snx 482  (Alomone Labs)


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    Structured Review

    Alomone Labs snx 482
    Glutamatergic transmission in the NL is predominantly triggered by Ca 2+ entry through N-type VGCCs. A : Both the ipsilateral (open circles) and the contralateral (filled circles) EPSCs recorded from the same NL neuron were largely and irreversibly blocked by the N-type blocker ω-Conotoxin-GVIA (ω-CTx-GVIA, 2.5 μM), with nearly identical time courses. Averaged traces under control (thin traces) and drug (thick traces) conditions are shown on the right. Stimulus artifacts are truncated for clarity. B-C : No inhibition of EPSCs was produced by the P/Q-type blocker ω-Agatoxin-IVA (ω-Aga-IVA, 0.1 μM) or the L-type blocker nimodipine (10 μM). D: A small and reversible inhibition of the EPSCs by the R-type blocker <t>SNX-482</t> (50 nM) was observed. The different time courses of the EPSCs observed in the sampled neurons may be due to different locations of the neurons along the tonotopic frequency axis. E : Summary of the effects of different VGCC blockers on EPSCs of NL neurons. ω-CTx-GVIA inhibited the ipsilateral and the contralateral EPSCs by 88% and 86%, respectively. Blockers for P/Q- and L-type VGCCs had no effects on EPSCs. SNX-482 produced a small inhibition with a large variation among cells. No differences in the percent inhibition by either drug were detected between the ipsilateral and the contralateral EPSCs. Error bars represent standard deviations. n.s.: non-significant (paired t-test, p > 0.05; the number of cells is indicated in parentheses).
    Snx 482, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 40 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Regulation of glutamatergic and GABAergic neurotransmission in the chick nucleus laminaris: role of N-type calcium channels"

    Article Title: Regulation of glutamatergic and GABAergic neurotransmission in the chick nucleus laminaris: role of N-type calcium channels

    Journal: Neuroscience

    doi: 10.1016/j.neuroscience.2009.09.013

    Glutamatergic transmission in the NL is predominantly triggered by Ca 2+ entry through N-type VGCCs. A : Both the ipsilateral (open circles) and the contralateral (filled circles) EPSCs recorded from the same NL neuron were largely and irreversibly blocked by the N-type blocker ω-Conotoxin-GVIA (ω-CTx-GVIA, 2.5 μM), with nearly identical time courses. Averaged traces under control (thin traces) and drug (thick traces) conditions are shown on the right. Stimulus artifacts are truncated for clarity. B-C : No inhibition of EPSCs was produced by the P/Q-type blocker ω-Agatoxin-IVA (ω-Aga-IVA, 0.1 μM) or the L-type blocker nimodipine (10 μM). D: A small and reversible inhibition of the EPSCs by the R-type blocker SNX-482 (50 nM) was observed. The different time courses of the EPSCs observed in the sampled neurons may be due to different locations of the neurons along the tonotopic frequency axis. E : Summary of the effects of different VGCC blockers on EPSCs of NL neurons. ω-CTx-GVIA inhibited the ipsilateral and the contralateral EPSCs by 88% and 86%, respectively. Blockers for P/Q- and L-type VGCCs had no effects on EPSCs. SNX-482 produced a small inhibition with a large variation among cells. No differences in the percent inhibition by either drug were detected between the ipsilateral and the contralateral EPSCs. Error bars represent standard deviations. n.s.: non-significant (paired t-test, p > 0.05; the number of cells is indicated in parentheses).
    Figure Legend Snippet: Glutamatergic transmission in the NL is predominantly triggered by Ca 2+ entry through N-type VGCCs. A : Both the ipsilateral (open circles) and the contralateral (filled circles) EPSCs recorded from the same NL neuron were largely and irreversibly blocked by the N-type blocker ω-Conotoxin-GVIA (ω-CTx-GVIA, 2.5 μM), with nearly identical time courses. Averaged traces under control (thin traces) and drug (thick traces) conditions are shown on the right. Stimulus artifacts are truncated for clarity. B-C : No inhibition of EPSCs was produced by the P/Q-type blocker ω-Agatoxin-IVA (ω-Aga-IVA, 0.1 μM) or the L-type blocker nimodipine (10 μM). D: A small and reversible inhibition of the EPSCs by the R-type blocker SNX-482 (50 nM) was observed. The different time courses of the EPSCs observed in the sampled neurons may be due to different locations of the neurons along the tonotopic frequency axis. E : Summary of the effects of different VGCC blockers on EPSCs of NL neurons. ω-CTx-GVIA inhibited the ipsilateral and the contralateral EPSCs by 88% and 86%, respectively. Blockers for P/Q- and L-type VGCCs had no effects on EPSCs. SNX-482 produced a small inhibition with a large variation among cells. No differences in the percent inhibition by either drug were detected between the ipsilateral and the contralateral EPSCs. Error bars represent standard deviations. n.s.: non-significant (paired t-test, p > 0.05; the number of cells is indicated in parentheses).

    Techniques Used: Transmission Assay, Inhibition, Produced

    2) Product Images from "Alternative splicing of auxiliary β2-subunits stabilizes Cav2.3 Ca2+ channel activity in continuously active midbrain dopamine neurons"

    Article Title: Alternative splicing of auxiliary β2-subunits stabilizes Cav2.3 Ca2+ channel activity in continuously active midbrain dopamine neurons

    Journal: bioRxiv

    doi: 10.1101/2021.02.10.430224

    SNX-482 inhibition of non-L-type I Ca in cultured midbrain DA neurons. A. Representative traces illustrating the inhibition of non-L-type I Ca by 100 nM SNX-482 (red). Cells were initially perfused with a bath solution containing 3 μM isradipine (ISR, black). Full block was obtained using 2 μM Cd 2+ (blue). Square pulses (50 ms) were applied to 0 mV from a holding potential of −70 mV (top) B. Current amplitude values plotted as a function of time. After stabilization of I Ca with ISR (black circles), 100 nM SNX-482 was applied. The remaining currents was blocked by 2 μM Cd 2+ . C. SNX-482 inhibition expressed as % of control I Ca after LTCC block using 3 μM ISR. D. Mean current amplitude at the end of ISR application and at the end of SNX-482 application. Data represent the means ± SEM for the indicated number of experiments (N=4). Statistical significance was determined using paired Student’s t-test: *** p
    Figure Legend Snippet: SNX-482 inhibition of non-L-type I Ca in cultured midbrain DA neurons. A. Representative traces illustrating the inhibition of non-L-type I Ca by 100 nM SNX-482 (red). Cells were initially perfused with a bath solution containing 3 μM isradipine (ISR, black). Full block was obtained using 2 μM Cd 2+ (blue). Square pulses (50 ms) were applied to 0 mV from a holding potential of −70 mV (top) B. Current amplitude values plotted as a function of time. After stabilization of I Ca with ISR (black circles), 100 nM SNX-482 was applied. The remaining currents was blocked by 2 μM Cd 2+ . C. SNX-482 inhibition expressed as % of control I Ca after LTCC block using 3 μM ISR. D. Mean current amplitude at the end of ISR application and at the end of SNX-482 application. Data represent the means ± SEM for the indicated number of experiments (N=4). Statistical significance was determined using paired Student’s t-test: *** p

    Techniques Used: Inhibition, Cell Culture, Blocking Assay

    SNX-482 effects on pacemaking of cultured mouse midbrain DA neurons. A. Representative recording of spontaneous firing activity of cultured midbrain dopaminergic neurons before, during and after the application (wash-out) of 100 nM SNX-482. Inset (bottom right): overlay of one single AP before (control) and during the application of 100 nM SNX-482. B. Firing frequency [Hz], coefficient of variation of the interspike interval [%], and AHP peak [mV] before (control) and during the application of 100 nM SNX-482. Data represent the means ± SEM for the indicated number of experiments (N=3). Statistical significance was determined using paired Student’s t-test.: *** p
    Figure Legend Snippet: SNX-482 effects on pacemaking of cultured mouse midbrain DA neurons. A. Representative recording of spontaneous firing activity of cultured midbrain dopaminergic neurons before, during and after the application (wash-out) of 100 nM SNX-482. Inset (bottom right): overlay of one single AP before (control) and during the application of 100 nM SNX-482. B. Firing frequency [Hz], coefficient of variation of the interspike interval [%], and AHP peak [mV] before (control) and during the application of 100 nM SNX-482. Data represent the means ± SEM for the indicated number of experiments (N=3). Statistical significance was determined using paired Student’s t-test.: *** p

    Techniques Used: Cell Culture, Activity Assay

    3) Product Images from "Low-threshold calcium currents contribute to locomotor-like activity in neonatal mice"

    Article Title: Low-threshold calcium currents contribute to locomotor-like activity in neonatal mice

    Journal: Journal of Neurophysiology

    doi: 10.1152/jn.00583.2011

    Application of the selective R-type calcium channel blocker SNX-482 does not alter fictive locomotor-like activity. A : paired extracellular recordings from iL2 and iL5 in an isolated whole-cord preparation with cocktail (3–10 μM NMDA,
    Figure Legend Snippet: Application of the selective R-type calcium channel blocker SNX-482 does not alter fictive locomotor-like activity. A : paired extracellular recordings from iL2 and iL5 in an isolated whole-cord preparation with cocktail (3–10 μM NMDA,

    Techniques Used: Activity Assay, Isolation

    4) Product Images from "Recruitment of apical dendritic T-type Ca2+ channels by backpropagating spikes underlies de novo intrinsic bursting in hippocampal epileptogenesis"

    Article Title: Recruitment of apical dendritic T-type Ca2+ channels by backpropagating spikes underlies de novo intrinsic bursting in hippocampal epileptogenesis

    Journal: The Journal of Physiology

    doi: 10.1113/jphysiol.2007.127670

    Effects of amiloride and SNX-482 on bursting
    Figure Legend Snippet: Effects of amiloride and SNX-482 on bursting

    Techniques Used:

    5) Product Images from "Spontaneous release of acetylcholine from autonomic nerves in the bladder"

    Article Title: Spontaneous release of acetylcholine from autonomic nerves in the bladder

    Journal: British Journal of Pharmacology

    doi: 10.1111/j.1476-5381.2009.00166.x

    Effects of CTX alone and of a cocktail of toxins (CTX, ATX and SNX 482) on physostigmine (Physo)- and EFS (10 Hz)-induced contractions in isolated muscle strips of the guinea pig bladder. (A) Averaged data from six guinea pigs shows the lack of effect of CTX (0.3 µmol·L −1 ) on physostigmine (1 µmol·L −1 )-induced contractions in the presence of TTX (1 µmol·L −1 ). (B) Averaged data ( N = 7) of the effect of CTX (0.3 µmol·L −1 ) on EFS (10 Hz)-induced contractions. (C) Averaged data from five guinea pigs of the effects of the cocktail of toxins [CTX (0.3 µmol·L −1 ), ATX (0.1 µmol·L −1 ) and SNX 482 (0.3 µmol·L −1 )] on physostigmine (1 µmol·L −1 )-induced contractions, in the presence of TTX (1 µmol·L −1 ). (D) Averaged data ( N = 5) of the effect of the same cocktail of toxins on EFS (10 Hz)-induced contractions revealing significant, but incomplete blockade. (E) Averaged data ( N = 6) of the corresponding time control for the effect of 1 µmol·L −1 physostigmine (physo 1 = 25–30 min and physo 2 = 45–50 min) alone. *, significant difference from TTX, P
    Figure Legend Snippet: Effects of CTX alone and of a cocktail of toxins (CTX, ATX and SNX 482) on physostigmine (Physo)- and EFS (10 Hz)-induced contractions in isolated muscle strips of the guinea pig bladder. (A) Averaged data from six guinea pigs shows the lack of effect of CTX (0.3 µmol·L −1 ) on physostigmine (1 µmol·L −1 )-induced contractions in the presence of TTX (1 µmol·L −1 ). (B) Averaged data ( N = 7) of the effect of CTX (0.3 µmol·L −1 ) on EFS (10 Hz)-induced contractions. (C) Averaged data from five guinea pigs of the effects of the cocktail of toxins [CTX (0.3 µmol·L −1 ), ATX (0.1 µmol·L −1 ) and SNX 482 (0.3 µmol·L −1 )] on physostigmine (1 µmol·L −1 )-induced contractions, in the presence of TTX (1 µmol·L −1 ). (D) Averaged data ( N = 5) of the effect of the same cocktail of toxins on EFS (10 Hz)-induced contractions revealing significant, but incomplete blockade. (E) Averaged data ( N = 6) of the corresponding time control for the effect of 1 µmol·L −1 physostigmine (physo 1 = 25–30 min and physo 2 = 45–50 min) alone. *, significant difference from TTX, P

    Techniques Used: Isolation

    6) 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: Science Advances

    doi: 10.1126/sciadv.abe6393

    Lamellar cells from Meissner corpuscles are excitable mechanosensors. ( A to D ) Exemplar action potentials (APs; left and middle) and spike quantification (right) obtained by current injection into Meissner lamellar cells in the presence of low (20 μM) extracellular Ca 2+ [(A), n = 6 cells], pan-Ca v blocker Cd 2+ [(B), n = 4 cells], Na v blocker tetrodotoxin (TTX; (C), n = 5 cells], R-type Ca v 2.3 blocker SNX-482 [(D), n = 11 cells]. Thin lines in quantification panels represent individual cells; thick lines connect means ± SEM. ( E ) Pharmacological profile of Meissner lamellar cell firing upon injection of a 100-pA current. Letters indicate Ca v type. Open circles represent individual cells. The effect of treatment is significant. F 11,53 = 75.57, P
    Figure Legend Snippet: Lamellar cells from Meissner corpuscles are excitable mechanosensors. ( A to D ) Exemplar action potentials (APs; left and middle) and spike quantification (right) obtained by current injection into Meissner lamellar cells in the presence of low (20 μM) extracellular Ca 2+ [(A), n = 6 cells], pan-Ca v blocker Cd 2+ [(B), n = 4 cells], Na v blocker tetrodotoxin (TTX; (C), n = 5 cells], R-type Ca v 2.3 blocker SNX-482 [(D), n = 11 cells]. Thin lines in quantification panels represent individual cells; thick lines connect means ± SEM. ( E ) Pharmacological profile of Meissner lamellar cell firing upon injection of a 100-pA current. Letters indicate Ca v type. Open circles represent individual cells. The effect of treatment is significant. F 11,53 = 75.57, P

    Techniques Used: Injection

    7) Product Images from "Control of Spontaneous Firing Patterns by the Selective Coupling of Calcium Currents to Calcium Activated Potassium Currents in Striatal Cholinergic Interneurons"

    Article Title: Control of Spontaneous Firing Patterns by the Selective Coupling of Calcium Currents to Calcium Activated Potassium Currents in Striatal Cholinergic Interneurons

    Journal: The Journal of neuroscience : the official journal of the Society for Neuroscience

    doi: 10.1523/JNEUROSCI.2734-05.2005

    Reduction of the mAHP current by Ca v 2.2 channel blockade can induce burst discharge, a. 1 μM omega-conotoxin GVIA (GVIA) that blocks Ca v 2.2 channels reduces the mAHP current (gray trace) relative to control (black trace). Inset: the mean±SEM value across cells of the mAHP current before (black boxes) and after (gray boxes) application of various calcium current blockers: 10 μM dihydropyridines (dihyd) that block Ca v 1 channels, 1 μM GVIA, 1 μM omega-conotoxin MVIIC (MVIIC) that blocks Ca v 2.1/2.2 channels and 100 nM SNX-482 (SNX) that blocks Ca v 2.3 channels. The current was measured 25 ms after the end of the pulse and averaged over 5 traces taken in a 20 sec interval. Only the GVIA treatment elicited a significant reduction in the value of the mAHP current (p
    Figure Legend Snippet: Reduction of the mAHP current by Ca v 2.2 channel blockade can induce burst discharge, a. 1 μM omega-conotoxin GVIA (GVIA) that blocks Ca v 2.2 channels reduces the mAHP current (gray trace) relative to control (black trace). Inset: the mean±SEM value across cells of the mAHP current before (black boxes) and after (gray boxes) application of various calcium current blockers: 10 μM dihydropyridines (dihyd) that block Ca v 1 channels, 1 μM GVIA, 1 μM omega-conotoxin MVIIC (MVIIC) that blocks Ca v 2.1/2.2 channels and 100 nM SNX-482 (SNX) that blocks Ca v 2.3 channels. The current was measured 25 ms after the end of the pulse and averaged over 5 traces taken in a 20 sec interval. Only the GVIA treatment elicited a significant reduction in the value of the mAHP current (p

    Techniques Used: Blocking Assay, Mass Spectrometry, Size-exclusion Chromatography

    8) Product Images from "Identification of a sensory neuron Cav2.3 inhibitor within a new superfamily of macro-conotoxins"

    Article Title: Identification of a sensory neuron Cav2.3 inhibitor within a new superfamily of macro-conotoxins

    Journal: bioRxiv

    doi: 10.1101/2022.07.04.498665

    Mu8.1 inhibits recombinant human Cav2.3-mediated currents in a concentration-dependent manner A. Representative whole-cell Cav2.3 currents in control (green) and in the presence of 1 µM (blue), 3 µM (purple) and 10 µM (mauve) Mu8.1. Depolarization-activated currents were elicited by a 50 ms test pulse to −10 mV (Vh −80 mV; 0.1 Hz). B. Concentration-response relationship for the inhibition of Cav2.3 peak currents (IC 50 = 5.8 µM; nH: 0.97; n = 5). C. Mu8.1 and SNX-482 target overlapping populations of peptidergic nociceptors and C-LTMRs. Cells were treated with 3 µM Mu8.1 (pink box), 10 µM Mu8.1 (mauve box) and 100 nM SNX-482 (red box). All other labels as in Fig. 7A . D. Relative quantification of peptidergic nociceptors (pep nocicep), C-LTMRs and non-peptidergic nociceptors (non-pep nocicep) sensitive to 3 µM and 10 µM Mu8.1 (purple and mauve, respectively) and 100 nM SNX-482 (pink). Percentages were calculated from the total number of cells recorded per class. Bars represent mean + SD from two independent DRG isolations (190-810 neurons per group).
    Figure Legend Snippet: Mu8.1 inhibits recombinant human Cav2.3-mediated currents in a concentration-dependent manner A. Representative whole-cell Cav2.3 currents in control (green) and in the presence of 1 µM (blue), 3 µM (purple) and 10 µM (mauve) Mu8.1. Depolarization-activated currents were elicited by a 50 ms test pulse to −10 mV (Vh −80 mV; 0.1 Hz). B. Concentration-response relationship for the inhibition of Cav2.3 peak currents (IC 50 = 5.8 µM; nH: 0.97; n = 5). C. Mu8.1 and SNX-482 target overlapping populations of peptidergic nociceptors and C-LTMRs. Cells were treated with 3 µM Mu8.1 (pink box), 10 µM Mu8.1 (mauve box) and 100 nM SNX-482 (red box). All other labels as in Fig. 7A . D. Relative quantification of peptidergic nociceptors (pep nocicep), C-LTMRs and non-peptidergic nociceptors (non-pep nocicep) sensitive to 3 µM and 10 µM Mu8.1 (purple and mauve, respectively) and 100 nM SNX-482 (pink). Percentages were calculated from the total number of cells recorded per class. Bars represent mean + SD from two independent DRG isolations (190-810 neurons per group).

    Techniques Used: Recombinant, Concentration Assay, Inhibition

    9) Product Images from "Spontaneous release of acetylcholine from autonomic nerves in the bladder"

    Article Title: Spontaneous release of acetylcholine from autonomic nerves in the bladder

    Journal: British Journal of Pharmacology

    doi: 10.1111/j.1476-5381.2009.00166.x

    Effects of CTX alone and of a cocktail of toxins (CTX, ATX and SNX 482) on physostigmine (Physo)- and EFS (10 Hz)-induced contractions in isolated muscle strips of the guinea pig bladder. (A) Averaged data from six guinea pigs shows the lack of effect of CTX (0.3 µmol·L −1 ) on physostigmine (1 µmol·L −1 )-induced contractions in the presence of TTX (1 µmol·L −1 ). (B) Averaged data ( N = 7) of the effect of CTX (0.3 µmol·L −1 ) on EFS (10 Hz)-induced contractions. (C) Averaged data from five guinea pigs of the effects of the cocktail of toxins [CTX (0.3 µmol·L −1 ), ATX (0.1 µmol·L −1 ) and SNX 482 (0.3 µmol·L −1 )] on physostigmine (1 µmol·L −1 )-induced contractions, in the presence of TTX (1 µmol·L −1 ). (D) Averaged data ( N = 5) of the effect of the same cocktail of toxins on EFS (10 Hz)-induced contractions revealing significant, but incomplete blockade. (E) Averaged data ( N = 6) of the corresponding time control for the effect of 1 µmol·L −1 physostigmine (physo 1 = 25–30 min and physo 2 = 45–50 min) alone. *, significant difference from TTX, P
    Figure Legend Snippet: Effects of CTX alone and of a cocktail of toxins (CTX, ATX and SNX 482) on physostigmine (Physo)- and EFS (10 Hz)-induced contractions in isolated muscle strips of the guinea pig bladder. (A) Averaged data from six guinea pigs shows the lack of effect of CTX (0.3 µmol·L −1 ) on physostigmine (1 µmol·L −1 )-induced contractions in the presence of TTX (1 µmol·L −1 ). (B) Averaged data ( N = 7) of the effect of CTX (0.3 µmol·L −1 ) on EFS (10 Hz)-induced contractions. (C) Averaged data from five guinea pigs of the effects of the cocktail of toxins [CTX (0.3 µmol·L −1 ), ATX (0.1 µmol·L −1 ) and SNX 482 (0.3 µmol·L −1 )] on physostigmine (1 µmol·L −1 )-induced contractions, in the presence of TTX (1 µmol·L −1 ). (D) Averaged data ( N = 5) of the effect of the same cocktail of toxins on EFS (10 Hz)-induced contractions revealing significant, but incomplete blockade. (E) Averaged data ( N = 6) of the corresponding time control for the effect of 1 µmol·L −1 physostigmine (physo 1 = 25–30 min and physo 2 = 45–50 min) alone. *, significant difference from TTX, P

    Techniques Used: Isolation

    10) Product Images from "Cellular and Molecular Properties of Neurons: Specificity in the interaction of high-voltage-activated Ca2+ channel types with Ca2+-dependent afterhyperpolarizations in magnocellular supraoptic neurons"

    Article Title: Cellular and Molecular Properties of Neurons: Specificity in the interaction of high-voltage-activated Ca2+ channel types with Ca2+-dependent afterhyperpolarizations in magnocellular supraoptic neurons

    Journal: Journal of Neurophysiology

    doi: 10.1152/jn.00285.2018

    Effect of R-type blocker SNX-482 (0.3 μM) on afterhyperpolarizations (AHPs) and their corresponding Ca 2+ transients in oxytocin (OT) ( n = 5) ( A – D ) and vasopressin (VP) ( n = 5) ( E – H ) neurons. 4-Aminopyridine (4-AP) was preapplied to block Kv4 channels and isolate the effect of SNX482 on R-type Ca 2+ channels. A : example AHP after a 20-Hz, 20-spike train from an OT neuron and its corresponding somatic Ca 2+ signal. B : example AHP after a 20-Hz, 5-spike train from an OT neuron and its corresponding somatic Ca 2+ signal. C : summary data for OT neuron AHP measurements at the 20-spike peak amplitude (medium and slow AHP, mAHP + sAHP), at 1 s after the (sAHP), and 5-spike AHPs at the peak amplitude (mAHP). Red points are individual cells, and black points are group averages. After 20 spikes, 4-AP significantly increased the AHP at peak (* P
    Figure Legend Snippet: Effect of R-type blocker SNX-482 (0.3 μM) on afterhyperpolarizations (AHPs) and their corresponding Ca 2+ transients in oxytocin (OT) ( n = 5) ( A – D ) and vasopressin (VP) ( n = 5) ( E – H ) neurons. 4-Aminopyridine (4-AP) was preapplied to block Kv4 channels and isolate the effect of SNX482 on R-type Ca 2+ channels. A : example AHP after a 20-Hz, 20-spike train from an OT neuron and its corresponding somatic Ca 2+ signal. B : example AHP after a 20-Hz, 5-spike train from an OT neuron and its corresponding somatic Ca 2+ signal. C : summary data for OT neuron AHP measurements at the 20-spike peak amplitude (medium and slow AHP, mAHP + sAHP), at 1 s after the (sAHP), and 5-spike AHPs at the peak amplitude (mAHP). Red points are individual cells, and black points are group averages. After 20 spikes, 4-AP significantly increased the AHP at peak (* P

    Techniques Used: Blocking Assay

    SNX-482 blocks transient outward rectification and broadens spikes [oxytocin (OT) and vasopressin (VP) n = 5]. A , i : example single action potential (AP) from an OT neuron treated with SNX-482 (0.3 μM) showing obvious broadening of the AP. A , ii : example single AP from a different OT neuron than Ai , treated first with 4 mM 4-aminopyridine (4-AP), followed by subsequent application of SNX-482. B : step injections of depolarizing current reveal a fast transient outward rectifier that is reduced by SNX-482 in the same cell as A , i . Positive steps (25 pA) were generated from cells at −80 mV. C : in 20-spike trains, we measured AP half-width of the 1st spike. In OT and VP neurons, 4-AP results in significant spike broadening (OT, * P
    Figure Legend Snippet: SNX-482 blocks transient outward rectification and broadens spikes [oxytocin (OT) and vasopressin (VP) n = 5]. A , i : example single action potential (AP) from an OT neuron treated with SNX-482 (0.3 μM) showing obvious broadening of the AP. A , ii : example single AP from a different OT neuron than Ai , treated first with 4 mM 4-aminopyridine (4-AP), followed by subsequent application of SNX-482. B : step injections of depolarizing current reveal a fast transient outward rectifier that is reduced by SNX-482 in the same cell as A , i . Positive steps (25 pA) were generated from cells at −80 mV. C : in 20-spike trains, we measured AP half-width of the 1st spike. In OT and VP neurons, 4-AP results in significant spike broadening (OT, * P

    Techniques Used: Generated

    11) Product Images from "Spontaneous release of acetylcholine from autonomic nerves in the bladder"

    Article Title: Spontaneous release of acetylcholine from autonomic nerves in the bladder

    Journal: British Journal of Pharmacology

    doi: 10.1111/j.1476-5381.2009.00166.x

    Effects of CTX alone and of a cocktail of toxins (CTX, ATX and SNX 482) on physostigmine (Physo)- and EFS (10 Hz)-induced contractions in isolated muscle strips of the guinea pig bladder. (A) Averaged data from six guinea pigs shows the lack of effect of CTX (0.3 µmol·L −1 ) on physostigmine (1 µmol·L −1 )-induced contractions in the presence of TTX (1 µmol·L −1 ). (B) Averaged data ( N = 7) of the effect of CTX (0.3 µmol·L −1 ) on EFS (10 Hz)-induced contractions. (C) Averaged data from five guinea pigs of the effects of the cocktail of toxins [CTX (0.3 µmol·L −1 ), ATX (0.1 µmol·L −1 ) and SNX 482 (0.3 µmol·L −1 )] on physostigmine (1 µmol·L −1 )-induced contractions, in the presence of TTX (1 µmol·L −1 ). (D) Averaged data ( N = 5) of the effect of the same cocktail of toxins on EFS (10 Hz)-induced contractions revealing significant, but incomplete blockade. (E) Averaged data ( N = 6) of the corresponding time control for the effect of 1 µmol·L −1 physostigmine (physo 1 = 25–30 min and physo 2 = 45–50 min) alone. *, significant difference from TTX, P
    Figure Legend Snippet: Effects of CTX alone and of a cocktail of toxins (CTX, ATX and SNX 482) on physostigmine (Physo)- and EFS (10 Hz)-induced contractions in isolated muscle strips of the guinea pig bladder. (A) Averaged data from six guinea pigs shows the lack of effect of CTX (0.3 µmol·L −1 ) on physostigmine (1 µmol·L −1 )-induced contractions in the presence of TTX (1 µmol·L −1 ). (B) Averaged data ( N = 7) of the effect of CTX (0.3 µmol·L −1 ) on EFS (10 Hz)-induced contractions. (C) Averaged data from five guinea pigs of the effects of the cocktail of toxins [CTX (0.3 µmol·L −1 ), ATX (0.1 µmol·L −1 ) and SNX 482 (0.3 µmol·L −1 )] on physostigmine (1 µmol·L −1 )-induced contractions, in the presence of TTX (1 µmol·L −1 ). (D) Averaged data ( N = 5) of the effect of the same cocktail of toxins on EFS (10 Hz)-induced contractions revealing significant, but incomplete blockade. (E) Averaged data ( N = 6) of the corresponding time control for the effect of 1 µmol·L −1 physostigmine (physo 1 = 25–30 min and physo 2 = 45–50 min) alone. *, significant difference from TTX, P

    Techniques Used: Isolation

    12) 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

    Lamellar cells from Meissner corpuscles are excitable mechanosensors. (A-D) Exemplar action potentials ( left, middle panels) and quantification of spikes ( right panels) obtained by current injection into Meissner lamellar cells. Firing is inhibited upon depletion of extracellular Ca 2+ to 20µM, Low Ca 2+ ( A , n=6 cells), in the presence of pan-Ca v channel blocker 300 µM Cd 2+ ( B , n=4 cells) and R-type Ca v 2.3 channel blocker 1 µM SNX-482 ( D , n=11 cells) but not by the voltage-gated sodium channel blocker 100 µM tetrodotoxin, TTX ( C , n=5 cells). Thin lines in quantification panels represent individual cells, thick lines connect means ± s.e.m. (E) Pharmacological profile of Meissner lamellar cell firing in response to a 100 pA current injection, normalized to control treatment. Letters indicate Ca v type selectivity. Na v , voltage-gated sodium channel. Data are means ± s.e.m. from at least two independent experiments. Open circles represent individual cells. The effect of treatment is significant, F 11,53 =75.57, p
    Figure Legend Snippet: Lamellar cells from Meissner corpuscles are excitable mechanosensors. (A-D) Exemplar action potentials ( left, middle panels) and quantification of spikes ( right panels) obtained by current injection into Meissner lamellar cells. Firing is inhibited upon depletion of extracellular Ca 2+ to 20µM, Low Ca 2+ ( A , n=6 cells), in the presence of pan-Ca v channel blocker 300 µM Cd 2+ ( B , n=4 cells) and R-type Ca v 2.3 channel blocker 1 µM SNX-482 ( D , n=11 cells) but not by the voltage-gated sodium channel blocker 100 µM tetrodotoxin, TTX ( C , n=5 cells). Thin lines in quantification panels represent individual cells, thick lines connect means ± s.e.m. (E) Pharmacological profile of Meissner lamellar cell firing in response to a 100 pA current injection, normalized to control treatment. Letters indicate Ca v type selectivity. Na v , voltage-gated sodium channel. Data are means ± s.e.m. from at least two independent experiments. Open circles represent individual cells. The effect of treatment is significant, F 11,53 =75.57, p

    Techniques Used: Injection

    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

    13) Product Images from "Mechanisms underlying cannabinoid inhibition of presynaptic Ca2+ influx at parallel fibre synapses of the rat cerebellum"

    Article Title: Mechanisms underlying cannabinoid inhibition of presynaptic Ca2+ influx at parallel fibre synapses of the rat cerebellum

    Journal: The Journal of Physiology

    doi: 10.1113/jphysiol.2004.063263

    Effects of SNX-482 or nifedipine preapplication on WIN55,212-2-mediated inhibition of presynaptic calcium influx
    Figure Legend Snippet: Effects of SNX-482 or nifedipine preapplication on WIN55,212-2-mediated inhibition of presynaptic calcium influx

    Techniques Used: Inhibition

    14) Product Images from "Recruitment of apical dendritic T-type Ca2+ channels by backpropagating spikes underlies de novo intrinsic bursting in hippocampal epileptogenesis"

    Article Title: Recruitment of apical dendritic T-type Ca2+ channels by backpropagating spikes underlies de novo intrinsic bursting in hippocampal epileptogenesis

    Journal: The Journal of Physiology

    doi: 10.1113/jphysiol.2007.127670

    Effects of amiloride and SNX-482 on bursting
    Figure Legend Snippet: Effects of amiloride and SNX-482 on bursting

    Techniques Used:

    15) Product Images from "Calcium Channel Dysfunction in Inferior Colliculus Neurons of the Genetically Epilepsy-Prone Rat"

    Article Title: Calcium Channel Dysfunction in Inferior Colliculus Neurons of the Genetically Epilepsy-Prone Rat

    Journal:

    doi: 10.1016/j.neuropharm.2008.11.005

    Enhancement of R-type current density in IC neurons of SN-GEPR-3. Ba 2+ currents were activated at 0 mV in absence and presence of 100 nM SNX 482 in IC neurons obtained from control SD rats and SN-GEPR-3s. A . Representative SNX482-sensitive current traces
    Figure Legend Snippet: Enhancement of R-type current density in IC neurons of SN-GEPR-3. Ba 2+ currents were activated at 0 mV in absence and presence of 100 nM SNX 482 in IC neurons obtained from control SD rats and SN-GEPR-3s. A . Representative SNX482-sensitive current traces

    Techniques Used:

    16) Product Images from "Recruitment of apical dendritic T-type Ca2+ channels by backpropagating spikes underlies de novo intrinsic bursting in hippocampal epileptogenesis"

    Article Title: Recruitment of apical dendritic T-type Ca2+ channels by backpropagating spikes underlies de novo intrinsic bursting in hippocampal epileptogenesis

    Journal: The Journal of Physiology

    doi: 10.1113/jphysiol.2007.127670

    Effects of amiloride and SNX-482 on bursting
    Figure Legend Snippet: Effects of amiloride and SNX-482 on bursting

    Techniques Used:

    17) Product Images from "Recruitment of apical dendritic T-type Ca2+ channels by backpropagating spikes underlies de novo intrinsic bursting in hippocampal epileptogenesis"

    Article Title: Recruitment of apical dendritic T-type Ca2+ channels by backpropagating spikes underlies de novo intrinsic bursting in hippocampal epileptogenesis

    Journal: The Journal of Physiology

    doi: 10.1113/jphysiol.2007.127670

    Effects of amiloride and SNX-482 on bursting
    Figure Legend Snippet: Effects of amiloride and SNX-482 on bursting

    Techniques Used:

    18) Product Images from "Low-threshold calcium currents contribute to locomotor-like activity in neonatal mice"

    Article Title: Low-threshold calcium currents contribute to locomotor-like activity in neonatal mice

    Journal: Journal of Neurophysiology

    doi: 10.1152/jn.00583.2011

    Application of the selective R-type calcium channel blocker SNX-482 does not alter fictive locomotor-like activity. A : paired extracellular recordings from iL2 and iL5 in an isolated whole-cord preparation with cocktail (3–10 μM NMDA,
    Figure Legend Snippet: Application of the selective R-type calcium channel blocker SNX-482 does not alter fictive locomotor-like activity. A : paired extracellular recordings from iL2 and iL5 in an isolated whole-cord preparation with cocktail (3–10 μM NMDA,

    Techniques Used: Activity Assay, Isolation

    19) Product Images from "β2-subunit alternative splicing stabilizes Cav2.3 Ca2+ channel activity during continuous midbrain dopamine neuron-like activity"

    Article Title: β2-subunit alternative splicing stabilizes Cav2.3 Ca2+ channel activity during continuous midbrain dopamine neuron-like activity

    Journal: eLife

    doi: 10.7554/eLife.67464

    Inhibition of I Ca in SN DA neurons of adult (12 weeks) mice by 100 nM SNX-482. To further prove the presence of SNX-482-sensitive R-type currents in SN DA neurons, we performed perforated-patch recordings. These allow stable recordings over a long period of time and to test for reversibility of channel block by 100 nM SNX-482. Recordings were performed with the pulse protocol shown in A (holding potential –60 mV) after blocking I A K + -currents known to be present in these cells to exclude block of I A by SNX-482 ( Kimm and Bean, 2014 ) as described previously ( Benkert et al., 2019 ). 100 nM SNX-482 significantly reduced current to 87% ± 4% of control I Ca (n=8, p=0.012, one-sample t-test, for statistics see Supplementary file 7 ) and this inhibition was slowly reversible. ( A ) I Ca before (black), during (red) and after (blue) SNX-482 application. ( B ) Example of peak I Ca plotted over time during SNX-482 application. The asterisks mark the time points of the recordings shown on the left. Single depolarizing voltage steps to 0 mV were applied from a holding potential of –60 mV every 10 s. ( C ) Mean effect of SNX-482 on peak I Ca . *, p
    Figure Legend Snippet: Inhibition of I Ca in SN DA neurons of adult (12 weeks) mice by 100 nM SNX-482. To further prove the presence of SNX-482-sensitive R-type currents in SN DA neurons, we performed perforated-patch recordings. These allow stable recordings over a long period of time and to test for reversibility of channel block by 100 nM SNX-482. Recordings were performed with the pulse protocol shown in A (holding potential –60 mV) after blocking I A K + -currents known to be present in these cells to exclude block of I A by SNX-482 ( Kimm and Bean, 2014 ) as described previously ( Benkert et al., 2019 ). 100 nM SNX-482 significantly reduced current to 87% ± 4% of control I Ca (n=8, p=0.012, one-sample t-test, for statistics see Supplementary file 7 ) and this inhibition was slowly reversible. ( A ) I Ca before (black), during (red) and after (blue) SNX-482 application. ( B ) Example of peak I Ca plotted over time during SNX-482 application. The asterisks mark the time points of the recordings shown on the left. Single depolarizing voltage steps to 0 mV were applied from a holding potential of –60 mV every 10 s. ( C ) Mean effect of SNX-482 on peak I Ca . *, p

    Techniques Used: Inhibition, Mouse Assay, Blocking Assay

    SNX-482 effects on pacemaking of cultured mouse midbrain DA neurons. ( A ) Representative recording of spontaneous firing activity of cultured midbrain dopaminergic neurons before, during and after the application (wash-out) of 100 nM SNX-482. Below, enlargements of action potentials within the highlighted regions are shown. ( B ) Firing frequency [Hz], coefficient of variation of the interspike interval [%], and AHP peak [mV] before (control) and during the application of 100 nM SNX-482. Data represent the means ± SEM for the indicated number of experiments. Statistical significance was determined using paired Student’s t-test.: *** p
    Figure Legend Snippet: SNX-482 effects on pacemaking of cultured mouse midbrain DA neurons. ( A ) Representative recording of spontaneous firing activity of cultured midbrain dopaminergic neurons before, during and after the application (wash-out) of 100 nM SNX-482. Below, enlargements of action potentials within the highlighted regions are shown. ( B ) Firing frequency [Hz], coefficient of variation of the interspike interval [%], and AHP peak [mV] before (control) and during the application of 100 nM SNX-482. Data represent the means ± SEM for the indicated number of experiments. Statistical significance was determined using paired Student’s t-test.: *** p

    Techniques Used: Cell Culture, Activity Assay

    20) Product Images from "Spontaneous release of acetylcholine from autonomic nerves in the bladder"

    Article Title: Spontaneous release of acetylcholine from autonomic nerves in the bladder

    Journal: British Journal of Pharmacology

    doi: 10.1111/j.1476-5381.2009.00166.x

    Effects of CTX alone and of a cocktail of toxins (CTX, ATX and SNX 482) on physostigmine (Physo)- and EFS (10 Hz)-induced contractions in isolated muscle strips of the guinea pig bladder. (A) Averaged data from six guinea pigs shows the lack of effect of CTX (0.3 µmol·L −1 ) on physostigmine (1 µmol·L −1 )-induced contractions in the presence of TTX (1 µmol·L −1 ). (B) Averaged data ( N = 7) of the effect of CTX (0.3 µmol·L −1 ) on EFS (10 Hz)-induced contractions. (C) Averaged data from five guinea pigs of the effects of the cocktail of toxins [CTX (0.3 µmol·L −1 ), ATX (0.1 µmol·L −1 ) and SNX 482 (0.3 µmol·L −1 )] on physostigmine (1 µmol·L −1 )-induced contractions, in the presence of TTX (1 µmol·L −1 ). (D) Averaged data ( N = 5) of the effect of the same cocktail of toxins on EFS (10 Hz)-induced contractions revealing significant, but incomplete blockade. (E) Averaged data ( N = 6) of the corresponding time control for the effect of 1 µmol·L −1 physostigmine (physo 1 = 25–30 min and physo 2 = 45–50 min) alone. *, significant difference from TTX, P
    Figure Legend Snippet: Effects of CTX alone and of a cocktail of toxins (CTX, ATX and SNX 482) on physostigmine (Physo)- and EFS (10 Hz)-induced contractions in isolated muscle strips of the guinea pig bladder. (A) Averaged data from six guinea pigs shows the lack of effect of CTX (0.3 µmol·L −1 ) on physostigmine (1 µmol·L −1 )-induced contractions in the presence of TTX (1 µmol·L −1 ). (B) Averaged data ( N = 7) of the effect of CTX (0.3 µmol·L −1 ) on EFS (10 Hz)-induced contractions. (C) Averaged data from five guinea pigs of the effects of the cocktail of toxins [CTX (0.3 µmol·L −1 ), ATX (0.1 µmol·L −1 ) and SNX 482 (0.3 µmol·L −1 )] on physostigmine (1 µmol·L −1 )-induced contractions, in the presence of TTX (1 µmol·L −1 ). (D) Averaged data ( N = 5) of the effect of the same cocktail of toxins on EFS (10 Hz)-induced contractions revealing significant, but incomplete blockade. (E) Averaged data ( N = 6) of the corresponding time control for the effect of 1 µmol·L −1 physostigmine (physo 1 = 25–30 min and physo 2 = 45–50 min) alone. *, significant difference from TTX, P

    Techniques Used: Isolation

    21) 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

    22) Product Images from "Calcium currents in striatal fast-spiking interneurons: dopaminergic modulation of CaV1 channels"

    Article Title: Calcium currents in striatal fast-spiking interneurons: dopaminergic modulation of CaV1 channels

    Journal: BMC Neuroscience

    doi: 10.1186/s12868-018-0441-0

    Calcium channels expressed in striatal FSI. a Left: representative time course of peak maximum Ca 2+ current amplitude during the sequential addition of 20 µM nicardipine, a Ca V 1 (L) channel antagonist, 1 µM ω-conotoxin GIVA (ω-CgTx), a Ca V 2.2 (N) channel antagonist, and 1 µM ω-agatoxin TK (ω-AgTx), a Ca V 2.1 (P/Q) channel antagonist. Right: Representative I–V plots obtained during sequential application of each Ca 2+ channel antagonist and the consequent Ca 2+ current reduction. Note remaining unblocked current. b Left: Time course of maximum Ca 2+ current amplitude showing the action of saturating concentrations of 1 µM SNX-482 (SNX), a Ca V 2.3 (R) channel antagonist and 1 µM TTA-P2 (TTA), a Ca V 3 (T) channel antagonist. Right: Representative I–V plots during sequential application of Ca 2+ channel antagonists with the consequent Ca 2+ current reduction. Average percentage of current reduction in a sample of experiments after each channel antagonist was taken as the contribution of a specific Ca 2+ channel class as seen in Table 1
    Figure Legend Snippet: Calcium channels expressed in striatal FSI. a Left: representative time course of peak maximum Ca 2+ current amplitude during the sequential addition of 20 µM nicardipine, a Ca V 1 (L) channel antagonist, 1 µM ω-conotoxin GIVA (ω-CgTx), a Ca V 2.2 (N) channel antagonist, and 1 µM ω-agatoxin TK (ω-AgTx), a Ca V 2.1 (P/Q) channel antagonist. Right: Representative I–V plots obtained during sequential application of each Ca 2+ channel antagonist and the consequent Ca 2+ current reduction. Note remaining unblocked current. b Left: Time course of maximum Ca 2+ current amplitude showing the action of saturating concentrations of 1 µM SNX-482 (SNX), a Ca V 2.3 (R) channel antagonist and 1 µM TTA-P2 (TTA), a Ca V 3 (T) channel antagonist. Right: Representative I–V plots during sequential application of Ca 2+ channel antagonists with the consequent Ca 2+ current reduction. Average percentage of current reduction in a sample of experiments after each channel antagonist was taken as the contribution of a specific Ca 2+ channel class as seen in Table 1

    Techniques Used:

    23) Product Images from "Recruitment of apical dendritic T-type Ca2+ channels by backpropagating spikes underlies de novo intrinsic bursting in hippocampal epileptogenesis"

    Article Title: Recruitment of apical dendritic T-type Ca2+ channels by backpropagating spikes underlies de novo intrinsic bursting in hippocampal epileptogenesis

    Journal: The Journal of Physiology

    doi: 10.1113/jphysiol.2007.127670

    Effects of amiloride and SNX-482 on bursting
    Figure Legend Snippet: Effects of amiloride and SNX-482 on bursting

    Techniques Used:

    24) Product Images from "Recruitment of apical dendritic T-type Ca2+ channels by backpropagating spikes underlies de novo intrinsic bursting in hippocampal epileptogenesis"

    Article Title: Recruitment of apical dendritic T-type Ca2+ channels by backpropagating spikes underlies de novo intrinsic bursting in hippocampal epileptogenesis

    Journal: The Journal of Physiology

    doi: 10.1113/jphysiol.2007.127670

    Effects of amiloride and SNX-482 on bursting
    Figure Legend Snippet: Effects of amiloride and SNX-482 on bursting

    Techniques Used:

    25) Product Images from "Recruitment of apical dendritic T-type Ca2+ channels by backpropagating spikes underlies de novo intrinsic bursting in hippocampal epileptogenesis"

    Article Title: Recruitment of apical dendritic T-type Ca2+ channels by backpropagating spikes underlies de novo intrinsic bursting in hippocampal epileptogenesis

    Journal: The Journal of Physiology

    doi: 10.1113/jphysiol.2007.127670

    Effects of amiloride and SNX-482 on bursting
    Figure Legend Snippet: Effects of amiloride and SNX-482 on bursting

    Techniques Used:

    26) Product Images from "A System for Performing High Throughput Assays of Synaptic Function"

    Article Title: A System for Performing High Throughput Assays of Synaptic Function

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0025999

    MANTRA system responses depend on action potential-mediated opening of presynaptic Ca ++ channels. ( A ) TTX concentration-response curve for response amplitudes to a 30 Hz, 10 sec pulse train from a single plate. Each point shows the mean ± SEM of 8 wells normalized to within-plate vehicle controls. Data were fit with a standard sigmoid concentration-response function (R 2 = 0.99). ( B ) SypHy fluorescence responses during a 30 Hz, 10 second stimulus train in the presence of the Cav2.1 inhibitor ω-agatoxin IVA (500 nM), the Cav2.2 inhibitor ω-conotoxin GVIA (1 µM), and the Cav2.3 inhibitor SNX-482 (1.2 µM). The waveforms depicted are an average of 24 wells for the vehicle and 8 wells for the treatment group. ( C,D ) Amplitudes (mean ± SEM) of the sypHy responses shown in (B) following (C) 30 pulses (1 sec) and (D) 300 pulses (10 sec) of the stimulus train (***: p
    Figure Legend Snippet: MANTRA system responses depend on action potential-mediated opening of presynaptic Ca ++ channels. ( A ) TTX concentration-response curve for response amplitudes to a 30 Hz, 10 sec pulse train from a single plate. Each point shows the mean ± SEM of 8 wells normalized to within-plate vehicle controls. Data were fit with a standard sigmoid concentration-response function (R 2 = 0.99). ( B ) SypHy fluorescence responses during a 30 Hz, 10 second stimulus train in the presence of the Cav2.1 inhibitor ω-agatoxin IVA (500 nM), the Cav2.2 inhibitor ω-conotoxin GVIA (1 µM), and the Cav2.3 inhibitor SNX-482 (1.2 µM). The waveforms depicted are an average of 24 wells for the vehicle and 8 wells for the treatment group. ( C,D ) Amplitudes (mean ± SEM) of the sypHy responses shown in (B) following (C) 30 pulses (1 sec) and (D) 300 pulses (10 sec) of the stimulus train (***: p

    Techniques Used: Concentration Assay, Size-exclusion Chromatography, Fluorescence

    27) Product Images from "Active Dendrites and Differential Distribution of Calcium Channels Enable Functional Compartmentalization of Golgi Cells"

    Article Title: Active Dendrites and Differential Distribution of Calcium Channels Enable Functional Compartmentalization of Golgi Cells

    Journal: The Journal of Neuroscience

    doi: 10.1523/JNEUROSCI.3132-15.2015

    Different calcium channels mediate proximal and distal calcium transients. A , Schematic of experiment. Bursts of action potentials are evoked somatically. Calcium transients are recorded at a proximal and a distal location; specific calcium channel antagonists are applied locally. B–D , Calcium transients in the presence and absence of calcium channel antagonists applied to the proximal and distal dendrites. B , Antagonists of P-type (ω-agatoxin IVA), N-type (ω-conotoxin GVIA), and L-type (nimodipine) channels were coapplied. C , Calcium transients in the presence and absence of the R-type channel antagonist SNX-482. D , Application of the T-type channel antagonist TTA-P2. E , Summary data of calcium channel pharmacology. *Denotes statistical significance.
    Figure Legend Snippet: Different calcium channels mediate proximal and distal calcium transients. A , Schematic of experiment. Bursts of action potentials are evoked somatically. Calcium transients are recorded at a proximal and a distal location; specific calcium channel antagonists are applied locally. B–D , Calcium transients in the presence and absence of calcium channel antagonists applied to the proximal and distal dendrites. B , Antagonists of P-type (ω-agatoxin IVA), N-type (ω-conotoxin GVIA), and L-type (nimodipine) channels were coapplied. C , Calcium transients in the presence and absence of the R-type channel antagonist SNX-482. D , Application of the T-type channel antagonist TTA-P2. E , Summary data of calcium channel pharmacology. *Denotes statistical significance.

    Techniques Used:

    The effect of calcium-dependent potassium channel and calcium channel inhibition on Golgi cell firing. A , Spontaneously firing GoC in the absence (black trace, left) or in the presence of the SK-type potassium channel blocker apamin (blue trace, right). B , Same experiment but blue trace in the presence of the BK-type potassium channel blocker paxilline. C , The N-type channel blocker ω-conotoxin GVIA. D , The L-type calcium channel antagonist nimodipine. E , The P-type calcium channel blocker ω-agatoxin IVA. F , The R-type and T-type channel blockers SNX-482 and TTA-P2, respectively. G , Summary data of action potential frequency. H , Action potential (AP) width. I , Afterhyperpolarization (AHP). *Denotes statistical significance.
    Figure Legend Snippet: The effect of calcium-dependent potassium channel and calcium channel inhibition on Golgi cell firing. A , Spontaneously firing GoC in the absence (black trace, left) or in the presence of the SK-type potassium channel blocker apamin (blue trace, right). B , Same experiment but blue trace in the presence of the BK-type potassium channel blocker paxilline. C , The N-type channel blocker ω-conotoxin GVIA. D , The L-type calcium channel antagonist nimodipine. E , The P-type calcium channel blocker ω-agatoxin IVA. F , The R-type and T-type channel blockers SNX-482 and TTA-P2, respectively. G , Summary data of action potential frequency. H , Action potential (AP) width. I , Afterhyperpolarization (AHP). *Denotes statistical significance.

    Techniques Used: Inhibition

    28) Product Images from "N-type calcium current, Cav2.2, is enhanced in small diameter sensory neurons isolated from Nf1+/− mice"

    Article Title: N-type calcium current, Cav2.2, is enhanced in small diameter sensory neurons isolated from Nf1+/− mice

    Journal: Neuroscience

    doi: 10.1016/j.neuroscience.2014.04.021

    The sensitivities of I Ca to AgTx and SNX-482 in Nf1+/− sensory neurons are not different compared to wildtype neurons. Shown are box plots for the sensitivities of I Ca to 200 nM AgTx for wildtype (WT, n=12) and Nf1+/− (n=8) neurons; these values were not different (P=0.19, t-test). For 200 nM SNX-482, the sensitivities were also not different (P=0.34, t-test) between wildtype (n=10) and Nf1+/− (n=12) sensory neurons. The mean is represented by the dotted line; the median by the solid line; the upper and lower bars are 95% and 5% percentiles, respectively.
    Figure Legend Snippet: The sensitivities of I Ca to AgTx and SNX-482 in Nf1+/− sensory neurons are not different compared to wildtype neurons. Shown are box plots for the sensitivities of I Ca to 200 nM AgTx for wildtype (WT, n=12) and Nf1+/− (n=8) neurons; these values were not different (P=0.19, t-test). For 200 nM SNX-482, the sensitivities were also not different (P=0.34, t-test) between wildtype (n=10) and Nf1+/− (n=12) sensory neurons. The mean is represented by the dotted line; the median by the solid line; the upper and lower bars are 95% and 5% percentiles, respectively.

    Techniques Used:

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    Alomone Labs snx 482
    Glutamatergic transmission in the NL is predominantly triggered by Ca 2+ entry through N-type VGCCs. A : Both the ipsilateral (open circles) and the contralateral (filled circles) EPSCs recorded from the same NL neuron were largely and irreversibly blocked by the N-type blocker ω-Conotoxin-GVIA (ω-CTx-GVIA, 2.5 μM), with nearly identical time courses. Averaged traces under control (thin traces) and drug (thick traces) conditions are shown on the right. Stimulus artifacts are truncated for clarity. B-C : No inhibition of EPSCs was produced by the P/Q-type blocker ω-Agatoxin-IVA (ω-Aga-IVA, 0.1 μM) or the L-type blocker nimodipine (10 μM). D: A small and reversible inhibition of the EPSCs by the R-type blocker <t>SNX-482</t> (50 nM) was observed. The different time courses of the EPSCs observed in the sampled neurons may be due to different locations of the neurons along the tonotopic frequency axis. E : Summary of the effects of different VGCC blockers on EPSCs of NL neurons. ω-CTx-GVIA inhibited the ipsilateral and the contralateral EPSCs by 88% and 86%, respectively. Blockers for P/Q- and L-type VGCCs had no effects on EPSCs. SNX-482 produced a small inhibition with a large variation among cells. No differences in the percent inhibition by either drug were detected between the ipsilateral and the contralateral EPSCs. Error bars represent standard deviations. n.s.: non-significant (paired t-test, p > 0.05; the number of cells is indicated in parentheses).
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    Glutamatergic transmission in the NL is predominantly triggered by Ca 2+ entry through N-type VGCCs. A : Both the ipsilateral (open circles) and the contralateral (filled circles) EPSCs recorded from the same NL neuron were largely and irreversibly blocked by the N-type blocker ω-Conotoxin-GVIA (ω-CTx-GVIA, 2.5 μM), with nearly identical time courses. Averaged traces under control (thin traces) and drug (thick traces) conditions are shown on the right. Stimulus artifacts are truncated for clarity. B-C : No inhibition of EPSCs was produced by the P/Q-type blocker ω-Agatoxin-IVA (ω-Aga-IVA, 0.1 μM) or the L-type blocker nimodipine (10 μM). D: A small and reversible inhibition of the EPSCs by the R-type blocker SNX-482 (50 nM) was observed. The different time courses of the EPSCs observed in the sampled neurons may be due to different locations of the neurons along the tonotopic frequency axis. E : Summary of the effects of different VGCC blockers on EPSCs of NL neurons. ω-CTx-GVIA inhibited the ipsilateral and the contralateral EPSCs by 88% and 86%, respectively. Blockers for P/Q- and L-type VGCCs had no effects on EPSCs. SNX-482 produced a small inhibition with a large variation among cells. No differences in the percent inhibition by either drug were detected between the ipsilateral and the contralateral EPSCs. Error bars represent standard deviations. n.s.: non-significant (paired t-test, p > 0.05; the number of cells is indicated in parentheses).

    Journal: Neuroscience

    Article Title: Regulation of glutamatergic and GABAergic neurotransmission in the chick nucleus laminaris: role of N-type calcium channels

    doi: 10.1016/j.neuroscience.2009.09.013

    Figure Lengend Snippet: Glutamatergic transmission in the NL is predominantly triggered by Ca 2+ entry through N-type VGCCs. A : Both the ipsilateral (open circles) and the contralateral (filled circles) EPSCs recorded from the same NL neuron were largely and irreversibly blocked by the N-type blocker ω-Conotoxin-GVIA (ω-CTx-GVIA, 2.5 μM), with nearly identical time courses. Averaged traces under control (thin traces) and drug (thick traces) conditions are shown on the right. Stimulus artifacts are truncated for clarity. B-C : No inhibition of EPSCs was produced by the P/Q-type blocker ω-Agatoxin-IVA (ω-Aga-IVA, 0.1 μM) or the L-type blocker nimodipine (10 μM). D: A small and reversible inhibition of the EPSCs by the R-type blocker SNX-482 (50 nM) was observed. The different time courses of the EPSCs observed in the sampled neurons may be due to different locations of the neurons along the tonotopic frequency axis. E : Summary of the effects of different VGCC blockers on EPSCs of NL neurons. ω-CTx-GVIA inhibited the ipsilateral and the contralateral EPSCs by 88% and 86%, respectively. Blockers for P/Q- and L-type VGCCs had no effects on EPSCs. SNX-482 produced a small inhibition with a large variation among cells. No differences in the percent inhibition by either drug were detected between the ipsilateral and the contralateral EPSCs. Error bars represent standard deviations. n.s.: non-significant (paired t-test, p > 0.05; the number of cells is indicated in parentheses).

    Article Snippet: All chemicals and drugs were obtained from Sigma (Saint Louis, MO), except for SNX-482, ω-Conotoxin-GVIA (ω-CTx-GVIA) and tACPD, which were obtained from Peptide International (Louisville, KY), Alomone Labs (Jerusalem, Israel), and Tocris (Ballwin, MO), respectively.

    Techniques: Transmission Assay, Inhibition, Produced

    SNX-482 inhibition of non-L-type I Ca in cultured midbrain DA neurons. A. Representative traces illustrating the inhibition of non-L-type I Ca by 100 nM SNX-482 (red). Cells were initially perfused with a bath solution containing 3 μM isradipine (ISR, black). Full block was obtained using 2 μM Cd 2+ (blue). Square pulses (50 ms) were applied to 0 mV from a holding potential of −70 mV (top) B. Current amplitude values plotted as a function of time. After stabilization of I Ca with ISR (black circles), 100 nM SNX-482 was applied. The remaining currents was blocked by 2 μM Cd 2+ . C. SNX-482 inhibition expressed as % of control I Ca after LTCC block using 3 μM ISR. D. Mean current amplitude at the end of ISR application and at the end of SNX-482 application. Data represent the means ± SEM for the indicated number of experiments (N=4). Statistical significance was determined using paired Student’s t-test: *** p

    Journal: bioRxiv

    Article Title: Alternative splicing of auxiliary β2-subunits stabilizes Cav2.3 Ca2+ channel activity in continuously active midbrain dopamine neurons

    doi: 10.1101/2021.02.10.430224

    Figure Lengend Snippet: SNX-482 inhibition of non-L-type I Ca in cultured midbrain DA neurons. A. Representative traces illustrating the inhibition of non-L-type I Ca by 100 nM SNX-482 (red). Cells were initially perfused with a bath solution containing 3 μM isradipine (ISR, black). Full block was obtained using 2 μM Cd 2+ (blue). Square pulses (50 ms) were applied to 0 mV from a holding potential of −70 mV (top) B. Current amplitude values plotted as a function of time. After stabilization of I Ca with ISR (black circles), 100 nM SNX-482 was applied. The remaining currents was blocked by 2 μM Cd 2+ . C. SNX-482 inhibition expressed as % of control I Ca after LTCC block using 3 μM ISR. D. Mean current amplitude at the end of ISR application and at the end of SNX-482 application. Data represent the means ± SEM for the indicated number of experiments (N=4). Statistical significance was determined using paired Student’s t-test: *** p

    Article Snippet: For inhibition experiments, 100 nM SNX-482 (Alomone, Cat # RTS-500 dissolved in ACSF) or 10 µM nifedipine (Alomone, Cat # N-120 diluted into ACSF from a freshly prepared 10 mM stock solution in DMSO) was bath applied (in ACSF).

    Techniques: Inhibition, Cell Culture, Blocking Assay

    SNX-482 effects on pacemaking of cultured mouse midbrain DA neurons. A. Representative recording of spontaneous firing activity of cultured midbrain dopaminergic neurons before, during and after the application (wash-out) of 100 nM SNX-482. Inset (bottom right): overlay of one single AP before (control) and during the application of 100 nM SNX-482. B. Firing frequency [Hz], coefficient of variation of the interspike interval [%], and AHP peak [mV] before (control) and during the application of 100 nM SNX-482. Data represent the means ± SEM for the indicated number of experiments (N=3). Statistical significance was determined using paired Student’s t-test.: *** p

    Journal: bioRxiv

    Article Title: Alternative splicing of auxiliary β2-subunits stabilizes Cav2.3 Ca2+ channel activity in continuously active midbrain dopamine neurons

    doi: 10.1101/2021.02.10.430224

    Figure Lengend Snippet: SNX-482 effects on pacemaking of cultured mouse midbrain DA neurons. A. Representative recording of spontaneous firing activity of cultured midbrain dopaminergic neurons before, during and after the application (wash-out) of 100 nM SNX-482. Inset (bottom right): overlay of one single AP before (control) and during the application of 100 nM SNX-482. B. Firing frequency [Hz], coefficient of variation of the interspike interval [%], and AHP peak [mV] before (control) and during the application of 100 nM SNX-482. Data represent the means ± SEM for the indicated number of experiments (N=3). Statistical significance was determined using paired Student’s t-test.: *** p

    Article Snippet: For inhibition experiments, 100 nM SNX-482 (Alomone, Cat # RTS-500 dissolved in ACSF) or 10 µM nifedipine (Alomone, Cat # N-120 diluted into ACSF from a freshly prepared 10 mM stock solution in DMSO) was bath applied (in ACSF).

    Techniques: Cell Culture, Activity Assay

    Application of the selective R-type calcium channel blocker SNX-482 does not alter fictive locomotor-like activity. A : paired extracellular recordings from iL2 and iL5 in an isolated whole-cord preparation with cocktail (3–10 μM NMDA,

    Journal: Journal of Neurophysiology

    Article Title: Low-threshold calcium currents contribute to locomotor-like activity in neonatal mice

    doi: 10.1152/jn.00583.2011

    Figure Lengend Snippet: Application of the selective R-type calcium channel blocker SNX-482 does not alter fictive locomotor-like activity. A : paired extracellular recordings from iL2 and iL5 in an isolated whole-cord preparation with cocktail (3–10 μM NMDA,

    Article Snippet: The cycle frequency was not significantly affected by SNX-482 (control, mean = 0.24 ± 0.04 Hz; SNX-482, mean = 0.23 ± 0.02 Hz; n = 3; t = 0.39; P = 0.72; ).

    Techniques: Activity Assay, Isolation

    Effects of amiloride and SNX-482 on bursting

    Journal: The Journal of Physiology

    Article Title: Recruitment of apical dendritic T-type Ca2+ channels by backpropagating spikes underlies de novo intrinsic bursting in hippocampal epileptogenesis

    doi: 10.1113/jphysiol.2007.127670

    Figure Lengend Snippet: Effects of amiloride and SNX-482 on bursting

    Article Snippet: We also examined the effects of SNX-482 on bursting in se -experienced neurons.

    Techniques: