, 2 µM ω-conotoxin GVIA, or both ( A ); 10 µM ISL, 0.5 µM ω-agatoxin IVA, or both ( B ); or 10 µM ISL, 1 µM nifedipine, or both ( C ). Insets compare the effects of N-, P/Q-, or L-type VGCC blockade on 4-AP-evoked glutamate release, or the inhibition by ISL (% control release 5 min after 4-AP addition). Data are the mean ± SEM (n = 5 per group). ***, p
    Figure Legend Snippet: ISL-mediated inhibition of 4-AP-evoked glutamate release in the presence of N-, P/Q-, or L-type VGCC blockade. ( A ) 4-AP-evoked glutamate release from synaptosomes incubated in the presence of 1.2 mM CaCl 2 , and in the absence (control) or presence of 10 µM ISL, 2 µM ω-conotoxin GVIA, or both ( A ); 10 µM ISL, 0.5 µM ω-agatoxin IVA, or both ( B ); or 10 µM ISL, 1 µM nifedipine, or both ( C ). Insets compare the effects of N-, P/Q-, or L-type VGCC blockade on 4-AP-evoked glutamate release, or the inhibition by ISL (% control release 5 min after 4-AP addition). Data are the mean ± SEM (n = 5 per group). ***, p

    Techniques Used: Inhibition, Incubation

    6) Product Images from "Auxiliary α2δ1 and α2δ3 Subunits of Calcium Channels Drive Excitatory and Inhibitory Neuronal Network Development"

    Article Title: Auxiliary α2δ1 and α2δ3 Subunits of Calcium Channels Drive Excitatory and Inhibitory Neuronal Network Development

    Journal: The Journal of Neuroscience

    doi: 10.1523/JNEUROSCI.1707-19.2020

    Overexpression of α2δ1 and α2δ3 subunits selectively increases the frequency of neurotransmitter release in excitatory and inhibitory synapses, respectively. A , A timeline of infection (green triangle) and electrophysiological recordings (orange triangles). B , Representative traces of mEPSCs recorded at DIV14 in control and α2δ1- and α2δ3-overexpressing cultures. C , D , The mean frequency ( C ) and the amplitude ( D ) of mEPSCs in α2δ1- and α2δ3-overexpressing cultures. E , Representative traces of mIPSCs recorded at DIV14 in control and α2δ1- and α2δ3-overexpressing cultures. F , G , The mean frequency ( F ) and the amplitude ( G ) of mIPSCs in α2δ1- and α2δ3-overexpressing cultures. H , The increase in the mEPSC and mIPSC frequency by α2δ1 and a2d3 subunits, respectively, is caused by bigger contribution of high voltage-activated VGCCs as demonstrated by Cd 2+ -induced reduction to respective values obtained in controls in the presence of Cd 2+ . I , J , The effects of α2δ1 and α2δ3 overexpression on the frequency of mEPSCs ( E ) and mIPSCs ( F ) are mediated by P/Q- and N-type calcium channels, respectively. CNTX, conotoxin, AGTX, agatoxin. * p
    Figure Legend Snippet: Overexpression of α2δ1 and α2δ3 subunits selectively increases the frequency of neurotransmitter release in excitatory and inhibitory synapses, respectively. A , A timeline of infection (green triangle) and electrophysiological recordings (orange triangles). B , Representative traces of mEPSCs recorded at DIV14 in control and α2δ1- and α2δ3-overexpressing cultures. C , D , The mean frequency ( C ) and the amplitude ( D ) of mEPSCs in α2δ1- and α2δ3-overexpressing cultures. E , Representative traces of mIPSCs recorded at DIV14 in control and α2δ1- and α2δ3-overexpressing cultures. F , G , The mean frequency ( F ) and the amplitude ( G ) of mIPSCs in α2δ1- and α2δ3-overexpressing cultures. H , The increase in the mEPSC and mIPSC frequency by α2δ1 and a2d3 subunits, respectively, is caused by bigger contribution of high voltage-activated VGCCs as demonstrated by Cd 2+ -induced reduction to respective values obtained in controls in the presence of Cd 2+ . I , J , The effects of α2δ1 and α2δ3 overexpression on the frequency of mEPSCs ( E ) and mIPSCs ( F ) are mediated by P/Q- and N-type calcium channels, respectively. CNTX, conotoxin, AGTX, agatoxin. * p

    Techniques Used: Over Expression, Infection

    7) Product Images from "Isoflurane Inhibits Dopaminergic Synaptic Vesicle Exocytosis Coupled to CaV2.1 and CaV2.2 in Rat Midbrain Neurons"

    Article Title: Isoflurane Inhibits Dopaminergic Synaptic Vesicle Exocytosis Coupled to CaV2.1 and CaV2.2 in Rat Midbrain Neurons

    Journal: eNeuro

    doi: 10.1523/ENEURO.0278-18.2018

    Ca V 2.1 and Ca V 2.2 contribute to SV exocytosis in VTA neurons. A , Schematic of protocol using trains of 100 APs in the absence (black) or presence of ω-conotoxin GVIA (cono, 1 μM, purple bar) alone, ω-agatoxin IVA (aga, 400 nM, orange bar) alone, or both toxins together. B , Comparison of the effect of conotoxin and agatoxin on dopaminergic and non-dopaminergic neurons. The combination of conotoxin and agatoxin abolished exocytosis in both dopaminergic (DA) and non-dopaminergic (non-DA) neurons; **** p
    Figure Legend Snippet: Ca V 2.1 and Ca V 2.2 contribute to SV exocytosis in VTA neurons. A , Schematic of protocol using trains of 100 APs in the absence (black) or presence of ω-conotoxin GVIA (cono, 1 μM, purple bar) alone, ω-agatoxin IVA (aga, 400 nM, orange bar) alone, or both toxins together. B , Comparison of the effect of conotoxin and agatoxin on dopaminergic and non-dopaminergic neurons. The combination of conotoxin and agatoxin abolished exocytosis in both dopaminergic (DA) and non-dopaminergic (non-DA) neurons; **** p

    Techniques Used:

    8) Product Images from "Isoflurane Inhibits Dopaminergic Synaptic Vesicle Exocytosis Coupled to CaV2.1 and CaV2.2 in Rat Midbrain Neurons"

    Article Title: Isoflurane Inhibits Dopaminergic Synaptic Vesicle Exocytosis Coupled to CaV2.1 and CaV2.2 in Rat Midbrain Neurons

    Journal: eNeuro

    doi: 10.1523/ENEURO.0278-18.2018

    Ca V 2.1 and Ca V 2.2 contribute to SV exocytosis in VTA neurons. A , Schematic of protocol using trains of 100 APs in the absence (black) or presence of ω-conotoxin GVIA (cono, 1 μM, purple bar) alone, ω-agatoxin IVA (aga, 400 nM, orange bar) alone, or both toxins together. B , Comparison of the effect of conotoxin and agatoxin on dopaminergic and non-dopaminergic neurons. The combination of conotoxin and agatoxin abolished exocytosis in both dopaminergic (DA) and non-dopaminergic (non-DA) neurons; **** p
    Figure Legend Snippet: Ca V 2.1 and Ca V 2.2 contribute to SV exocytosis in VTA neurons. A , Schematic of protocol using trains of 100 APs in the absence (black) or presence of ω-conotoxin GVIA (cono, 1 μM, purple bar) alone, ω-agatoxin IVA (aga, 400 nM, orange bar) alone, or both toxins together. B , Comparison of the effect of conotoxin and agatoxin on dopaminergic and non-dopaminergic neurons. The combination of conotoxin and agatoxin abolished exocytosis in both dopaminergic (DA) and non-dopaminergic (non-DA) neurons; **** p

    Techniques Used:

    9) Product Images from "CaV2.1 α1 Subunit Expression Regulates Presynaptic CaV2.1 Abundance and Synaptic Strength at a Central Synapse"

    Article Title: CaV2.1 α1 Subunit Expression Regulates Presynaptic CaV2.1 Abundance and Synaptic Strength at a Central Synapse

    Journal: Neuron

    doi: 10.1016/j.neuron.2018.11.028

    Ca V 2.1 α 1 OE Results in Increased Ca V 2.1 Currents and Almost Complete Loss of Ca V 2.2 Currents at the P7 Calyx (A) Schematic of auditory brainstem. Globular bushy cells (GBC) which give rise to the calyx of Held are depicted for clarity. (B) (Top) Developmental transition of calyx of Held from multiple Ca V 2 subtype synapse to Ca V 2 exclusive at onset of hearing (P12). (Bottom) Experimental timeline from virus injection into VCN at P1 to electrophysiological recordings at P7. (C) Schematic of HdAd constructs expressing either Ca V 2.1 or Ca V 2.2 cDNAs (light blue) driven by the Punisher overexpression cassette and mEGFP marker (green) driven by a 470 bp human synapsin promoter; arrows indicate viral inverted terminal repeat sequences; J indicates the viral genome packaging signal sequence. (D) Pharmacological isolation of Ca V 2 isoforms expressed in the presynaptic terminal at P7 in control (n = 5), Ca V 2.1 α 1 OE (n = 4), or Ca V 2.2 α 1 OE (n = 6). Average traces before application of blockers (black), after applying 200 nM ω-agatoxin IVA to specifically block Ca V 2.1 (Aga, brown), after 2 μM ω-conotoxin GVIA to block Ca V 2.2 (Cono, blue) and 50 μM Cd 2+ to block the remaining Ca 2+ currents (gray). (E–H) Ca 2+ current amplitudes before blocker application (Ca V 2.1 α 1 OE versus control, p = 0.0328 Mood’s median test and post hoc Bonferroni test), Aga-sensitive Ca 2+ current amplitudes (Ca V 2.1 α 1 OE versus control, p = 0.0328), Cono-sensitive Ca 2+ current amplitudes (Ca V 2.1 α 1 OE versus control, p = 0.0054), and Cd 2+ -sensitive Ca 2+ current amplitudes (n.s., Kruskal Wallis and post hoc Dunn’s test, n = 5/4/6 for control, Ca V 2.1 α 1 OE, and Ca V 2.2 α 1 OE, respectively). (I) Relative Ca 2+ current fractions sensitive to respective blockers. (J and K) Average Ca 2+ current traces to 10 ms step depolarizations from −80 mV holding to voltages between −50 and +40 mV for control (J and K, left, black) and Ca V 2.1 α 1 OE (J, right, brown) or Ca V 2.2 α 1 OE (K, right, blue). (L–O) Current-voltage relationships of either steady-state Ca 2+ currents (L and N) or tail Ca 2+ currents (M and O, n = 10 for control, Ca V 2.1 α 1 OE and Ca V 2.2 α 1 .
    Figure Legend Snippet: Ca V 2.1 α 1 OE Results in Increased Ca V 2.1 Currents and Almost Complete Loss of Ca V 2.2 Currents at the P7 Calyx (A) Schematic of auditory brainstem. Globular bushy cells (GBC) which give rise to the calyx of Held are depicted for clarity. (B) (Top) Developmental transition of calyx of Held from multiple Ca V 2 subtype synapse to Ca V 2 exclusive at onset of hearing (P12). (Bottom) Experimental timeline from virus injection into VCN at P1 to electrophysiological recordings at P7. (C) Schematic of HdAd constructs expressing either Ca V 2.1 or Ca V 2.2 cDNAs (light blue) driven by the Punisher overexpression cassette and mEGFP marker (green) driven by a 470 bp human synapsin promoter; arrows indicate viral inverted terminal repeat sequences; J indicates the viral genome packaging signal sequence. (D) Pharmacological isolation of Ca V 2 isoforms expressed in the presynaptic terminal at P7 in control (n = 5), Ca V 2.1 α 1 OE (n = 4), or Ca V 2.2 α 1 OE (n = 6). Average traces before application of blockers (black), after applying 200 nM ω-agatoxin IVA to specifically block Ca V 2.1 (Aga, brown), after 2 μM ω-conotoxin GVIA to block Ca V 2.2 (Cono, blue) and 50 μM Cd 2+ to block the remaining Ca 2+ currents (gray). (E–H) Ca 2+ current amplitudes before blocker application (Ca V 2.1 α 1 OE versus control, p = 0.0328 Mood’s median test and post hoc Bonferroni test), Aga-sensitive Ca 2+ current amplitudes (Ca V 2.1 α 1 OE versus control, p = 0.0328), Cono-sensitive Ca 2+ current amplitudes (Ca V 2.1 α 1 OE versus control, p = 0.0054), and Cd 2+ -sensitive Ca 2+ current amplitudes (n.s., Kruskal Wallis and post hoc Dunn’s test, n = 5/4/6 for control, Ca V 2.1 α 1 OE, and Ca V 2.2 α 1 OE, respectively). (I) Relative Ca 2+ current fractions sensitive to respective blockers. (J and K) Average Ca 2+ current traces to 10 ms step depolarizations from −80 mV holding to voltages between −50 and +40 mV for control (J and K, left, black) and Ca V 2.1 α 1 OE (J, right, brown) or Ca V 2.2 α 1 OE (K, right, blue). (L–O) Current-voltage relationships of either steady-state Ca 2+ currents (L and N) or tail Ca 2+ currents (M and O, n = 10 for control, Ca V 2.1 α 1 OE and Ca V 2.2 α 1 .

    Techniques Used: Injection, Construct, Expressing, Over Expression, Marker, Sequencing, Isolation, Blocking Assay, Mass Spectrometry

    Ca V 2.2 α 1 OE Results in Slight Loss of Ca V 2.1 Currents, while Ca V 2.1 α 1 OE Results in an Increase in Ca V 2.1 Currents at P20/21 Calyx (A) Experimental timeline from virus injection into CN at P14 to electrophysiological recordings at P20/21. (B) Confocal images of brainstem slices injected with Ca V 2.1 α 1 OE construct. (Left) CN injection site. (Right) Contralateral MNTB with mEGFP-expressing calyx of Held terminals. (C) Pharmacological isolation of Ca V 2 isoforms expressed in the presynaptic terminal at P21 in control (n = 3) and Ca V 2.2 α 1 OE (n = 3). Average current traces before application of blockers (black), after applying 200 nM ω-agatoxin IVA to specifically block Ca V 2.1 (Aga, brown) and after applying 2 μM ω-conotoxin GVIA to specifically block Ca V 2.2 (Cono, blue). (D) Ca 2+ current amplitudes before blocker application (black, n.s., two-tailed t test), Aga-sensitive Ca 2+ current amplitudes (brown, n.s., one-tailed t test), and Cono-sensitive Ca 2+ current amplitudes (blue, 0.016, one-tailed t test). (E) Relative Ca 2+ current fractions sensitive to blockers. (F) Average Ca 2+ -current traces to 10 ms step depolarizations from −80 mV holding to voltages between −50 and +40 mV for control (left, n = 9) and Ca V 2.1 α 1 OE (right, n = 10). (G and H) Current-voltage relationships of either peak Ca 2+ currents (G) or tail Ca 2+ .
    Figure Legend Snippet: Ca V 2.2 α 1 OE Results in Slight Loss of Ca V 2.1 Currents, while Ca V 2.1 α 1 OE Results in an Increase in Ca V 2.1 Currents at P20/21 Calyx (A) Experimental timeline from virus injection into CN at P14 to electrophysiological recordings at P20/21. (B) Confocal images of brainstem slices injected with Ca V 2.1 α 1 OE construct. (Left) CN injection site. (Right) Contralateral MNTB with mEGFP-expressing calyx of Held terminals. (C) Pharmacological isolation of Ca V 2 isoforms expressed in the presynaptic terminal at P21 in control (n = 3) and Ca V 2.2 α 1 OE (n = 3). Average current traces before application of blockers (black), after applying 200 nM ω-agatoxin IVA to specifically block Ca V 2.1 (Aga, brown) and after applying 2 μM ω-conotoxin GVIA to specifically block Ca V 2.2 (Cono, blue). (D) Ca 2+ current amplitudes before blocker application (black, n.s., two-tailed t test), Aga-sensitive Ca 2+ current amplitudes (brown, n.s., one-tailed t test), and Cono-sensitive Ca 2+ current amplitudes (blue, 0.016, one-tailed t test). (E) Relative Ca 2+ current fractions sensitive to blockers. (F) Average Ca 2+ -current traces to 10 ms step depolarizations from −80 mV holding to voltages between −50 and +40 mV for control (left, n = 9) and Ca V 2.1 α 1 OE (right, n = 10). (G and H) Current-voltage relationships of either peak Ca 2+ currents (G) or tail Ca 2+ .

    Techniques Used: Injection, Construct, Expressing, Isolation, Blocking Assay, Two Tailed Test, One-tailed Test, Mass Spectrometry

    10) Product Images from "GABAB receptors modulate Ca2+ but not G protein‐gated inwardly rectifying K+ channels in cerebrospinal‐fluid contacting neurones of mouse brainstem"

    Article Title: GABAB receptors modulate Ca2+ but not G protein‐gated inwardly rectifying K+ channels in cerebrospinal‐fluid contacting neurones of mouse brainstem

    Journal: The Journal of Physiology

    doi: 10.1113/JP277172

    CSF‐cNs express N‐type voltage‐gated Ca 2+ channels A , representative whole‐cell current traces recorded in response to voltage steps from −60 mV to +30 mV ( V Step , +10 mV increments, protocol illustrated under the current traces) from a holding potential of −70 mV ( V h ) to elicit Ca 2+ current in a CSF‐cN. The inset represents the recorded CSF‐cN after cell dialysis with Alexa 594 (10 μM) to confirm the morphology. CC: central canal. B , average current‐voltage relationship for the Ca 2+ currents recorded in CSF‐cNs ( n = 13). Data are fitted using a Boltzmann function (red trace, see Methods for more details). The inset in red gives the values defining the properties of the Ca 2+ current in CSF‐cNs obtained from the Boltzmann fit of the average data (see text for details). C , summary box‐and‐whiskers plots of the averaged percentage of Ca 2+ current blockade in the presence of cadmium (Cd 2+ ; 105 ± 3%; black box, n = 12), ω‐conotoxin GVIA (ω‐CnTx GVIA; 64 ± 6%; grey box, n = 7), ω‐agatoxin IVA (ω‐AgaTx IVA; 11 ± 2%, light grey box, n = 11), and nifedipine (14 ± 3%; white box, n = 9). Ca 2+ current sensitivity to cadmium and ω‐CnTx GVIA is significantly higher compared to that observed in the presence of ω‐agatoxin IVA ( **** P
    Figure Legend Snippet: CSF‐cNs express N‐type voltage‐gated Ca 2+ channels A , representative whole‐cell current traces recorded in response to voltage steps from −60 mV to +30 mV ( V Step , +10 mV increments, protocol illustrated under the current traces) from a holding potential of −70 mV ( V h ) to elicit Ca 2+ current in a CSF‐cN. The inset represents the recorded CSF‐cN after cell dialysis with Alexa 594 (10 μM) to confirm the morphology. CC: central canal. B , average current‐voltage relationship for the Ca 2+ currents recorded in CSF‐cNs ( n = 13). Data are fitted using a Boltzmann function (red trace, see Methods for more details). The inset in red gives the values defining the properties of the Ca 2+ current in CSF‐cNs obtained from the Boltzmann fit of the average data (see text for details). C , summary box‐and‐whiskers plots of the averaged percentage of Ca 2+ current blockade in the presence of cadmium (Cd 2+ ; 105 ± 3%; black box, n = 12), ω‐conotoxin GVIA (ω‐CnTx GVIA; 64 ± 6%; grey box, n = 7), ω‐agatoxin IVA (ω‐AgaTx IVA; 11 ± 2%, light grey box, n = 11), and nifedipine (14 ± 3%; white box, n = 9). Ca 2+ current sensitivity to cadmium and ω‐CnTx GVIA is significantly higher compared to that observed in the presence of ω‐agatoxin IVA ( **** P

    Techniques Used:

    11) Product Images from "Altered Synaptic Vesicle Release and Ca2+ Influx at Single Presynaptic Terminals of Cortical Neurons in a Knock-in Mouse Model of Huntington’s Disease"

    Article Title: Altered Synaptic Vesicle Release and Ca2+ Influx at Single Presynaptic Terminals of Cortical Neurons in a Knock-in Mouse Model of Huntington’s Disease

    Journal: Frontiers in Molecular Neuroscience

    doi: 10.3389/fnmol.2018.00478

    Blocking N-type voltage-gated Ca 2+ channels reduces Ca 2+ influx in HD cortical neurons. (A) Average Δ F/F 0 traces of Cal-520 measured in the untreated ( n = 254 boutons, N = 6 experiments) and ω-conotoxin GVIA-treated HD neurons ( n = 162 boutons, N = 6 experiment). Where indicated, 1,200 1-ms field stimuli were delivered at 10 Hz for 120 s. (B) The peak Δ F/F 0 of Cal-520 during electrical stimulation in the untreated and ω-conotoxin GVIA-treated HD neurons. ** p
    Figure Legend Snippet: Blocking N-type voltage-gated Ca 2+ channels reduces Ca 2+ influx in HD cortical neurons. (A) Average Δ F/F 0 traces of Cal-520 measured in the untreated ( n = 254 boutons, N = 6 experiments) and ω-conotoxin GVIA-treated HD neurons ( n = 162 boutons, N = 6 experiment). Where indicated, 1,200 1-ms field stimuli were delivered at 10 Hz for 120 s. (B) The peak Δ F/F 0 of Cal-520 during electrical stimulation in the untreated and ω-conotoxin GVIA-treated HD neurons. ** p

    Techniques Used: Blocking Assay

    Blocking N-type voltage-gated Ca 2+ channels reduces the increased release of synaptic vesicles in HD cortical neurons. (A) Average traces of normalized FM 1–43 fluorescence intensity in untreated HD ( n = 36 boutons, N = 4 experiments) and WT cortical neurons ( n = 49 boutons, N = 5 experiments), HD ( n = 31 boutons, N = 5 experiments) and WT cortical neurons ( n = 29 boutons, N = 4 experiments) treated with 100 nM ω-conotoxin GVIA (Ctx-GVIA). Where indicated, 1,200 1-ms field stimuli were delivered at 10 Hz for 120 s. (B) The percent fluorescence loss of FM 1–43 in untreated and ω-conotoxin GVIA-treated HD and WT neurons. The average change in fluorescence loss in response to ω-conotoxin GVIA treatment was considerably smaller in WT cortical neurons (10.5%) compared with HD neurons (17.8%). (C) The time constant of FM 1–43 destaining in untreated and ω-conotoxin GVIA-treated HD and WT cortical neurons. The destaining rates of FM 1–43 in WT cortical neurons with ω-conotoxin GVIA were not significantly different from those without ω-conotoxin GVIA ( p > 0.08). NS, not significant, and **** p
    Figure Legend Snippet: Blocking N-type voltage-gated Ca 2+ channels reduces the increased release of synaptic vesicles in HD cortical neurons. (A) Average traces of normalized FM 1–43 fluorescence intensity in untreated HD ( n = 36 boutons, N = 4 experiments) and WT cortical neurons ( n = 49 boutons, N = 5 experiments), HD ( n = 31 boutons, N = 5 experiments) and WT cortical neurons ( n = 29 boutons, N = 4 experiments) treated with 100 nM ω-conotoxin GVIA (Ctx-GVIA). Where indicated, 1,200 1-ms field stimuli were delivered at 10 Hz for 120 s. (B) The percent fluorescence loss of FM 1–43 in untreated and ω-conotoxin GVIA-treated HD and WT neurons. The average change in fluorescence loss in response to ω-conotoxin GVIA treatment was considerably smaller in WT cortical neurons (10.5%) compared with HD neurons (17.8%). (C) The time constant of FM 1–43 destaining in untreated and ω-conotoxin GVIA-treated HD and WT cortical neurons. The destaining rates of FM 1–43 in WT cortical neurons with ω-conotoxin GVIA were not significantly different from those without ω-conotoxin GVIA ( p > 0.08). NS, not significant, and **** p

    Techniques Used: Blocking Assay, Fluorescence

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    Alomone Labs ω conotoxin gvia
    Isosaponarin inhibits the [Ca 2+ ] C and the N- and P/Q-type Ca 2+ channel-mediated glutamate release. ( A ) [Ca 2+ ] C was monitored using Fura-2. Synaptosomes were stimulated with 4-AP (1 mM) in the absence (control) or presence of isosaponarin that was added 10 min before stimulation. ( B ) Effect of isosaponarin on 4-AP-evoked glutamate release in the presence of the Ca 2+ channel toxins <t>ω-conotoxin</t> <t>GVIA</t> or ω-agatoxin IVA, which was added either alone or in combination. Data are presented as mean ± SEM (n = 5 per group). *** p
    ω Conotoxin Gvia, 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
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    Isosaponarin inhibits the [Ca 2+ ] C and the N- and P/Q-type Ca 2+ channel-mediated glutamate release. ( A ) [Ca 2+ ] C was monitored using Fura-2. Synaptosomes were stimulated with 4-AP (1 mM) in the absence (control) or presence of isosaponarin that was added 10 min before stimulation. ( B ) Effect of isosaponarin on 4-AP-evoked glutamate release in the presence of the Ca 2+ channel toxins ω-conotoxin GVIA or ω-agatoxin IVA, which was added either alone or in combination. Data are presented as mean ± SEM (n = 5 per group). *** p

    Journal: International Journal of Molecular Sciences

    Article Title: The Effect of Isosaponarin Derived from Wasabi Leaves on Glutamate Release in Rat Synaptosomes and Its Underlying Mechanism

    doi: 10.3390/ijms23158752

    Figure Lengend Snippet: Isosaponarin inhibits the [Ca 2+ ] C and the N- and P/Q-type Ca 2+ channel-mediated glutamate release. ( A ) [Ca 2+ ] C was monitored using Fura-2. Synaptosomes were stimulated with 4-AP (1 mM) in the absence (control) or presence of isosaponarin that was added 10 min before stimulation. ( B ) Effect of isosaponarin on 4-AP-evoked glutamate release in the presence of the Ca 2+ channel toxins ω-conotoxin GVIA or ω-agatoxin IVA, which was added either alone or in combination. Data are presented as mean ± SEM (n = 5 per group). *** p

    Article Snippet: The agents 4-AP, bafilomycin A1, GF109203X, Go6976, and rottlerin were purchased by Tocris Bioscience (Bristol, UK). ω-conotoxin GVIA and ω-agatoxin IVA were purchased from Alomone labs (Jerusalem, Israel).

    Techniques:

    P/Q-type are the predominant VGCC controlling presynaptic Ca 2+ and GABAergic transmission at the indirect pathway projections to the GPe. A: Timecourse of VGCC blocker application effects on PreCaTs and raw photometry traces. B: Summary of drug effects: baseline, last 2 minutes of drug, last 2 minutes of washout. Blockade of P/Q -type VGGCs (Agatoxin, n = 6 slices) significantly decreased PreCaTs from baseline, whereas no significant effect on PreCaTs was observed by blocking N-type VGCCs (Conotoxin, n= 8 slices) or L-type VGCCs (Nifedipine, n = 5 slices). C: Timecourse of VGCC blocker application effects on oIPSCs and raw electrophysiological traces. D: Comparison of drug effects: baseline, last 2 minutes of drug, last 2 minutes of washout. Blockade of P/Q -type VGGCs (Agatoxin, n = 5 cells) significantly decreased PreCaTs from baseline, and smaller but significant effects were induced by blocking N-type VGCCs (Conotoxin, n = 5 cells) or L-type VGCCs (Nifedipine, n = 5 cells). * p

    Journal: bioRxiv

    Article Title: Distinct mechanisms of CB1 and GABAB receptor presynaptic modulation of striatal indirect pathway projections to mouse Globus Pallidus

    doi: 10.1101/2022.07.21.500979

    Figure Lengend Snippet: P/Q-type are the predominant VGCC controlling presynaptic Ca 2+ and GABAergic transmission at the indirect pathway projections to the GPe. A: Timecourse of VGCC blocker application effects on PreCaTs and raw photometry traces. B: Summary of drug effects: baseline, last 2 minutes of drug, last 2 minutes of washout. Blockade of P/Q -type VGGCs (Agatoxin, n = 6 slices) significantly decreased PreCaTs from baseline, whereas no significant effect on PreCaTs was observed by blocking N-type VGCCs (Conotoxin, n= 8 slices) or L-type VGCCs (Nifedipine, n = 5 slices). C: Timecourse of VGCC blocker application effects on oIPSCs and raw electrophysiological traces. D: Comparison of drug effects: baseline, last 2 minutes of drug, last 2 minutes of washout. Blockade of P/Q -type VGGCs (Agatoxin, n = 5 cells) significantly decreased PreCaTs from baseline, and smaller but significant effects were induced by blocking N-type VGCCs (Conotoxin, n = 5 cells) or L-type VGCCs (Nifedipine, n = 5 cells). * p

    Article Snippet: QX-314 bromide was dissolved fresh in internal solution. ω-conotoxin GVIA and ω -agatoxin IVA were purchased form Alomone Labs (Jerusalem, Israel), QX-314 bromide and 4-AP from Millipore Sigma (St. Louis, MO, USA), and all other drugs from Tocris Biosciences (Minneapolis, MN, USA).

    Techniques: Transmission Assay, Blocking Assay