ω agatoxin iva  (Alomone Labs)


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    Alomone Labs ω agatoxin iva
    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, <t>ω-agatoxin</t> <t>IVA</t> (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
    ω Agatoxin Iva, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) 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:

    2) Product Images from "Identification and Modulation of Voltage-Gated Ca2+ Currents in Zebrafish Rohon-Beard Neurons"

    Article Title: Identification and Modulation of Voltage-Gated Ca2+ Currents in Zebrafish Rohon-Beard Neurons

    Journal: Journal of Neurophysiology

    doi: 10.1152/jn.00625.2010

    Pharmacological dissection of high-voltage-activated (HVA)- I Ca in R-B neurons. A and B : time courses of I Ca amplitude during serial application of 10 μM nifedipine, 0.5 μM ω-agatoxin IVA, 3 μM ω-conotoxin GVIA,
    Figure Legend Snippet: Pharmacological dissection of high-voltage-activated (HVA)- I Ca in R-B neurons. A and B : time courses of I Ca amplitude during serial application of 10 μM nifedipine, 0.5 μM ω-agatoxin IVA, 3 μM ω-conotoxin GVIA,

    Techniques Used: Dissection

    3) 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

    4) 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:

    5) Product Images from "Two delta opioid receptor subtypes are functional in single ventral tegmental area neurons, and can interact with the mu opioid receptor"

    Article Title: Two delta opioid receptor subtypes are functional in single ventral tegmental area neurons, and can interact with the mu opioid receptor

    Journal: Neuropharmacology

    doi: 10.1016/j.neuropharm.2017.06.019

    Both DOR subtypes hyperpolarize VTA neurons via K + channel activation and excite VTA neurons through activation of Ca v 2.1 (A) In control experiments, VTA neurons respond similarly to the first and second application of the same DOR agonist, regardless of the magnitude or direction of the response. (1 μM DPDPE, n = 7; 1 μM deltorphin II, n = 5) (B) In neurons responding to DPDPE or deltorphin II with a hyperpolarization, the K + channel blocker BaCl 2 (100 μM) prevented a hyperpolarization in response to a second agonist application (DPDPE n = 6; deltorphin II n = 9). (C) In neurons where the initial response to DPDPE (n = 5) or deltorphin II (n = 5) was a depolarization, this response was blocked by the Ca v 2.1 blocker ω-agatoxin-IVA (100 nM). In an additional neuron that first responded to deltorphin II with a hyperpolarization, the response was larger in the presence of ω-agatoxin-IVA. Paired t-tests, * p
    Figure Legend Snippet: Both DOR subtypes hyperpolarize VTA neurons via K + channel activation and excite VTA neurons through activation of Ca v 2.1 (A) In control experiments, VTA neurons respond similarly to the first and second application of the same DOR agonist, regardless of the magnitude or direction of the response. (1 μM DPDPE, n = 7; 1 μM deltorphin II, n = 5) (B) In neurons responding to DPDPE or deltorphin II with a hyperpolarization, the K + channel blocker BaCl 2 (100 μM) prevented a hyperpolarization in response to a second agonist application (DPDPE n = 6; deltorphin II n = 9). (C) In neurons where the initial response to DPDPE (n = 5) or deltorphin II (n = 5) was a depolarization, this response was blocked by the Ca v 2.1 blocker ω-agatoxin-IVA (100 nM). In an additional neuron that first responded to deltorphin II with a hyperpolarization, the response was larger in the presence of ω-agatoxin-IVA. Paired t-tests, * p

    Techniques Used: Activation Assay

    6) Product Images from "Ginsenoside Rb1 selectively inhibits the activity of L-type voltage-gated calcium channels in cultured rat hippocampal neurons"

    Article Title: Ginsenoside Rb1 selectively inhibits the activity of L-type voltage-gated calcium channels in cultured rat hippocampal neurons

    Journal: Acta Pharmacologica Sinica

    doi: 10.1038/aps.2011.181

    Rb1 inhibited the I Ba in hippocampal neurons, and this inhibitory effect was eliminated after the application of nifedipine (A). Neither ω-conotoxin-GVIA nor ω-agatoxin IVA diminished the Rb1-sensitive I Ba (B and C, respectively). Upper panel, pairs of the inward currents evoked by pulses from −60 to +0 mV (0–+20 mV) at the times indicated in the lower panel. Lower panel, time course of the effects of 10 μmol/L Rb1 on the I Ba amplitude before and after application of the Ca 2+ channel antagonists (10 μmol/L nifedipine, 1 μmol/L ω-conotoxin GVIA and 30 nmol/L ω-agatoxin IVA). The bar graphs for Rb1 inhibition (mean±SEM, n =5 for Rb1) on the I Ba in cells untreated or treated with Ca 2+ channel antagonists. c P
    Figure Legend Snippet: Rb1 inhibited the I Ba in hippocampal neurons, and this inhibitory effect was eliminated after the application of nifedipine (A). Neither ω-conotoxin-GVIA nor ω-agatoxin IVA diminished the Rb1-sensitive I Ba (B and C, respectively). Upper panel, pairs of the inward currents evoked by pulses from −60 to +0 mV (0–+20 mV) at the times indicated in the lower panel. Lower panel, time course of the effects of 10 μmol/L Rb1 on the I Ba amplitude before and after application of the Ca 2+ channel antagonists (10 μmol/L nifedipine, 1 μmol/L ω-conotoxin GVIA and 30 nmol/L ω-agatoxin IVA). The bar graphs for Rb1 inhibition (mean±SEM, n =5 for Rb1) on the I Ba in cells untreated or treated with Ca 2+ channel antagonists. c P

    Techniques Used: Inhibition

    (A) Phase-contrast image showing a single patch recording from 7-d cultured hippocampal neurons for the recording of the VGCCs. Scale bar, 10 μm. (B) Pharmacological separation of the VGCC subtypes in hippocampal neurons. Upper panel, inward Ca 2+ channel Ba 2+ currents evoked by pulses from −60 mV to 0 mV at the times indicated in the lower panel. Lower panel, time course of effects of ω-conotoxin GVIA (1 μmol/L), ω-agatoxin IVA (30 nmol/L) and nifedipine (10 μmol/L) on the Ba 2+ current amplitude.
    Figure Legend Snippet: (A) Phase-contrast image showing a single patch recording from 7-d cultured hippocampal neurons for the recording of the VGCCs. Scale bar, 10 μm. (B) Pharmacological separation of the VGCC subtypes in hippocampal neurons. Upper panel, inward Ca 2+ channel Ba 2+ currents evoked by pulses from −60 mV to 0 mV at the times indicated in the lower panel. Lower panel, time course of effects of ω-conotoxin GVIA (1 μmol/L), ω-agatoxin IVA (30 nmol/L) and nifedipine (10 μmol/L) on the Ba 2+ current amplitude.

    Techniques Used: Cell Culture

    7) Product Images from "Effects of IgG anti-GM1 monoclonal antibodies on neuromuscular transmission and calcium channel binding in rat neuromuscular junctions"

    Article Title: Effects of IgG anti-GM1 monoclonal antibodies on neuromuscular transmission and calcium channel binding in rat neuromuscular junctions

    Journal: Experimental and Therapeutic Medicine

    doi: 10.3892/etm.2015.2575

    Effects of pretreatment with the P/Q-type calcium channel blocker, ω-agatoxin IVA, on the inhibitory effect of IgG anti-GM1 mAb (1:100) on spontaneous muscle action potentials (SMAPs) in the spinal cord-muscle co-culture system. (A) Inhibition
    Figure Legend Snippet: Effects of pretreatment with the P/Q-type calcium channel blocker, ω-agatoxin IVA, on the inhibitory effect of IgG anti-GM1 mAb (1:100) on spontaneous muscle action potentials (SMAPs) in the spinal cord-muscle co-culture system. (A) Inhibition

    Techniques Used: Co-Culture Assay, Inhibition

    8) Product Images from "Characterization of Na+ and Ca2+ Channels in Zebrafish Dorsal Root Ganglion Neurons"

    Article Title: Characterization of Na+ and Ca2+ Channels in Zebrafish Dorsal Root Ganglion Neurons

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0042602

    Pharmacological dissection of HVA- I Ca in zebrafish DRG neurons. A , Left , Time courses of I Ca amplitude during serial application of nifedipine (10 µM), ω-agatoxin IVA (0.5 µM), ω-conotoxin GVIA (3 µM), SNX-482 (300 nM) and CdCl 2 (100 µM). I Ca was evoked every 10 s by 70 ms test pulses to 0 mV from a holding potential of −80 mV. The horizontal bars indicate the duration of drug application. Right , superimposed current traces obtained at different time points during drug application (labeled as a–f). B , Bar graph representing the mean I Ca inhibition (%) produced by application of the indicated antagonists or toxins. Error bars represent s . e . m . The number of neurons tested is indicated in parentheses. C , Effect of non-dihydropyridine Ca 2+ channel agonist FPL 64176 (FPL) on I Ca in DRG neurons. FPL (1 µM) was applied to rat superior cervical ganglion (SCG) neurons as a positive control (left panel). Note that FPL applied to zebrafish DRG I Ca display neither an increase in macroscopic inward currents nor greatly prolonged trajectory of the tail currents (right panel).
    Figure Legend Snippet: Pharmacological dissection of HVA- I Ca in zebrafish DRG neurons. A , Left , Time courses of I Ca amplitude during serial application of nifedipine (10 µM), ω-agatoxin IVA (0.5 µM), ω-conotoxin GVIA (3 µM), SNX-482 (300 nM) and CdCl 2 (100 µM). I Ca was evoked every 10 s by 70 ms test pulses to 0 mV from a holding potential of −80 mV. The horizontal bars indicate the duration of drug application. Right , superimposed current traces obtained at different time points during drug application (labeled as a–f). B , Bar graph representing the mean I Ca inhibition (%) produced by application of the indicated antagonists or toxins. Error bars represent s . e . m . The number of neurons tested is indicated in parentheses. C , Effect of non-dihydropyridine Ca 2+ channel agonist FPL 64176 (FPL) on I Ca in DRG neurons. FPL (1 µM) was applied to rat superior cervical ganglion (SCG) neurons as a positive control (left panel). Note that FPL applied to zebrafish DRG I Ca display neither an increase in macroscopic inward currents nor greatly prolonged trajectory of the tail currents (right panel).

    Techniques Used: Dissection, Mass Spectrometry, Labeling, Inhibition, Produced, Positive Control

    9) 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:

    10) 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

    11) 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:

    12) Product Images from "Differential regulation of nimodipine-sensitive and -insensitive Ca2+ influx by the Na+/Ca2+ exchanger and mitochondria in the rat suprachiasmatic nucleus neurons"

    Article Title: Differential regulation of nimodipine-sensitive and -insensitive Ca2+ influx by the Na+/Ca2+ exchanger and mitochondria in the rat suprachiasmatic nucleus neurons

    Journal: Journal of Biomedical Science

    doi: 10.1186/s12929-018-0447-z

    Effects of CaV2 channel blockers on nimodipine-insensitive Ca 2+ transients. a A representative experiment showing the effect of FCCP on nimodipine-insensitive Ca 2+ transients (an average of 11 cells). b Two representative experiments showing the effects of CaV2 channel blockers, applied additively in order of 0.2 μM SNX-482, 0.2 μM ω-agatoxin IVA, and 2 μM ω-conotoxin GVIA, on the nimodipine-insensitive Ca 2+ transients in the absence (dark grey trace) and presence (black trace) of FCCP. c Summary of experiments showing the amplitude of nimodipine-insensitive Ca 2+ transients reduced by each drug and the amplitude of Ca 2+ transients resistant to the blocker cocktail in the absence (dark grey bars) and presence (black bars) of FCCP. Note that FCCP induced a 3- to 4-hold increase (indicated by the number on top of black bars) in the Ca 2+ transient sensitive to ω-agatoxin IVA or ω-conotoxin GVIA or resistant to the cocktail of blockers. *** P
    Figure Legend Snippet: Effects of CaV2 channel blockers on nimodipine-insensitive Ca 2+ transients. a A representative experiment showing the effect of FCCP on nimodipine-insensitive Ca 2+ transients (an average of 11 cells). b Two representative experiments showing the effects of CaV2 channel blockers, applied additively in order of 0.2 μM SNX-482, 0.2 μM ω-agatoxin IVA, and 2 μM ω-conotoxin GVIA, on the nimodipine-insensitive Ca 2+ transients in the absence (dark grey trace) and presence (black trace) of FCCP. c Summary of experiments showing the amplitude of nimodipine-insensitive Ca 2+ transients reduced by each drug and the amplitude of Ca 2+ transients resistant to the blocker cocktail in the absence (dark grey bars) and presence (black bars) of FCCP. Note that FCCP induced a 3- to 4-hold increase (indicated by the number on top of black bars) in the Ca 2+ transient sensitive to ω-agatoxin IVA or ω-conotoxin GVIA or resistant to the cocktail of blockers. *** P

    Techniques Used:

    13) Product Images from "Conditionally immortalized stem cell lines from human spinal cord retain regional identity and generate functional V2a interneurons and motorneurons"

    Article Title: Conditionally immortalized stem cell lines from human spinal cord retain regional identity and generate functional V2a interneurons and motorneurons

    Journal: Stem Cell Research & Therapy

    doi: 10.1186/scrt220

    SPC-01 generates functional neurons. (a) Preincubation with Cd 2+ (100 μ M ) together with Ni 2+ (50 μ M ), for 5 minutes significantly reduced the [Ca 2+ ] i responses induced by K + in all cells tested by 93% ± 9.2% ( n = 5), indicating the involvement of voltage-activated Ca 2+ channels in depolarization-induced Ca 2+ entry. (b) The specific L-type Ca 2+ channel blocker nicardipine (1 μ M ) reduced the [Ca 2+ ] i responses by 28% ± 7% ( n = 5; P = 0.002). The trace in (c) shows the [Ca 2+ ] i responses observed in a selected SPC-01-derived neuron induced by 50 m M K + , preincubated for 2 minutes with Ω -GVIA (800 n M ) and then stimulated with K + . After a washout of 10 minutes, the same cells were subjected to K + to observe recovery. Similarly, the effect of the P/Q-Ca 2+ channel blocker, Ω -Aga-IVA, 300 n M was tested before and during stimulation with high K + (d) . After washout of the toxin, the [Ca 2+ ] i response was shown to be reversible. The histogram (e) summarizes the results presented in (c) and (d) . The resting [Ca 2+ ] i level in these cells is indicated as basal. The results are expressed as mean ± SEM; n = 4 (Ω-GVIA) and n = 5 (Ω-Aga-IVA). Asterisks indicate the statistical significance ( P > 0.05) versus control K + stimulus.
    Figure Legend Snippet: SPC-01 generates functional neurons. (a) Preincubation with Cd 2+ (100 μ M ) together with Ni 2+ (50 μ M ), for 5 minutes significantly reduced the [Ca 2+ ] i responses induced by K + in all cells tested by 93% ± 9.2% ( n = 5), indicating the involvement of voltage-activated Ca 2+ channels in depolarization-induced Ca 2+ entry. (b) The specific L-type Ca 2+ channel blocker nicardipine (1 μ M ) reduced the [Ca 2+ ] i responses by 28% ± 7% ( n = 5; P = 0.002). The trace in (c) shows the [Ca 2+ ] i responses observed in a selected SPC-01-derived neuron induced by 50 m M K + , preincubated for 2 minutes with Ω -GVIA (800 n M ) and then stimulated with K + . After a washout of 10 minutes, the same cells were subjected to K + to observe recovery. Similarly, the effect of the P/Q-Ca 2+ channel blocker, Ω -Aga-IVA, 300 n M was tested before and during stimulation with high K + (d) . After washout of the toxin, the [Ca 2+ ] i response was shown to be reversible. The histogram (e) summarizes the results presented in (c) and (d) . The resting [Ca 2+ ] i level in these cells is indicated as basal. The results are expressed as mean ± SEM; n = 4 (Ω-GVIA) and n = 5 (Ω-Aga-IVA). Asterisks indicate the statistical significance ( P > 0.05) versus control K + stimulus.

    Techniques Used: Functional Assay, Derivative Assay

    14) Product Images from "Fragile X mental retardation protein controls synaptic vesicle exocytosis by modulating N-type calcium channel density"

    Article Title: Fragile X mental retardation protein controls synaptic vesicle exocytosis by modulating N-type calcium channel density

    Journal: Nature Communications

    doi: 10.1038/ncomms4628

    FMRP knockdown enhances synaptic vesicle exocytosis in presynaptic terminals of DRG neurons via Ca V 2.2 channels. ( a ) Presynaptic terminals of DRG neurons expressing vGpH (vGpH). Images show vGpH fluorescence (green) colocalized with endogenous synapsin 1 and 2 (left panel, red) and apposed to endogenous PSD-95 (right panel, red). Synapses are indicated by the white arrows. Scale bars, 5 μm. ( b ) Fluorescence changes (ΔF) of vGpH in presynaptic terminals of DRG neurons transfected with Ctrl shRNA (top panels) or FMRP shRNA (bottom panels) in response to electrical stimulation. Left panels: at rest; middle panels: after 40 action potentials (AP) at 10 Hz; right panels: after a brief application of NH 4 Cl. Responsive terminals are indicated by the black arrows. Pseudocolor scale is shown to the right (min, max:minimum and maximum fluorescence intensity). Scale bar, 10 μm. ( c , d ) vGpH response to 40 AP at 10 Hz from presynaptic terminals of DRG neurons transfected with Ctrl shRNA ( c ) or FMRP shRNA ( d ) before and after treatment with toxins (10 min with ω-conotoxin GVIA (1 μM) and ω-agatoxin IVA (300 nM)). Fluorescence intensities were normalized to the peak of a brief application of NH 4 Cl. ( e ) Normalized vGpH responses to 40 AP at 10 Hz from presynaptic terminals of DRG neurons transfected with Ctrl shRNA (black-filled bar, 100±10.6%, n =38) or FMRP shRNA (red open bar, 137.0±12.6%, n =25, P =0.027). ω-conotoxin GVIA (ConoTx, 1 μM) reduces Ctrl shRNA and FMRP shRNA responses to a similar level (44.7±4.9%, n =15 and 41.6±3.3%, n =24, respectively). ω-conotoxin GVIA (1 μM) and ω-agatoxin IVA (AgaTx, 300 nM) application reduces further the responses: Ctrl shRNA=17.3±3.2%, n =38, and FMRP shRNA=18.1±5.0%, n =27. A dot plot graph for the data is presented in Supplementary Fig. 9 . Means±s.e.m., * P
    Figure Legend Snippet: FMRP knockdown enhances synaptic vesicle exocytosis in presynaptic terminals of DRG neurons via Ca V 2.2 channels. ( a ) Presynaptic terminals of DRG neurons expressing vGpH (vGpH). Images show vGpH fluorescence (green) colocalized with endogenous synapsin 1 and 2 (left panel, red) and apposed to endogenous PSD-95 (right panel, red). Synapses are indicated by the white arrows. Scale bars, 5 μm. ( b ) Fluorescence changes (ΔF) of vGpH in presynaptic terminals of DRG neurons transfected with Ctrl shRNA (top panels) or FMRP shRNA (bottom panels) in response to electrical stimulation. Left panels: at rest; middle panels: after 40 action potentials (AP) at 10 Hz; right panels: after a brief application of NH 4 Cl. Responsive terminals are indicated by the black arrows. Pseudocolor scale is shown to the right (min, max:minimum and maximum fluorescence intensity). Scale bar, 10 μm. ( c , d ) vGpH response to 40 AP at 10 Hz from presynaptic terminals of DRG neurons transfected with Ctrl shRNA ( c ) or FMRP shRNA ( d ) before and after treatment with toxins (10 min with ω-conotoxin GVIA (1 μM) and ω-agatoxin IVA (300 nM)). Fluorescence intensities were normalized to the peak of a brief application of NH 4 Cl. ( e ) Normalized vGpH responses to 40 AP at 10 Hz from presynaptic terminals of DRG neurons transfected with Ctrl shRNA (black-filled bar, 100±10.6%, n =38) or FMRP shRNA (red open bar, 137.0±12.6%, n =25, P =0.027). ω-conotoxin GVIA (ConoTx, 1 μM) reduces Ctrl shRNA and FMRP shRNA responses to a similar level (44.7±4.9%, n =15 and 41.6±3.3%, n =24, respectively). ω-conotoxin GVIA (1 μM) and ω-agatoxin IVA (AgaTx, 300 nM) application reduces further the responses: Ctrl shRNA=17.3±3.2%, n =38, and FMRP shRNA=18.1±5.0%, n =27. A dot plot graph for the data is presented in Supplementary Fig. 9 . Means±s.e.m., * P

    Techniques Used: Expressing, Fluorescence, Transfection, shRNA

    15) Product Images from "Otoprotective Effects of Stephania tetrandra S. Moore Herb Isolate against Acoustic Trauma"

    Article Title: Otoprotective Effects of Stephania tetrandra S. Moore Herb Isolate against Acoustic Trauma

    Journal: JARO: Journal of the Association for Research in Otolaryngology

    doi: 10.1007/s10162-018-00690-3

    Whole-cell Ca 2+ currents in SGNs resistant to a cocktail of L-, N-, P/Q-, and R-type current blockers is sensitive to TET. We used a cocktail of 10 μM nimodipine, 1 μM ω-agatoxin IVA, 1 μM conotoxin MVIIA, and 200 nM rSNX-482. a Current traces for control (in black) recorded using a holding voltage of − 100 mV to step voltages (in mV, − 60, − 40, − 30, and − 10). The middle (in blue) and the right (in magenta) depict the effects of 0.5 M and 2 M TET, respectively on the transient Ca 2+ current. b The corresponding current-voltage relations are shown from data from eight SGNs isolated from the basal one third of the cochlea. c The dose-response data was fitted using a Hill equation of the form I/I max = IC 50 /(IC 50 + [TET] n ), where IC 50 = half blocking concentration, and n = Hill’s coefficient. The IC 50 for TET was 0.6 ± 0.1 mM ( n = 6), and n = 1.2
    Figure Legend Snippet: Whole-cell Ca 2+ currents in SGNs resistant to a cocktail of L-, N-, P/Q-, and R-type current blockers is sensitive to TET. We used a cocktail of 10 μM nimodipine, 1 μM ω-agatoxin IVA, 1 μM conotoxin MVIIA, and 200 nM rSNX-482. a Current traces for control (in black) recorded using a holding voltage of − 100 mV to step voltages (in mV, − 60, − 40, − 30, and − 10). The middle (in blue) and the right (in magenta) depict the effects of 0.5 M and 2 M TET, respectively on the transient Ca 2+ current. b The corresponding current-voltage relations are shown from data from eight SGNs isolated from the basal one third of the cochlea. c The dose-response data was fitted using a Hill equation of the form I/I max = IC 50 /(IC 50 + [TET] n ), where IC 50 = half blocking concentration, and n = Hill’s coefficient. The IC 50 for TET was 0.6 ± 0.1 mM ( n = 6), and n = 1.2

    Techniques Used: Isolation, Blocking Assay, Concentration Assay

    16) Product Images from "Numb deficiency in cerebellar Purkinje cells impairs synaptic expression of metabotropic glutamate receptor and motor coordination"

    Article Title: Numb deficiency in cerebellar Purkinje cells impairs synaptic expression of metabotropic glutamate receptor and motor coordination

    Journal: Proceedings of the National Academy of Sciences of the United States of America

    doi: 10.1073/pnas.1512915112

    P/Q channel-mediated Ca 2+ transient is not changed in Numb-cKO mice. ( A ) A projected z-stack image of a PC filled with Alexa Fluor 594. (Scale bar: 20 μm.) ( B ) Fluo-4 signals in the dendritic field of PCs from control (ctrl) and Numb-cKO mice (P21). The same microscopic fields are shown at basal ( Left ) and peak ( Center ) [Ca 2+ ] i and after application of ω-Agatoxin IVA ( Right ). (Scale bars: 10 μm.) ( C ) ω-Agatoxin–sensitive [Ca 2+ ] i in the cells shown in B . Arrows show the initiation of depolarization. ( D ) Mean amplitudes of changes in Fluo-4 fluorescence (Δ F / F 0 ) in control and Numb-cKO mice. Ctrl: 3.0 ± 0.5 ( n = 17 dendritic regions in 10 PCs). Numb-cKO: 3.1 ± 0.6 ( n = 20 dendritic regions in 10 PCs).
    Figure Legend Snippet: P/Q channel-mediated Ca 2+ transient is not changed in Numb-cKO mice. ( A ) A projected z-stack image of a PC filled with Alexa Fluor 594. (Scale bar: 20 μm.) ( B ) Fluo-4 signals in the dendritic field of PCs from control (ctrl) and Numb-cKO mice (P21). The same microscopic fields are shown at basal ( Left ) and peak ( Center ) [Ca 2+ ] i and after application of ω-Agatoxin IVA ( Right ). (Scale bars: 10 μm.) ( C ) ω-Agatoxin–sensitive [Ca 2+ ] i in the cells shown in B . Arrows show the initiation of depolarization. ( D ) Mean amplitudes of changes in Fluo-4 fluorescence (Δ F / F 0 ) in control and Numb-cKO mice. Ctrl: 3.0 ± 0.5 ( n = 17 dendritic regions in 10 PCs). Numb-cKO: 3.1 ± 0.6 ( n = 20 dendritic regions in 10 PCs).

    Techniques Used: Mouse Assay, Fluorescence

    17) Product Images from "Calcium current homeostasis and synaptic deficits in hippocampal neurons from Kelch-like 1 knockout mice"

    Article Title: Calcium current homeostasis and synaptic deficits in hippocampal neurons from Kelch-like 1 knockout mice

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2014.00444

    Characterization of HVA currents . (A) Example time course response of a neuron exposed to: nifedipine (1 μM), ω-Agatoxin IVA (400 nM) and ω-Conotoxin GVIA (2 μM). Right: Current traces obtained before (a) and after addition of the drugs (b–d) (V T = +10 mV, V H = −50 mV). (B) Percentage block of HVA current by antagonists in WT and KO neurons. (C) Western blot analysis of HVA channel subunits. Top: Examples of protein levels of HVA channel subunits in WT and KO hippocampus. Bottom: Quantification of α 1A , α 1C , α 1D , α 1B protein ratios (KO/WT). * p
    Figure Legend Snippet: Characterization of HVA currents . (A) Example time course response of a neuron exposed to: nifedipine (1 μM), ω-Agatoxin IVA (400 nM) and ω-Conotoxin GVIA (2 μM). Right: Current traces obtained before (a) and after addition of the drugs (b–d) (V T = +10 mV, V H = −50 mV). (B) Percentage block of HVA current by antagonists in WT and KO neurons. (C) Western blot analysis of HVA channel subunits. Top: Examples of protein levels of HVA channel subunits in WT and KO hippocampus. Bottom: Quantification of α 1A , α 1C , α 1D , α 1B protein ratios (KO/WT). * p

    Techniques Used: Blocking Assay, Western Blot

    18) Product Images from "Bicistronic CACNA1A Gene Expression in Neurons Derived from Spinocerebellar Ataxia Type 6 Patient-Induced Pluripotent Stem Cells"

    Article Title: Bicistronic CACNA1A Gene Expression in Neurons Derived from Spinocerebellar Ataxia Type 6 Patient-Induced Pluripotent Stem Cells

    Journal: Stem Cells and Development

    doi: 10.1089/scd.2017.0085

    Cav2.1 and α1ACT functions in SCA6 neurons. ( A) Cultured human neurons of all genotypes express functional VGCCs. Ba 2+ I/V curves in SCA6 and control 5w neurons. Currents are normalized to cell capacitance (pA/pF). (B) Cultured human neurons of all genotypes express functional P/Q type channels. Representative traces (300 ms depolarization from −70 to 0 mV) of Ba 2+ currents before and after application of 400 nM ω-Agatoxin IVA, specific blocker of P/Q type currents in SCA6 and control 5w neurons. Traces represent normalized to I max without ω-Agatoxin IVA currents ( I / I max ), showing current amplitude reduction on toxin perfusion, demonstrating the expression of ω-Agatoxin IVA-sensitive Cav2.1 channels. (C) mRNA expression levels of the α1ACT target genes GRN , BTG1 , and TAF1 in SCA6 and control 5w neuronal cultures. Expression levels are normalized to control. GRN gene transcripts are significantly reduced in cultures of SCA6 neurons compared with the control. Each bar represents mean ± s.e.m. from three independent experiments. One-way ANOVA test, Tukey's multiple-comparisons test: * P
    Figure Legend Snippet: Cav2.1 and α1ACT functions in SCA6 neurons. ( A) Cultured human neurons of all genotypes express functional VGCCs. Ba 2+ I/V curves in SCA6 and control 5w neurons. Currents are normalized to cell capacitance (pA/pF). (B) Cultured human neurons of all genotypes express functional P/Q type channels. Representative traces (300 ms depolarization from −70 to 0 mV) of Ba 2+ currents before and after application of 400 nM ω-Agatoxin IVA, specific blocker of P/Q type currents in SCA6 and control 5w neurons. Traces represent normalized to I max without ω-Agatoxin IVA currents ( I / I max ), showing current amplitude reduction on toxin perfusion, demonstrating the expression of ω-Agatoxin IVA-sensitive Cav2.1 channels. (C) mRNA expression levels of the α1ACT target genes GRN , BTG1 , and TAF1 in SCA6 and control 5w neuronal cultures. Expression levels are normalized to control. GRN gene transcripts are significantly reduced in cultures of SCA6 neurons compared with the control. Each bar represents mean ± s.e.m. from three independent experiments. One-way ANOVA test, Tukey's multiple-comparisons test: * P

    Techniques Used: Cell Culture, Functional Assay, Mass Spectrometry, Expressing

    19) 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

    20) Product Images from "Ion Channel Expression in the Developing Enteric Nervous System"

    Article Title: Ion Channel Expression in the Developing Enteric Nervous System

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0123436

    Expression of Ca 2+ channels and the lack of effect of Ca 2+ channel blockers on ENCC migration and neuritogenesis. A. RT-PCR confirming expression of transcripts encoding 8 calcium channels in purified (FACS-sorted) ENCCs from E11.5 gut. Adult mouse brain (Br) was used as a positive control and-RT was a negative control (-). B, C. Immunohistochemistry using antisera to Ca v 2.1 ( B ) and Ca v 2.2 ( C ) of dissociated E14.5 gut cultured for 48 hours revealed Ca v 2.1 and Ca v 2.2 immunostaining of Tuj1+ neurites ( arrows ). Tuj1+ cell bodies show some Ca v 2.1 staining, but little, if any, Ca v 2.2 immunostaining. D. There was no significant difference in the distance migrated by ENCCs in explants grown in the presence of the N-type blocker, ω-conotoxin GVIA (n = 9), the P/Q-type blocker, ω-agatoxin IVA (n = 10), the L-type blocker, nicardipine (n = 9) or the T-type blocker, mibefradil (n = 10) compared to controls (n = 11) (mean ± SEM; one way ANOVA; minimum of 2 experiments). E. Effects of calcium channel blockers on neuritogenesis. There was no significant difference in the percentage of Tuj1+ cells that extended neurites between control and drug-treated cultures of E14.5 dissociated gut (for controls and each drug, a minimum of 950 Tuj1+ cells was examined from 5 or 6 coverslips from 2 experiments).
    Figure Legend Snippet: Expression of Ca 2+ channels and the lack of effect of Ca 2+ channel blockers on ENCC migration and neuritogenesis. A. RT-PCR confirming expression of transcripts encoding 8 calcium channels in purified (FACS-sorted) ENCCs from E11.5 gut. Adult mouse brain (Br) was used as a positive control and-RT was a negative control (-). B, C. Immunohistochemistry using antisera to Ca v 2.1 ( B ) and Ca v 2.2 ( C ) of dissociated E14.5 gut cultured for 48 hours revealed Ca v 2.1 and Ca v 2.2 immunostaining of Tuj1+ neurites ( arrows ). Tuj1+ cell bodies show some Ca v 2.1 staining, but little, if any, Ca v 2.2 immunostaining. D. There was no significant difference in the distance migrated by ENCCs in explants grown in the presence of the N-type blocker, ω-conotoxin GVIA (n = 9), the P/Q-type blocker, ω-agatoxin IVA (n = 10), the L-type blocker, nicardipine (n = 9) or the T-type blocker, mibefradil (n = 10) compared to controls (n = 11) (mean ± SEM; one way ANOVA; minimum of 2 experiments). E. Effects of calcium channel blockers on neuritogenesis. There was no significant difference in the percentage of Tuj1+ cells that extended neurites between control and drug-treated cultures of E14.5 dissociated gut (for controls and each drug, a minimum of 950 Tuj1+ cells was examined from 5 or 6 coverslips from 2 experiments).

    Techniques Used: Expressing, Migration, Reverse Transcription Polymerase Chain Reaction, Purification, FACS, Positive Control, Negative Control, Immunohistochemistry, Cell Culture, Immunostaining, Staining

    21) Product Images from "Mechanistic insights into the detection of free fatty and bile acids by ileal glucagon-like peptide-1 secreting cells"

    Article Title: Mechanistic insights into the detection of free fatty and bile acids by ileal glucagon-like peptide-1 secreting cells

    Journal: Molecular Metabolism

    doi: 10.1016/j.molmet.2017.11.005

    Electrophysiological characterization of organoid-derived ileal L-cells. (A) Perforated-patch current clamp recording of an organoid-derived ileal L-cell, firing action potentials in response to depolarizing current injections. Current was injected to maintain the cell at −70 mV, and a series of 10 ms current pulses were applied, increasing in magnitude by 2 pA. The pulse protocol is illustrated below. (B) Perforated-patch current clamp recording of spontaneous action potential firing from an ileal L-cell. (C) Representative traces using the same protocol as in (A), before (Ci) and during application of 0.3 μM tetrodotoxin (TTX, Cii) and during application of TTX + 0.5 μM ω-agatoxin-IVA (Ciii). Dashed line represents the threshold of action potential firing. The insets show spontaneous action potential firing under the same treatment conditions. (Civ) Threshold for action potential firing (n = 5) and (Cv) % inhibition of action potential peak following application of channel blockers, expressed as a % of total block by application of TTX (0.3 μM) + Cd 2+ (100 μM). (Di) Inward current from a perforated-patch voltage clamp recording and sample traces following application of 0.3 μM TTX (Dii, orange trace) or 100 μM Cd 2+ (Diii, gray trace). Currents were elicited from a series of 70 ms voltage steps from −110 to +60 mV, from a holding potential of −80 mV. Only the current response to the +10 mV voltage step is shown and is illustrated below the current traces. (Div) Peak current amplitude of the fast and slow current components. Gene expression data of Scn (Ei) or Cacna (Eii) genes by RNA sequencing of FACS-sorted L-cells from mouse ileum (white circles) and colon (black circles). Individual data points represent fragments per kilobase of transcript per million mapped reads (FPKM) from 1 mouse. Mean values (n = 3) are presented as lines. (Fi) Superimposed Ca 2+ currents from an ileal L-cell before and during exposure to Ca 2+ channel blockers. Red trace represents calcium current ( I Ca ) recorded in the presence of ω-agatoxin-IVA (0.5 μM), pink trace represents I Ca recorded following subsequent application of isradipine (10 μM), and gray trace represents I Ca recorded following application of cadmium (Cd 2+ , 100 μM). Currents were elicited using the protocol described in (D) and only the current responses to the +10 mV voltage step are shown. (Fii) Contribution of Ca 2+ channel subtype to total Ca 2+ current measured. (Fiii) The peak I Ca –voltage relationship for a representative organoid ileal L-cell following application of Ca 2+ channel blockers. Statistical analysis performed using either by Wilcoxon matched-pairs signed rank test (Civ), one-way ANOVA with Tukey's multiple comparison (Cv) or multiple t-tests with Holm-Sidak multiple comparisons correction (E), p
    Figure Legend Snippet: Electrophysiological characterization of organoid-derived ileal L-cells. (A) Perforated-patch current clamp recording of an organoid-derived ileal L-cell, firing action potentials in response to depolarizing current injections. Current was injected to maintain the cell at −70 mV, and a series of 10 ms current pulses were applied, increasing in magnitude by 2 pA. The pulse protocol is illustrated below. (B) Perforated-patch current clamp recording of spontaneous action potential firing from an ileal L-cell. (C) Representative traces using the same protocol as in (A), before (Ci) and during application of 0.3 μM tetrodotoxin (TTX, Cii) and during application of TTX + 0.5 μM ω-agatoxin-IVA (Ciii). Dashed line represents the threshold of action potential firing. The insets show spontaneous action potential firing under the same treatment conditions. (Civ) Threshold for action potential firing (n = 5) and (Cv) % inhibition of action potential peak following application of channel blockers, expressed as a % of total block by application of TTX (0.3 μM) + Cd 2+ (100 μM). (Di) Inward current from a perforated-patch voltage clamp recording and sample traces following application of 0.3 μM TTX (Dii, orange trace) or 100 μM Cd 2+ (Diii, gray trace). Currents were elicited from a series of 70 ms voltage steps from −110 to +60 mV, from a holding potential of −80 mV. Only the current response to the +10 mV voltage step is shown and is illustrated below the current traces. (Div) Peak current amplitude of the fast and slow current components. Gene expression data of Scn (Ei) or Cacna (Eii) genes by RNA sequencing of FACS-sorted L-cells from mouse ileum (white circles) and colon (black circles). Individual data points represent fragments per kilobase of transcript per million mapped reads (FPKM) from 1 mouse. Mean values (n = 3) are presented as lines. (Fi) Superimposed Ca 2+ currents from an ileal L-cell before and during exposure to Ca 2+ channel blockers. Red trace represents calcium current ( I Ca ) recorded in the presence of ω-agatoxin-IVA (0.5 μM), pink trace represents I Ca recorded following subsequent application of isradipine (10 μM), and gray trace represents I Ca recorded following application of cadmium (Cd 2+ , 100 μM). Currents were elicited using the protocol described in (D) and only the current responses to the +10 mV voltage step are shown. (Fii) Contribution of Ca 2+ channel subtype to total Ca 2+ current measured. (Fiii) The peak I Ca –voltage relationship for a representative organoid ileal L-cell following application of Ca 2+ channel blockers. Statistical analysis performed using either by Wilcoxon matched-pairs signed rank test (Civ), one-way ANOVA with Tukey's multiple comparison (Cv) or multiple t-tests with Holm-Sidak multiple comparisons correction (E), p

    Techniques Used: Derivative Assay, Injection, Mass Spectrometry, Inhibition, Blocking Assay, Expressing, RNA Sequencing Assay, FACS

    22) Product Images from "TRPM8 and Nav1.8 sodium channels are required for transthyretin-induced calcium influx in growth cones of small-diameter TrkA-positive sensory neurons"

    Article Title: TRPM8 and Nav1.8 sodium channels are required for transthyretin-induced calcium influx in growth cones of small-diameter TrkA-positive sensory neurons

    Journal: Molecular Neurodegeneration

    doi: 10.1186/1750-1326-6-19

    Effect of ion channel blockers on L55P TTR-induced calcium influx and analysis of sensitivity to icilin and capsaicin , (A) L55P was applied to DRG growth cones in the presence of VGCC inhibitors (nifedipine, ω-agatoxin IVA, ω-conotoxin GIVA), Na V inhibitors (tetrodotoxin, ambroxol and carbamazepine) and TRP inhibitors (SKF-96365, BCTC). The resulting maximal calcium influx (max ΔF/F 0 ) calculated over the imaging period (7 min) was calculated. (B) Effect of capsaicin (1 μM) and icilin (100 μM) on cytosolic calcium in DRG growth cones in culture. When DRG cultures were pre-treated with ambroxol (5 μM), icilin-induced calcium fluorescence was significantly decreased. All graphs show maximal ΔF/F 0 ± SEM for n = 12-24 growth cones. Significant differences from control values are depicted as: * p
    Figure Legend Snippet: Effect of ion channel blockers on L55P TTR-induced calcium influx and analysis of sensitivity to icilin and capsaicin , (A) L55P was applied to DRG growth cones in the presence of VGCC inhibitors (nifedipine, ω-agatoxin IVA, ω-conotoxin GIVA), Na V inhibitors (tetrodotoxin, ambroxol and carbamazepine) and TRP inhibitors (SKF-96365, BCTC). The resulting maximal calcium influx (max ΔF/F 0 ) calculated over the imaging period (7 min) was calculated. (B) Effect of capsaicin (1 μM) and icilin (100 μM) on cytosolic calcium in DRG growth cones in culture. When DRG cultures were pre-treated with ambroxol (5 μM), icilin-induced calcium fluorescence was significantly decreased. All graphs show maximal ΔF/F 0 ± SEM for n = 12-24 growth cones. Significant differences from control values are depicted as: * p

    Techniques Used: Imaging, Fluorescence

    23) Product Images from "The Immediately Releasable Pool of Mouse Chromaffin Cell Vesicles Is Coupled to P/Q-Type Calcium Channels via the Synaptic Protein Interaction Site"

    Article Title: The Immediately Releasable Pool of Mouse Chromaffin Cell Vesicles Is Coupled to P/Q-Type Calcium Channels via the Synaptic Protein Interaction Site

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0054846

    Synprint transfection does not modify the relative contributions of calcium current subtypes. The figures on the top show the calcium current vs. voltage relationships for ( A ) Syn + cells in control conditions (Syn + ) (n = 9), Syn + cells treated with 200 nM ω-agatoxin-IVA (Syn + +AGA) (n = 9), and Syn + cells treated with 10 µM nitrendipine (Syn + +NITRE) (n = 7); and for ( B ) nontransfected cells in control conditions (Control) (n = 11), nontransfected cells treated with 200 nM ω-agatoxin-IVA (Control+AGA) (n = 9), and nontransfected cells treated with 10 µM nitrendipine (Control+NITRE) (n = 9). The cells were stimulated with 50 ms square voltage pulses, from a holding potential of −80 mV to the potentials indicated in the abscissas of panels A and B. C . Original records of Ca 2+ currents obtained in response to square depolarizations to +10 mV for the same three conditions detailed in panel A. D . Original records of Ca 2+ currents obtained in response to a square depolarization to +10 mV for the same three conditions detailed in panel B.
    Figure Legend Snippet: Synprint transfection does not modify the relative contributions of calcium current subtypes. The figures on the top show the calcium current vs. voltage relationships for ( A ) Syn + cells in control conditions (Syn + ) (n = 9), Syn + cells treated with 200 nM ω-agatoxin-IVA (Syn + +AGA) (n = 9), and Syn + cells treated with 10 µM nitrendipine (Syn + +NITRE) (n = 7); and for ( B ) nontransfected cells in control conditions (Control) (n = 11), nontransfected cells treated with 200 nM ω-agatoxin-IVA (Control+AGA) (n = 9), and nontransfected cells treated with 10 µM nitrendipine (Control+NITRE) (n = 9). The cells were stimulated with 50 ms square voltage pulses, from a holding potential of −80 mV to the potentials indicated in the abscissas of panels A and B. C . Original records of Ca 2+ currents obtained in response to square depolarizations to +10 mV for the same three conditions detailed in panel A. D . Original records of Ca 2+ currents obtained in response to a square depolarization to +10 mV for the same three conditions detailed in panel B.

    Techniques Used: Transfection, Mass Spectrometry

    Synprint mediates the coupling of IRP with P/Q-type calcium channels. A: Examples of original records of Ca 2+ currents (top) and membrane capacitance changes (bottom) in response to the application of the dual 10 ms pulse protocol, in Syn − (i) or Syn + (ii) cells. B. (i) Calcium current densities obtained in Syn − (n = 30), EGFP (n = 7), Syn + (n = 14), and Syn + cells treated with 200 nM ω-agatoxin-IVA (Syn + +AGA) (n = 10). (ii) Averaged estimations of B min and B max for the IRP, obtained in response to the application of the dual 10 ms pulse protocol under the same conditions mentioned in (i). Please note that while Syn − , EGFP and Syn + have almost identical I Ca2+ values, a highly significant decrease (p
    Figure Legend Snippet: Synprint mediates the coupling of IRP with P/Q-type calcium channels. A: Examples of original records of Ca 2+ currents (top) and membrane capacitance changes (bottom) in response to the application of the dual 10 ms pulse protocol, in Syn − (i) or Syn + (ii) cells. B. (i) Calcium current densities obtained in Syn − (n = 30), EGFP (n = 7), Syn + (n = 14), and Syn + cells treated with 200 nM ω-agatoxin-IVA (Syn + +AGA) (n = 10). (ii) Averaged estimations of B min and B max for the IRP, obtained in response to the application of the dual 10 ms pulse protocol under the same conditions mentioned in (i). Please note that while Syn − , EGFP and Syn + have almost identical I Ca2+ values, a highly significant decrease (p

    Techniques Used: Mass Spectrometry

    24) 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

    25) Product Images from "CRMP-2 peptide mediated decrease of high and low voltage-activated calcium channels, attenuation of nociceptor excitability, and anti-nociception in a model of AIDS therapy-induced painful peripheral neuropathy"

    Article Title: CRMP-2 peptide mediated decrease of high and low voltage-activated calcium channels, attenuation of nociceptor excitability, and anti-nociception in a model of AIDS therapy-induced painful peripheral neuropathy

    Journal: Molecular Pain

    doi: 10.1186/1744-8069-8-54

    Pharmacological and biophysical dissection of TAT-CBD3A6K-mediated block of T-and R-type calcium currents in DRG neurons. ( A ) Representative T- (top) and R-type (bottom) current traces obtained from two separate DRG neurons evoked by 200 ms steps in 5 mV increments from −60 mV to +50 mV, from a holding potential of −90 mV. The extracellular bath solution contained 5 mM Nifedipine (Nif), 200 nM ω-Agatoxin IVA (Aga) and 500 nM ω-Conotoxin GVIA (CTX) to block L-, P/Q-, and N-type calcium currents, respectively. ( B ) Summary of the normalized conductance (G) versus voltage relations for DRG neurons with T- (filled squares) or R- (open squares) type calcium currents. The dotted line at −10 mV highlights the clear discrimination in conductances between T- and R-type currents. ( C ) Representative currents, evoked by a ramp depolarizations from −60 mV to +20 mV for 2 s, illustrating the presence of both T- and R-type currents in the same DRG neuron before (left trace) and 2 min after application 10 μM TAT-CBD3A6K (right trace)
    Figure Legend Snippet: Pharmacological and biophysical dissection of TAT-CBD3A6K-mediated block of T-and R-type calcium currents in DRG neurons. ( A ) Representative T- (top) and R-type (bottom) current traces obtained from two separate DRG neurons evoked by 200 ms steps in 5 mV increments from −60 mV to +50 mV, from a holding potential of −90 mV. The extracellular bath solution contained 5 mM Nifedipine (Nif), 200 nM ω-Agatoxin IVA (Aga) and 500 nM ω-Conotoxin GVIA (CTX) to block L-, P/Q-, and N-type calcium currents, respectively. ( B ) Summary of the normalized conductance (G) versus voltage relations for DRG neurons with T- (filled squares) or R- (open squares) type calcium currents. The dotted line at −10 mV highlights the clear discrimination in conductances between T- and R-type currents. ( C ) Representative currents, evoked by a ramp depolarizations from −60 mV to +20 mV for 2 s, illustrating the presence of both T- and R-type currents in the same DRG neuron before (left trace) and 2 min after application 10 μM TAT-CBD3A6K (right trace)

    Techniques Used: Dissection, Blocking Assay, Mass Spectrometry

    Characterization of TAT-CBD3A6K-mediated inhibition of T- and R-type calcium currents. ( A ) Representative family of traces from a DRG neuron with both T- and R-type calcium currents before ( left ), 2 min ( middle ) and 5 min ( right ) after addition of 10 μM TAT-CBD3A6K. Currents were elicited in response to the voltage protocol described in the legend to Figure 5 A. To isolate T- and R-type calcium currents, the extracellular bath solution contained 5 mM Nifedipine (Nif), 200 nM ω-Agatoxin IVA (Aga) and 500 nM ω-Conotoxin GVIA (CTX) to block L-, P/Q-, and N-type calcium currents, respectively. ( B , C ) Time course of TAT-CBD3A6K mediated inhibition (“run-down”) of T-type ( B ) and R-type ( C ) calcium currents. Time course of inhibition is shown as averaged normalized current density (pA pF -1 ) before peptide addition and at intervals of 30 s for 5 min. Averaged values are shown with standard error for 4–6 control cells and 4 cells following addition of 10 μM TAT-CBD3A6K. The asterisk denotes statistical significance (p
    Figure Legend Snippet: Characterization of TAT-CBD3A6K-mediated inhibition of T- and R-type calcium currents. ( A ) Representative family of traces from a DRG neuron with both T- and R-type calcium currents before ( left ), 2 min ( middle ) and 5 min ( right ) after addition of 10 μM TAT-CBD3A6K. Currents were elicited in response to the voltage protocol described in the legend to Figure 5 A. To isolate T- and R-type calcium currents, the extracellular bath solution contained 5 mM Nifedipine (Nif), 200 nM ω-Agatoxin IVA (Aga) and 500 nM ω-Conotoxin GVIA (CTX) to block L-, P/Q-, and N-type calcium currents, respectively. ( B , C ) Time course of TAT-CBD3A6K mediated inhibition (“run-down”) of T-type ( B ) and R-type ( C ) calcium currents. Time course of inhibition is shown as averaged normalized current density (pA pF -1 ) before peptide addition and at intervals of 30 s for 5 min. Averaged values are shown with standard error for 4–6 control cells and 4 cells following addition of 10 μM TAT-CBD3A6K. The asterisk denotes statistical significance (p

    Techniques Used: Inhibition, Blocking Assay

    26) 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

    27) Product Images from "Alteration of the mu opioid receptor: Ca2+ channel signaling pathway in a subset of rat sensory neurons following chronic femoral artery occlusion"

    Article Title: Alteration of the mu opioid receptor: Ca2+ channel signaling pathway in a subset of rat sensory neurons following chronic femoral artery occlusion

    Journal: Journal of Neurophysiology

    doi: 10.1152/jn.00630.2014

    A and B : summary scatter plots of Ca 2+ current density (pA/pF) and membrane capacitance (pF) in acutely isolated DiI-labeled and EGFP-expressing DRG neurons from rats with freely perfused and 72 h-ligated femoral arteries. Current density was calculated from the peak Ca 2+ current amplitude normalized to membrane capacitance. The lines on the plots indicate the means (±SE), and the numbers in parentheses indicate the number of neurons tested. C : summary plot of the mean (±SE) Ca 2+ current inhibition produced by the N (ω-conotoxin GVIA; 10 μM)- and P/Q [ω-agatoxin IVA (AgaIVa]; 0.2 μM)-type Ca 2+ channel blockers in DRG neurons from freely perfused and ligated rats. The number of cells tested is indicated in parentheses.
    Figure Legend Snippet: A and B : summary scatter plots of Ca 2+ current density (pA/pF) and membrane capacitance (pF) in acutely isolated DiI-labeled and EGFP-expressing DRG neurons from rats with freely perfused and 72 h-ligated femoral arteries. Current density was calculated from the peak Ca 2+ current amplitude normalized to membrane capacitance. The lines on the plots indicate the means (±SE), and the numbers in parentheses indicate the number of neurons tested. C : summary plot of the mean (±SE) Ca 2+ current inhibition produced by the N (ω-conotoxin GVIA; 10 μM)- and P/Q [ω-agatoxin IVA (AgaIVa]; 0.2 μM)-type Ca 2+ channel blockers in DRG neurons from freely perfused and ligated rats. The number of cells tested is indicated in parentheses.

    Techniques Used: Isolation, Labeling, Expressing, Inhibition, Produced

    28) Product Images from "Use-dependent potentiation of voltage-gated calcium channels rescues neurotransmission in nerve terminals intoxicated by botulinum neurotoxin serotype A"

    Article Title: Use-dependent potentiation of voltage-gated calcium channels rescues neurotransmission in nerve terminals intoxicated by botulinum neurotoxin serotype A

    Journal: Scientific Reports

    doi: 10.1038/s41598-017-16064-3

    Rescue of spontaneous synaptic activity in BoNT/A-silenced synapses by elevated extracellular Ca 2+ requires VGCCs. ( A ) Representative whole-cell recordings and mean mEPSC frequencies from non-intoxicated cultures in the presence of 2, 4, 8, or 16 mM Ca 2+ . Representative whole-cell recordings and mean mEPSC frequencies from BoNT/A-intoxicated cultures, in the presence of 2, 4, 8, or 16 mM Ca 2+ as well in 16 mM Ca 2+ with VGCC antagonists (10 µM nimodipine, 0.5 µM ω-agatoxin IVA and 0.5 µM ω-conotoxin MVIIC). ( C ) Representative whole-cell recordings and mean mEPSC frequencies from neurons intoxicated by BoNT/D or BoNT/E and incubated in 2 or 16 mM Ca 2+ . mEPSC frequencies are normalized to recordings from age-matched, non-intoxicated control cultures. Scale bars represent 5 s (x-axis) and 40 pA (y-axis). All data presented as mean ± SEM and n ≥ 10 neurons for all conditions. **Indicates p
    Figure Legend Snippet: Rescue of spontaneous synaptic activity in BoNT/A-silenced synapses by elevated extracellular Ca 2+ requires VGCCs. ( A ) Representative whole-cell recordings and mean mEPSC frequencies from non-intoxicated cultures in the presence of 2, 4, 8, or 16 mM Ca 2+ . Representative whole-cell recordings and mean mEPSC frequencies from BoNT/A-intoxicated cultures, in the presence of 2, 4, 8, or 16 mM Ca 2+ as well in 16 mM Ca 2+ with VGCC antagonists (10 µM nimodipine, 0.5 µM ω-agatoxin IVA and 0.5 µM ω-conotoxin MVIIC). ( C ) Representative whole-cell recordings and mean mEPSC frequencies from neurons intoxicated by BoNT/D or BoNT/E and incubated in 2 or 16 mM Ca 2+ . mEPSC frequencies are normalized to recordings from age-matched, non-intoxicated control cultures. Scale bars represent 5 s (x-axis) and 40 pA (y-axis). All data presented as mean ± SEM and n ≥ 10 neurons for all conditions. **Indicates p

    Techniques Used: Activity Assay, Incubation

    29) Product Images from "Effects of IgG anti-GM1 monoclonal antibodies on neuromuscular transmission and calcium channel binding in rat neuromuscular junctions"

    Article Title: Effects of IgG anti-GM1 monoclonal antibodies on neuromuscular transmission and calcium channel binding in rat neuromuscular junctions

    Journal: Experimental and Therapeutic Medicine

    doi: 10.3892/etm.2015.2575

    Effects of pretreatment with the P/Q-type calcium channel blocker, ω-agatoxin IVA, on the inhibitory effect of IgG anti-GM1 mAb (1:100) on spontaneous muscle action potentials (SMAPs) in the spinal cord-muscle co-culture system. (A) Inhibition
    Figure Legend Snippet: Effects of pretreatment with the P/Q-type calcium channel blocker, ω-agatoxin IVA, on the inhibitory effect of IgG anti-GM1 mAb (1:100) on spontaneous muscle action potentials (SMAPs) in the spinal cord-muscle co-culture system. (A) Inhibition

    Techniques Used: Co-Culture Assay, Inhibition

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    Alomone Labs ω agatoxin iva
    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, <t>ω-agatoxin</t> <t>IVA</t> (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
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    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

    Journal: eNeuro

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

    doi: 10.1523/ENEURO.0278-18.2018

    Figure Lengend 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

    Article Snippet: Reagents and solutions Isoflurane was obtained from Abbott, ω-conotoxin GVIA and ω-agatoxin IVA from Alomone Labs, and 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and (2R )-amino-5-phosphonovaleric acid (AP5) from Tocris.

    Techniques:

    Pharmacological dissection of high-voltage-activated (HVA)- I Ca in R-B neurons. A and B : time courses of I Ca amplitude during serial application of 10 μM nifedipine, 0.5 μM ω-agatoxin IVA, 3 μM ω-conotoxin GVIA,

    Journal: Journal of Neurophysiology

    Article Title: Identification and Modulation of Voltage-Gated Ca2+ Currents in Zebrafish Rohon-Beard Neurons

    doi: 10.1152/jn.00625.2010

    Figure Lengend Snippet: Pharmacological dissection of high-voltage-activated (HVA)- I Ca in R-B neurons. A and B : time courses of I Ca amplitude during serial application of 10 μM nifedipine, 0.5 μM ω-agatoxin IVA, 3 μM ω-conotoxin GVIA,

    Article Snippet: Stock solutions were made for the following drugs: γ-aminobutyric acid (GABA), (rs)-baclofen, l-glutamic acid hydrochloride, oxotremorine M (all from TOCRIS Cookson, Ellisville, MO), nifedipine (EMD Chemicals, Gibbstown, NJ), tetrodotoxin (TTX), ω-agatoxin IVA, ω-conotoxin GVIA, ω-conotoxin MVIIA, SNX-482 (all from Alomone Labs, Jerusalem, Israel), guanylyl 5′-imidodiphosphate [Gpp(NH)p], (±)-norepinephrine, serotonin hydrochloride (5-hydroxytryptamine, 5-HT), NiCl2 , and CdCl2 (all from Sigma-Aldrich).

    Techniques: Dissection

    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

    Journal: Frontiers in Cellular Neuroscience

    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

    doi: 10.3389/fncel.2019.00278

    Figure Lengend 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

    Article Snippet: L-, P/Q-, N-, R-, and T-type Ca2+ currents were isolated with 10 μM nimodipine (Sigma-Aldrich, St. Louis, MO, United States), 1 μM ω-agatoxin IVA, 1 μM ω-conotoxin, 1 μM SNX482 (from Alomone Labs, Jerusalem, Israel) and 5 μM mibefradil (Tocris Bioscience, Bristol, United Kingdom), respectively.

    Techniques: 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

    Journal: Frontiers in Cellular Neuroscience

    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

    doi: 10.3389/fncel.2019.00278

    Figure Lengend 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

    Article Snippet: L-, P/Q-, N-, R-, and T-type Ca2+ currents were isolated with 10 μM nimodipine (Sigma-Aldrich, St. Louis, MO, United States), 1 μM ω-agatoxin IVA, 1 μM ω-conotoxin, 1 μM SNX482 (from Alomone Labs, Jerusalem, Israel) and 5 μM mibefradil (Tocris Bioscience, Bristol, United Kingdom), respectively.

    Techniques: Mouse Assay, Whisker Assay

    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

    Journal: The Journal of Physiology

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

    doi: 10.1113/JP277172

    Figure Lengend 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

    Article Snippet: 6,7‐dinitroquinoxaline‐2,3‐dione disodium salt (DNQX) from Abcam Biochemicals. (R)‐baclofen and gabazine (SR 95531) from Tocris Bioscience (Bristol, UK). ω‐conotoxin GVIA, ω‐agatoxin IVA and nifedipine from Alomone labs (Jerusalem, Israel).

    Techniques: