ω agatoxin iva  (Alomone Labs)


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    Structured Review

    Alomone Labs ω agatoxin iva
    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> GVIA or <t>ω-agatoxin</t> <t>IVA,</t> which was added either alone or in combination. Data are presented as mean ± SEM (n = 5 per group). *** p
    ω Agatoxin Iva, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 6 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 94 stars, based on 6 article reviews
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    ω agatoxin iva - by Bioz Stars, 2022-12
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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 "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

    3) Product Images from "An Anthranilate Derivative Inhibits Glutamate Release and Glutamate Excitotoxicity in Rats"

    Article Title: An Anthranilate Derivative Inhibits Glutamate Release and Glutamate Excitotoxicity in Rats

    Journal: International Journal of Molecular Sciences

    doi: 10.3390/ijms23052641

    Effect of HFP034 on 4-AP-evoked glutamate release in the presence of N-type Ca 2+ channel blocker ω-CgTX GVIA, P/Q-type Ca 2+ channel blocker ω-AgTX IVA, ryanodine receptor inhibitor dantrolene, or mitochondrial Na + /Ca 2+ exchanger inhibitor CGP37157. HFP034 was added 10 min before the addition of 4-AP, and other drugs were added 10 min before this. Each dot represents the value for an individual experiment. Data are presented as mean ± S.E.M. ( n = 5 per group). *** p
    Figure Legend Snippet: Effect of HFP034 on 4-AP-evoked glutamate release in the presence of N-type Ca 2+ channel blocker ω-CgTX GVIA, P/Q-type Ca 2+ channel blocker ω-AgTX IVA, ryanodine receptor inhibitor dantrolene, or mitochondrial Na + /Ca 2+ exchanger inhibitor CGP37157. HFP034 was added 10 min before the addition of 4-AP, and other drugs were added 10 min before this. Each dot represents the value for an individual experiment. Data are presented as mean ± S.E.M. ( n = 5 per group). *** p

    Techniques Used:

    4) Product Images from "Enmein Decreases Synaptic Glutamate Release and Protects against Kainic Acid-Induced Brain Injury in Rats"

    Article Title: Enmein Decreases Synaptic Glutamate Release and Protects against Kainic Acid-Induced Brain Injury in Rats

    Journal: International Journal of Molecular Sciences

    doi: 10.3390/ijms222312966

    Blockade of N- and P/Q-type Ca 2+ channels abolishes enmein inhibition of glutamate release. Glutamate release was evoked by 1 mM 4-AP in the absence (control) or presence of enmein, ω-CgTX GVIA + ω-AgTX IVA, or ω-CgTX GVIA + ω-AgTX IVA + enmein. Effect of enmein on the release of glutamate evoked by 15 mM KCl was also examined. Enmein was added 10 min before the addition of 4-AP, and other drugs were added 10 min before this. Data are presented as mean ± S.E.M. ( n = 5 per group). ***, p
    Figure Legend Snippet: Blockade of N- and P/Q-type Ca 2+ channels abolishes enmein inhibition of glutamate release. Glutamate release was evoked by 1 mM 4-AP in the absence (control) or presence of enmein, ω-CgTX GVIA + ω-AgTX IVA, or ω-CgTX GVIA + ω-AgTX IVA + enmein. Effect of enmein on the release of glutamate evoked by 15 mM KCl was also examined. Enmein was added 10 min before the addition of 4-AP, and other drugs were added 10 min before this. Data are presented as mean ± S.E.M. ( n = 5 per group). ***, p

    Techniques Used: Inhibition

    5) Product Images from "Chlorogenic Acid Decreases Glutamate Release from Rat Cortical Nerve Terminals by P/Q-Type Ca2+ Channel Suppression: A Possible Neuroprotective Mechanism"

    Article Title: Chlorogenic Acid Decreases Glutamate Release from Rat Cortical Nerve Terminals by P/Q-Type Ca2+ Channel Suppression: A Possible Neuroprotective Mechanism

    Journal: International Journal of Molecular Sciences

    doi: 10.3390/ijms222111447

    Effect of CGA on 4-AP-evoked glutamate release in the presence of N-type Ca 2+ channel blocker ω-CgTX GVIA, P/Q-type Ca 2+ channel blocker ω-AgTX IVA, ryanodine receptor inhibitor dantrolene, or mitochondrial Na + /Ca 2+ exchange inhibitor CGP37157. Inset, effect of CGA on the release of glutamate evoked by 15 mM KCl. CGA was added 10 min before the addition of 4-AP, and other drugs were added 10 min before this. Data are presented as mean ± S.E.M. ( n = 5 per group). ***, p
    Figure Legend Snippet: Effect of CGA on 4-AP-evoked glutamate release in the presence of N-type Ca 2+ channel blocker ω-CgTX GVIA, P/Q-type Ca 2+ channel blocker ω-AgTX IVA, ryanodine receptor inhibitor dantrolene, or mitochondrial Na + /Ca 2+ exchange inhibitor CGP37157. Inset, effect of CGA on the release of glutamate evoked by 15 mM KCl. CGA was added 10 min before the addition of 4-AP, and other drugs were added 10 min before this. Data are presented as mean ± S.E.M. ( n = 5 per group). ***, p

    Techniques Used:

    6) 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

    7) Product Images from "Conserved biophysical features of the CaV2 presynaptic Ca2+ channel homologue from the early-diverging animal Trichoplax adhaerens"

    Article Title: Conserved biophysical features of the CaV2 presynaptic Ca2+ channel homologue from the early-diverging animal Trichoplax adhaerens

    Journal: The Journal of Biological Chemistry

    doi: 10.1074/jbc.RA120.015725

    TCa V 2 is relatively insensitive to block by divalent metal cations Cd 2+ and Ni 2+ and Ca V 2 isotype–specific peptide toxins ω -conotoxin GVIA and ω -agatoxin IVA. A , dose-response curve for block of peak macroscopic currents of TCa V 2 and hCa V 2.1 with increasing concentrations of perfused external Cd 2+ ions. TCa V 2 is significantly less sensitive to Cd 2+ block than hCa V 2.1, with a roughly 19-fold higher IC 50 ( p
    Figure Legend Snippet: TCa V 2 is relatively insensitive to block by divalent metal cations Cd 2+ and Ni 2+ and Ca V 2 isotype–specific peptide toxins ω -conotoxin GVIA and ω -agatoxin IVA. A , dose-response curve for block of peak macroscopic currents of TCa V 2 and hCa V 2.1 with increasing concentrations of perfused external Cd 2+ ions. TCa V 2 is significantly less sensitive to Cd 2+ block than hCa V 2.1, with a roughly 19-fold higher IC 50 ( p

    Techniques Used: Blocking Assay, High Content Screening

    8) Product Images from "Lamellar cells in Pacinian and Meissner corpuscles are touch sensors"

    Article Title: Lamellar cells in Pacinian and Meissner corpuscles are touch sensors

    Journal: bioRxiv

    doi: 10.1101/2020.08.24.265231

    Pharmacological profile of Meissner lamellar cell firing. Quantification of the number of action potentials in response to current injection in the presence of indicated pharmacological agents: 10 µM Felodipine, a mix of 10 µM Nimodipine and 5 µM Isradipine, 10 µM Nifedipine, Agatoxin mix (1 µM ω-Agatoxin IVA and 1 µM ω-Agatoxin TK), Conotoxin mix (5 µM ω-Conotoxin CnVIIA, 10 nM ω-Conotoxin CVIB, 10 nM ω-Conotoxin CVIE, 1 µM ω-Conotoxin MVIIC and 1 µM ω-Conotoxin MVIID), 1 µM SNX-482, 5 µM Mibefradil, 200 nM Kurtoxin. Thin lines represent individual cells, thick lines connect means ± s.e.m. Data were obtained from at least two independent experiments.
    Figure Legend Snippet: Pharmacological profile of Meissner lamellar cell firing. Quantification of the number of action potentials in response to current injection in the presence of indicated pharmacological agents: 10 µM Felodipine, a mix of 10 µM Nimodipine and 5 µM Isradipine, 10 µM Nifedipine, Agatoxin mix (1 µM ω-Agatoxin IVA and 1 µM ω-Agatoxin TK), Conotoxin mix (5 µM ω-Conotoxin CnVIIA, 10 nM ω-Conotoxin CVIB, 10 nM ω-Conotoxin CVIE, 1 µM ω-Conotoxin MVIIC and 1 µM ω-Conotoxin MVIID), 1 µM SNX-482, 5 µM Mibefradil, 200 nM Kurtoxin. Thin lines represent individual cells, thick lines connect means ± s.e.m. Data were obtained from at least two independent experiments.

    Techniques Used: Injection

    9) 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

    10) Product Images from "Neuronal input triggers Ca2+ influx through AMPA receptors and voltage‐gated Ca2+ channels in oligodendrocytes. Neuronal input triggers Ca2+ influx through AMPA receptors and voltage‐gated Ca2+ channels in oligodendrocytes"

    Article Title: Neuronal input triggers Ca2+ influx through AMPA receptors and voltage‐gated Ca2+ channels in oligodendrocytes. Neuronal input triggers Ca2+ influx through AMPA receptors and voltage‐gated Ca2+ channels in oligodendrocytes

    Journal: Glia

    doi: 10.1002/glia.23670

    P/Q‐ and L‐type Ca v channels mediated Ca 2+ influx in response to glutamate input. (a) Glutamate‐induced Ca 2+ rise in a GCaMP6f + OL in the presence of Naspm, agatoxin (200 nM) and nifedipine (100 μM). (b) Summary of Ca 2+ responses after application of nifedipine or agatoxin, and combinations of agatoxin + nifedipine and agatoxin + CdCl 2 . (c) Ca v channel currents in the presence of 4‐AP (2 mM), TEA (10 mM), BaCl 2 (1 mM), and TTX (1 μM) in voltage‐clamp recording (holding at −65 mV), which were inhibited by CdCl 2 . Inset, step‐like depolarization protocol. (d) Current–voltage (I‐V) relationship of OL Ca 2+ current ( I Ca ). I Ca was partially inhibited by agatoxin and completely inhibited by CdCl 2 . (e) Ca 2+ rise in a GCaMP6f + OL when directly depolarized using a depolarizing pulse (diagram) during voltage‐clamp recording in the presence of agatoxin and nifedipine. The OL was brought from resting membrane potential at −65 mV to −40, −20, or 0 mV over the course of 100 ms, held at 0 mV for 100 ms, and brought back to resting membrane potential over a period of 2 s. (f) Summary of depolarization‐induced Ca 2+ rise in the presence of agatoxin and nifedipine. Data are represented as ± SEM . *** represents p
    Figure Legend Snippet: P/Q‐ and L‐type Ca v channels mediated Ca 2+ influx in response to glutamate input. (a) Glutamate‐induced Ca 2+ rise in a GCaMP6f + OL in the presence of Naspm, agatoxin (200 nM) and nifedipine (100 μM). (b) Summary of Ca 2+ responses after application of nifedipine or agatoxin, and combinations of agatoxin + nifedipine and agatoxin + CdCl 2 . (c) Ca v channel currents in the presence of 4‐AP (2 mM), TEA (10 mM), BaCl 2 (1 mM), and TTX (1 μM) in voltage‐clamp recording (holding at −65 mV), which were inhibited by CdCl 2 . Inset, step‐like depolarization protocol. (d) Current–voltage (I‐V) relationship of OL Ca 2+ current ( I Ca ). I Ca was partially inhibited by agatoxin and completely inhibited by CdCl 2 . (e) Ca 2+ rise in a GCaMP6f + OL when directly depolarized using a depolarizing pulse (diagram) during voltage‐clamp recording in the presence of agatoxin and nifedipine. The OL was brought from resting membrane potential at −65 mV to −40, −20, or 0 mV over the course of 100 ms, held at 0 mV for 100 ms, and brought back to resting membrane potential over a period of 2 s. (f) Summary of depolarization‐induced Ca 2+ rise in the presence of agatoxin and nifedipine. Data are represented as ± SEM . *** represents p

    Techniques Used:

    11) Product Images from "Deletion of the Ca2+ Channel Subunit α2δ3 Differentially Affects Cav2.1 and Cav2.2 Currents in Cultured Spiral Ganglion Neurons Before and After the Onset of Hearing"

    Article Title: Deletion of the Ca2+ Channel Subunit α2δ3 Differentially Affects Cav2.1 and Cav2.2 Currents in Cultured Spiral Ganglion Neurons Before and After the Onset of Hearing

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2019.00278

    Small P/Q-type Ca 2+ currents are not altered in neonatal SG neurons of α 2 δ3 –/– mice at P5 + 2 DIV. (A,B) Maximum I Ca traces of an α 2 δ3 +/+ ( A , top) and an α 2 δ3 –/– SG neuron ( B , top) in response to 100 ms depolarizing voltage steps before (α 2 δ3 +/+ , black; α 2 δ3 –/– , magenta) and during application of 1 μM ω-agatoxin IVA (blue). Corresponding steady-state I – V curves are shown below the traces. (C) Box-and-whisker plots of I Ca before (ctrl) and under superfusion of 1 μM ω-agatoxin IVA (aga) of SG neurons isolated from α 2 δ3 +/+ (+/+) and α 2 δ3 –/– (–/–) mice. Numbers under the box plots denote the numbers of SG neurons. Wilcoxon signed test, ∗∗∗ p
    Figure Legend Snippet: Small P/Q-type Ca 2+ currents are not altered in neonatal SG neurons of α 2 δ3 –/– mice at P5 + 2 DIV. (A,B) Maximum I Ca traces of an α 2 δ3 +/+ ( A , top) and an α 2 δ3 –/– SG neuron ( B , top) in response to 100 ms depolarizing voltage steps before (α 2 δ3 +/+ , black; α 2 δ3 –/– , magenta) and during application of 1 μM ω-agatoxin IVA (blue). Corresponding steady-state I – V curves are shown below the traces. (C) Box-and-whisker plots of I Ca before (ctrl) and under superfusion of 1 μM ω-agatoxin IVA (aga) of SG neurons isolated from α 2 δ3 +/+ (+/+) and α 2 δ3 –/– (–/–) mice. Numbers under the box plots denote the numbers of SG neurons. Wilcoxon signed test, ∗∗∗ p

    Techniques Used: Mouse Assay, Whisker Assay, Isolation

    P/Q-type Ca 2+ currents are strongly reduced in SG neurons of α 2 δ3 –/– mice at P20 + 3 DIV. (A,B) Maximum I Ca traces of an α 2 δ3 +/+ ( A , top) and an α 2 δ3 –/– SG neuron ( B , top) in response to 100 ms depolarizing voltage steps before (α 2 δ3 +/+ , black; α 2 δ3 –/– , magenta) and during application of 1 μM ω-agatoxin IVA (blue). Corresponding steady-state I – V curves are shown below the traces. (C) Box-and-whisker plots of I Ca before and during application of 1 μM ω-agatoxin IVA (aga) of SG neurons from α 2 δ3 +/+ (+/+) and α 2 δ3 –/– (–/–) mice. Numbers under the box plots denote the numbers of SG neurons. Wilcoxon signed test, ∗∗∗ p
    Figure Legend Snippet: P/Q-type Ca 2+ currents are strongly reduced in SG neurons of α 2 δ3 –/– mice at P20 + 3 DIV. (A,B) Maximum I Ca traces of an α 2 δ3 +/+ ( A , top) and an α 2 δ3 –/– SG neuron ( B , top) in response to 100 ms depolarizing voltage steps before (α 2 δ3 +/+ , black; α 2 δ3 –/– , magenta) and during application of 1 μM ω-agatoxin IVA (blue). Corresponding steady-state I – V curves are shown below the traces. (C) Box-and-whisker plots of I Ca before and during application of 1 μM ω-agatoxin IVA (aga) of SG neurons from α 2 δ3 +/+ (+/+) and α 2 δ3 –/– (–/–) mice. Numbers under the box plots denote the numbers of SG neurons. Wilcoxon signed test, ∗∗∗ p

    Techniques Used: Mouse Assay, Whisker Assay

    12) 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:

    13) 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:

    14) 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

    15) 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:

    16) 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 P/Q-type voltage-gated Ca 2+ channels does not affect the increased release of synaptic vesicles in HD cortical neurons compared to WT neurons. (A) Average traces of normalized FM 1–43 fluorescence intensity in untreated ( n = 36 boutons, N = 4 experiments) and 200 nM ω-agatoxin IVA(ATX-IVA)-treated WT neurons ( n = 31 boutons, N = 5 experiments; A1 ), and untreated ( n = 36 boutons, N = 4 experiments) and 200 nM ω-agatoxin IVA(ATX-IVA)-treated HD neurons ( n = 31 boutons, N = 5 experiments; A2 ). Where indicated, a train of 1,200 1-ms field stimuli was applied at 10 Hz for 120 s. (B) The percent loss of FM 1–43 fluorescence measured in WT and HD neurons in the presence or absence of ATX-IVA. Note that ω-agatoxin IVA caused a similar change in percent fluorescence loss in WT and HD neurons (18.7% and 20.3%, respectively). (C) The time constant of FM1–43 destaining measured in WT and HD neurons in the presence or absence of ATX-IVA. **** p
    Figure Legend Snippet: Blocking P/Q-type voltage-gated Ca 2+ channels does not affect the increased release of synaptic vesicles in HD cortical neurons compared to WT neurons. (A) Average traces of normalized FM 1–43 fluorescence intensity in untreated ( n = 36 boutons, N = 4 experiments) and 200 nM ω-agatoxin IVA(ATX-IVA)-treated WT neurons ( n = 31 boutons, N = 5 experiments; A1 ), and untreated ( n = 36 boutons, N = 4 experiments) and 200 nM ω-agatoxin IVA(ATX-IVA)-treated HD neurons ( n = 31 boutons, N = 5 experiments; A2 ). Where indicated, a train of 1,200 1-ms field stimuli was applied at 10 Hz for 120 s. (B) The percent loss of FM 1–43 fluorescence measured in WT and HD neurons in the presence or absence of ATX-IVA. Note that ω-agatoxin IVA caused a similar change in percent fluorescence loss in WT and HD neurons (18.7% and 20.3%, respectively). (C) The time constant of FM1–43 destaining measured in WT and HD neurons in the presence or absence of ATX-IVA. **** p

    Techniques Used: Blocking Assay, Fluorescence

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    Alomone Labs ω agatoxin iva
    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> GVIA or <t>ω-agatoxin</t> <t>IVA,</t> which was added either alone or in combination. Data are presented as mean ± SEM (n = 5 per group). *** p
    ω Agatoxin Iva, 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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    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:

    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

    Journal: Biology Open

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

    doi: 10.1242/bio.058840

    Figure Lengend 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

    Article Snippet: All reagents were purchased from the Sigma Chemical Company (St. Louis, MO, USA) with the exceptions of ZD7288 from the Tocris company (UK), ω-Agatoxin IVA, ω-Conotoxin GVIA and pimozide from Alomone Labs (Isreal).

    Techniques: Blocking Assay

    Effect of HFP034 on 4-AP-evoked glutamate release in the presence of N-type Ca 2+ channel blocker ω-CgTX GVIA, P/Q-type Ca 2+ channel blocker ω-AgTX IVA, ryanodine receptor inhibitor dantrolene, or mitochondrial Na + /Ca 2+ exchanger inhibitor CGP37157. HFP034 was added 10 min before the addition of 4-AP, and other drugs were added 10 min before this. Each dot represents the value for an individual experiment. Data are presented as mean ± S.E.M. ( n = 5 per group). *** p

    Journal: International Journal of Molecular Sciences

    Article Title: An Anthranilate Derivative Inhibits Glutamate Release and Glutamate Excitotoxicity in Rats

    doi: 10.3390/ijms23052641

    Figure Lengend Snippet: Effect of HFP034 on 4-AP-evoked glutamate release in the presence of N-type Ca 2+ channel blocker ω-CgTX GVIA, P/Q-type Ca 2+ channel blocker ω-AgTX IVA, ryanodine receptor inhibitor dantrolene, or mitochondrial Na + /Ca 2+ exchanger inhibitor CGP37157. HFP034 was added 10 min before the addition of 4-AP, and other drugs were added 10 min before this. Each dot represents the value for an individual experiment. Data are presented as mean ± S.E.M. ( n = 5 per group). *** p

    Article Snippet: DiSC3 (5) and fura-2-acetoxymethyl ester (Fura-2-AM) were purchased from Thermo (Waltham, MA, USA). ω-CgTX GVIA and ω-Aga IVA were purchased from the Alomone lab (Jerusalem, Israel).

    Techniques: