ω agatoxin tk  (Alomone Labs)


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    Structured Review

    Alomone Labs ω agatoxin tk
    Modulation of the inhibitory effects of CP 55,940 ( A ) and morphine ( B ) by blockers of voltage-dependent Ca 2+ channels: nimodipine (NIM), ω-conotoxin (ω-CTX), and <t>ω-agatoxin</t> (ω-ATX). The relative response was defined as the amplitude of the response to KCl at 10 min ( A ) or 5 min ( B ) after superfusion with an agonist plus a VDCC blocker, divided by the amplitude of the response to the first application (absence of drug) and multiplied by 100. The mean somal area of small neurons tested was 505 μm 2 (range, 298-764 μm 2 ) and was 1062 μm 2 (range, 856-1275 μm 2 ) for intermediate-size neurons. Values are the means ± SEM for the treatment group; the number in each bar is the number of neurons tested. * p
    ω Agatoxin Tk, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/ω agatoxin tk/product/Alomone Labs
    Average 91 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    ω agatoxin tk - by Bioz Stars, 2021-12
    91/100 stars

    Images

    1) Product Images from "Differential Effects of CB1 and Opioid Agonists on Two Populations of Adult Rat Dorsal Root Ganglion Neurons"

    Article Title: Differential Effects of CB1 and Opioid Agonists on Two Populations of Adult Rat Dorsal Root Ganglion Neurons

    Journal: The Journal of Neuroscience

    doi: 10.1523/JNEUROSCI.4298-03.2004

    Modulation of the inhibitory effects of CP 55,940 ( A ) and morphine ( B ) by blockers of voltage-dependent Ca 2+ channels: nimodipine (NIM), ω-conotoxin (ω-CTX), and ω-agatoxin (ω-ATX). The relative response was defined as the amplitude of the response to KCl at 10 min ( A ) or 5 min ( B ) after superfusion with an agonist plus a VDCC blocker, divided by the amplitude of the response to the first application (absence of drug) and multiplied by 100. The mean somal area of small neurons tested was 505 μm 2 (range, 298-764 μm 2 ) and was 1062 μm 2 (range, 856-1275 μm 2 ) for intermediate-size neurons. Values are the means ± SEM for the treatment group; the number in each bar is the number of neurons tested. * p
    Figure Legend Snippet: Modulation of the inhibitory effects of CP 55,940 ( A ) and morphine ( B ) by blockers of voltage-dependent Ca 2+ channels: nimodipine (NIM), ω-conotoxin (ω-CTX), and ω-agatoxin (ω-ATX). The relative response was defined as the amplitude of the response to KCl at 10 min ( A ) or 5 min ( B ) after superfusion with an agonist plus a VDCC blocker, divided by the amplitude of the response to the first application (absence of drug) and multiplied by 100. The mean somal area of small neurons tested was 505 μm 2 (range, 298-764 μm 2 ) and was 1062 μm 2 (range, 856-1275 μm 2 ) for intermediate-size neurons. Values are the means ± SEM for the treatment group; the number in each bar is the number of neurons tested. * p

    Techniques Used:

    2) Product Images from "N- and L-type calcium channel involvement in depolarization-induced suppression of inhibition in rat hippocampal CA1 cells"

    Article Title: N- and L-type calcium channel involvement in depolarization-induced suppression of inhibition in rat hippocampal CA1 cells

    Journal: The Journal of Physiology

    doi: 10.1111/j.1469-7793.1998.061bf.x

    Effects of Ca 2+ channel blockers on I Ca A , voltage steps to −10 or 0 mV for 500 ms elicited inward currents that were Cd 2+ or leak subtracted. Cd 2+ was applied at the end of the experiments, and occasionally the cell was lost prior to its application. In these cells leak subtraction only was possible. The peak current in control conditions and after drug administration for the cell was measured. Calibration values in top left panel apply to all other panels in A . B , the averaged data for each channel blocker are displayed in the histogram as a percentage of the control Ca 2+ current. NiCl 2 , 93.2 ± 3.3 %, n = 6; ω-conotoxin GVIA, 76.2 ± 8.0 %, n = 7; ω-agatoxin TK, 73.3 ± 8.0 %, n = 5; nifedipine, 58.9 ± 13.4 %, n = 7.
    Figure Legend Snippet: Effects of Ca 2+ channel blockers on I Ca A , voltage steps to −10 or 0 mV for 500 ms elicited inward currents that were Cd 2+ or leak subtracted. Cd 2+ was applied at the end of the experiments, and occasionally the cell was lost prior to its application. In these cells leak subtraction only was possible. The peak current in control conditions and after drug administration for the cell was measured. Calibration values in top left panel apply to all other panels in A . B , the averaged data for each channel blocker are displayed in the histogram as a percentage of the control Ca 2+ current. NiCl 2 , 93.2 ± 3.3 %, n = 6; ω-conotoxin GVIA, 76.2 ± 8.0 %, n = 7; ω-agatoxin TK, 73.3 ± 8.0 %, n = 5; nifedipine, 58.9 ± 13.4 %, n = 7.

    Techniques Used: Mass Spectrometry

    3) Product Images from "Differential inhibition of N and P/Q Ca2+ currents by 5-HT1A and 5-HT1D receptors in spinal neurons of Xenopus larvae"

    Article Title: Differential inhibition of N and P/Q Ca2+ currents by 5-HT1A and 5-HT1D receptors in spinal neurons of Xenopus larvae

    Journal: The Journal of Physiology

    doi: 10.1111/j.1469-7793.1998.103bz.x

    Summary of the effects of ω-CgTx and agatoxin on inhibition of HVA currents by 5-HT The 5-HT-sensitive current was divided into two components: a voltage-dependent component, which was relieved by a conditioning prepulse, and a voltage-independent component, which was unaffected. A, agatoxin reduced the 5-HT-sensitive current, predominantly through the reduction of the voltage-independent component ( P
    Figure Legend Snippet: Summary of the effects of ω-CgTx and agatoxin on inhibition of HVA currents by 5-HT The 5-HT-sensitive current was divided into two components: a voltage-dependent component, which was relieved by a conditioning prepulse, and a voltage-independent component, which was unaffected. A, agatoxin reduced the 5-HT-sensitive current, predominantly through the reduction of the voltage-independent component ( P

    Techniques Used: Inhibition

    Inhibition of HVA currents by 5-HT was totally occluded by agatoxin and ω-CgTx applied together A, HVA currents elicited by steps to +20 mV in control ( a ), 100 n M agatoxin ( d ) and 1 μM ω-CgTx ( g ). 5-HT (1 μM) caused different amounts of inhibition in the presence of control ( b ), agatoxin ( e ), and agatoxin + ω-CgTx ( h ); B, time series measurements from the same neuron. In control the inhibition was partially relieved by a prepulse to +120 mV (arrow; ○ shows steady-state inhibition). After agatoxin was applied, the amount of voltage-dependent inhibition relieved by the prepulse (arrows) remained almost unchanged, but the voltage-independent inhibition (difference between ○ and • at f ) was reduced. In the presence of both toxins, 5-HT had very little effect on the currents.
    Figure Legend Snippet: Inhibition of HVA currents by 5-HT was totally occluded by agatoxin and ω-CgTx applied together A, HVA currents elicited by steps to +20 mV in control ( a ), 100 n M agatoxin ( d ) and 1 μM ω-CgTx ( g ). 5-HT (1 μM) caused different amounts of inhibition in the presence of control ( b ), agatoxin ( e ), and agatoxin + ω-CgTx ( h ); B, time series measurements from the same neuron. In control the inhibition was partially relieved by a prepulse to +120 mV (arrow; ○ shows steady-state inhibition). After agatoxin was applied, the amount of voltage-dependent inhibition relieved by the prepulse (arrows) remained almost unchanged, but the voltage-independent inhibition (difference between ○ and • at f ) was reduced. In the presence of both toxins, 5-HT had very little effect on the currents.

    Techniques Used: Inhibition

    Composition of the HVA currents in Xenopus spinal neurons Aa, HVA Ca 2+ current elicited by a test pulse to +20 mV from a holding potential of −50 mV in control, agatoxin (200 nM), ω-CgTx (1 μM) and nifedipine (10 μM). b, time course of block measured at the points indicated in a. B, summary showing that agatoxin blocked 21.8 ± 0.9 % of total HVA current ( n = 24, P/Q-type), ω-CgTx blocked 66.3 ± 1.1 % of total HVA current ( n = 21, N-type), and nifedipine blocked 4.2 ± 0.8 % ( n = 5, L-type).
    Figure Legend Snippet: Composition of the HVA currents in Xenopus spinal neurons Aa, HVA Ca 2+ current elicited by a test pulse to +20 mV from a holding potential of −50 mV in control, agatoxin (200 nM), ω-CgTx (1 μM) and nifedipine (10 μM). b, time course of block measured at the points indicated in a. B, summary showing that agatoxin blocked 21.8 ± 0.9 % of total HVA current ( n = 24, P/Q-type), ω-CgTx blocked 66.3 ± 1.1 % of total HVA current ( n = 21, N-type), and nifedipine blocked 4.2 ± 0.8 % ( n = 5, L-type).

    Techniques Used: Blocking Assay

    P/Q-type Ca 2+ currents are reduced only through voltage-independent mechanisms A, agatoxin occluded the voltage-dependent block by 5-HT. Example traces of an experiment are shown in a and the time course measurements at 5 (•) and 70 ms (○) are shown in b. In agatoxin (100 nM), 5-HT caused a ‘pure’ voltage-dependent reduction which almost totally reversed at the end of the test pulse. Ba, a prepulse to +120 mV partially reversed the 5-HT inhibition in control (*, prepulse). b, agatoxin blocked around 20 % of the total HVA current, and in the presence of agatoxin, the prepulse relieved almost the same amount of current (*). However, some voltage-independent inhibition remained. Ca, in Ca 2+ currents elicited by a test pulse to +10 mV from a holding potential of −50 mV, the reduction of Ca 2+ currents by 8-OH-DPAT was not changed by a prepulse (*), suggesting voltage-independent inhibition. b, in the presence of agatoxin (100 nM), 8-OH-DPAT (1 μM) did not produce further inhibition in the same cell.
    Figure Legend Snippet: P/Q-type Ca 2+ currents are reduced only through voltage-independent mechanisms A, agatoxin occluded the voltage-dependent block by 5-HT. Example traces of an experiment are shown in a and the time course measurements at 5 (•) and 70 ms (○) are shown in b. In agatoxin (100 nM), 5-HT caused a ‘pure’ voltage-dependent reduction which almost totally reversed at the end of the test pulse. Ba, a prepulse to +120 mV partially reversed the 5-HT inhibition in control (*, prepulse). b, agatoxin blocked around 20 % of the total HVA current, and in the presence of agatoxin, the prepulse relieved almost the same amount of current (*). However, some voltage-independent inhibition remained. Ca, in Ca 2+ currents elicited by a test pulse to +10 mV from a holding potential of −50 mV, the reduction of Ca 2+ currents by 8-OH-DPAT was not changed by a prepulse (*), suggesting voltage-independent inhibition. b, in the presence of agatoxin (100 nM), 8-OH-DPAT (1 μM) did not produce further inhibition in the same cell.

    Techniques Used: Blocking Assay, Mass Spectrometry, Inhibition

    4) Product Images from "Voltage-activated Ca2+ channels and their role in the endocrine function of the pituitary gland in newborn and adult mice"

    Article Title: Voltage-activated Ca2+ channels and their role in the endocrine function of the pituitary gland in newborn and adult mice

    Journal: The Journal of Physiology

    doi: 10.1113/jphysiol.2003.058271

    The effects of nifedipine, ω-conotoxin GVIA, ω-conotoxin MVIIC with ω-agatoxin TK and CdCl 2 on Ba 2+ currents In panels A , B , C and D left plots present data from the newborn and right plots from the adult animals. A , Ba 2+ currents were evoked during 30 ms voltage steps from −80 mV to +60 mV. All recordings were obtained after preincubation (2 min) with different VACC blockers as indicated. B , current densities from the same cells were plotted to obtain the Ba 2+ current I–V relationship. C , the effect of VACC blockers on the Ba 2+ current I–V relationship obtained from 300 ms voltage ramps. D , the time course of the effect of nifedipine (1), GVIA (2), MVIIC/TK (3) and CdCl 2 (4) on Ba 2+ currents. LVA currents in adults are shown as red triangles and the HVA are shown as black triangles. Note that current values were normalized to the peak amplitude of both VACC components. Nifedipine blocked about 50% of the LVA component; however, other toxins than Cd 2+ did not affect the LVA component.
    Figure Legend Snippet: The effects of nifedipine, ω-conotoxin GVIA, ω-conotoxin MVIIC with ω-agatoxin TK and CdCl 2 on Ba 2+ currents In panels A , B , C and D left plots present data from the newborn and right plots from the adult animals. A , Ba 2+ currents were evoked during 30 ms voltage steps from −80 mV to +60 mV. All recordings were obtained after preincubation (2 min) with different VACC blockers as indicated. B , current densities from the same cells were plotted to obtain the Ba 2+ current I–V relationship. C , the effect of VACC blockers on the Ba 2+ current I–V relationship obtained from 300 ms voltage ramps. D , the time course of the effect of nifedipine (1), GVIA (2), MVIIC/TK (3) and CdCl 2 (4) on Ba 2+ currents. LVA currents in adults are shown as red triangles and the HVA are shown as black triangles. Note that current values were normalized to the peak amplitude of both VACC components. Nifedipine blocked about 50% of the LVA component; however, other toxins than Cd 2+ did not affect the LVA component.

    Techniques Used: Mass Spectrometry

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    Alomone Labs ω agatoxin tk
    Modulation of the inhibitory effects of CP 55,940 ( A ) and morphine ( B ) by blockers of voltage-dependent Ca 2+ channels: nimodipine (NIM), ω-conotoxin (ω-CTX), and <t>ω-agatoxin</t> (ω-ATX). The relative response was defined as the amplitude of the response to KCl at 10 min ( A ) or 5 min ( B ) after superfusion with an agonist plus a VDCC blocker, divided by the amplitude of the response to the first application (absence of drug) and multiplied by 100. The mean somal area of small neurons tested was 505 μm 2 (range, 298-764 μm 2 ) and was 1062 μm 2 (range, 856-1275 μm 2 ) for intermediate-size neurons. Values are the means ± SEM for the treatment group; the number in each bar is the number of neurons tested. * p
    ω Agatoxin Tk, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/ω agatoxin tk/product/Alomone Labs
    Average 91 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    ω agatoxin tk - by Bioz Stars, 2021-12
    91/100 stars
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    Modulation of the inhibitory effects of CP 55,940 ( A ) and morphine ( B ) by blockers of voltage-dependent Ca 2+ channels: nimodipine (NIM), ω-conotoxin (ω-CTX), and ω-agatoxin (ω-ATX). The relative response was defined as the amplitude of the response to KCl at 10 min ( A ) or 5 min ( B ) after superfusion with an agonist plus a VDCC blocker, divided by the amplitude of the response to the first application (absence of drug) and multiplied by 100. The mean somal area of small neurons tested was 505 μm 2 (range, 298-764 μm 2 ) and was 1062 μm 2 (range, 856-1275 μm 2 ) for intermediate-size neurons. Values are the means ± SEM for the treatment group; the number in each bar is the number of neurons tested. * p

    Journal: The Journal of Neuroscience

    Article Title: Differential Effects of CB1 and Opioid Agonists on Two Populations of Adult Rat Dorsal Root Ganglion Neurons

    doi: 10.1523/JNEUROSCI.4298-03.2004

    Figure Lengend Snippet: Modulation of the inhibitory effects of CP 55,940 ( A ) and morphine ( B ) by blockers of voltage-dependent Ca 2+ channels: nimodipine (NIM), ω-conotoxin (ω-CTX), and ω-agatoxin (ω-ATX). The relative response was defined as the amplitude of the response to KCl at 10 min ( A ) or 5 min ( B ) after superfusion with an agonist plus a VDCC blocker, divided by the amplitude of the response to the first application (absence of drug) and multiplied by 100. The mean somal area of small neurons tested was 505 μm 2 (range, 298-764 μm 2 ) and was 1062 μm 2 (range, 856-1275 μm 2 ) for intermediate-size neurons. Values are the means ± SEM for the treatment group; the number in each bar is the number of neurons tested. * p

    Article Snippet: Solutions of ω-conotoxin GVIA and ω-agatoxin TK (Alomone Labs, Jerusalem, Israel) were prepared at their final concentration in HEPES buffer on the day of use.

    Techniques:

    Effects of Ca 2+ channel blockers on I Ca A , voltage steps to −10 or 0 mV for 500 ms elicited inward currents that were Cd 2+ or leak subtracted. Cd 2+ was applied at the end of the experiments, and occasionally the cell was lost prior to its application. In these cells leak subtraction only was possible. The peak current in control conditions and after drug administration for the cell was measured. Calibration values in top left panel apply to all other panels in A . B , the averaged data for each channel blocker are displayed in the histogram as a percentage of the control Ca 2+ current. NiCl 2 , 93.2 ± 3.3 %, n = 6; ω-conotoxin GVIA, 76.2 ± 8.0 %, n = 7; ω-agatoxin TK, 73.3 ± 8.0 %, n = 5; nifedipine, 58.9 ± 13.4 %, n = 7.

    Journal: The Journal of Physiology

    Article Title: N- and L-type calcium channel involvement in depolarization-induced suppression of inhibition in rat hippocampal CA1 cells

    doi: 10.1111/j.1469-7793.1998.061bf.x

    Figure Lengend Snippet: Effects of Ca 2+ channel blockers on I Ca A , voltage steps to −10 or 0 mV for 500 ms elicited inward currents that were Cd 2+ or leak subtracted. Cd 2+ was applied at the end of the experiments, and occasionally the cell was lost prior to its application. In these cells leak subtraction only was possible. The peak current in control conditions and after drug administration for the cell was measured. Calibration values in top left panel apply to all other panels in A . B , the averaged data for each channel blocker are displayed in the histogram as a percentage of the control Ca 2+ current. NiCl 2 , 93.2 ± 3.3 %, n = 6; ω-conotoxin GVIA, 76.2 ± 8.0 %, n = 7; ω-agatoxin TK, 73.3 ± 8.0 %, n = 5; nifedipine, 58.9 ± 13.4 %, n = 7.

    Article Snippet: CNQX and QX-314 were purchased from Research Biochemicals International, and BAPTA was purchased from Molecular Probes. ω-Agatoxin TK, a selective blocker of both P- and Q-type Ca2+ channels , was purchased from Alomone Labs (Jerusalem, Israel).

    Techniques: Mass Spectrometry

    Summary of the effects of ω-CgTx and agatoxin on inhibition of HVA currents by 5-HT The 5-HT-sensitive current was divided into two components: a voltage-dependent component, which was relieved by a conditioning prepulse, and a voltage-independent component, which was unaffected. A, agatoxin reduced the 5-HT-sensitive current, predominantly through the reduction of the voltage-independent component ( P

    Journal: The Journal of Physiology

    Article Title: Differential inhibition of N and P/Q Ca2+ currents by 5-HT1A and 5-HT1D receptors in spinal neurons of Xenopus larvae

    doi: 10.1111/j.1469-7793.1998.103bz.x

    Figure Lengend Snippet: Summary of the effects of ω-CgTx and agatoxin on inhibition of HVA currents by 5-HT The 5-HT-sensitive current was divided into two components: a voltage-dependent component, which was relieved by a conditioning prepulse, and a voltage-independent component, which was unaffected. A, agatoxin reduced the 5-HT-sensitive current, predominantly through the reduction of the voltage-independent component ( P

    Article Snippet: The ion channel blockers used were: ω-agatoxin-IVA and ω-agatoxin-TK (agatoxin, Alomone Labs, Jerusalem, Israel), ω-conotoxin GVIA (ω-CgTx, Bachem, Torrance, CA, USA), ω-conotoxin MVIIC (Alomone Labs), nifedipine (Sigma), tetraethylammonium chloride (TEA, Aldrich) and tetrodotoxin (TTX, Sigma).

    Techniques: Inhibition

    Inhibition of HVA currents by 5-HT was totally occluded by agatoxin and ω-CgTx applied together A, HVA currents elicited by steps to +20 mV in control ( a ), 100 n M agatoxin ( d ) and 1 μM ω-CgTx ( g ). 5-HT (1 μM) caused different amounts of inhibition in the presence of control ( b ), agatoxin ( e ), and agatoxin + ω-CgTx ( h ); B, time series measurements from the same neuron. In control the inhibition was partially relieved by a prepulse to +120 mV (arrow; ○ shows steady-state inhibition). After agatoxin was applied, the amount of voltage-dependent inhibition relieved by the prepulse (arrows) remained almost unchanged, but the voltage-independent inhibition (difference between ○ and • at f ) was reduced. In the presence of both toxins, 5-HT had very little effect on the currents.

    Journal: The Journal of Physiology

    Article Title: Differential inhibition of N and P/Q Ca2+ currents by 5-HT1A and 5-HT1D receptors in spinal neurons of Xenopus larvae

    doi: 10.1111/j.1469-7793.1998.103bz.x

    Figure Lengend Snippet: Inhibition of HVA currents by 5-HT was totally occluded by agatoxin and ω-CgTx applied together A, HVA currents elicited by steps to +20 mV in control ( a ), 100 n M agatoxin ( d ) and 1 μM ω-CgTx ( g ). 5-HT (1 μM) caused different amounts of inhibition in the presence of control ( b ), agatoxin ( e ), and agatoxin + ω-CgTx ( h ); B, time series measurements from the same neuron. In control the inhibition was partially relieved by a prepulse to +120 mV (arrow; ○ shows steady-state inhibition). After agatoxin was applied, the amount of voltage-dependent inhibition relieved by the prepulse (arrows) remained almost unchanged, but the voltage-independent inhibition (difference between ○ and • at f ) was reduced. In the presence of both toxins, 5-HT had very little effect on the currents.

    Article Snippet: The ion channel blockers used were: ω-agatoxin-IVA and ω-agatoxin-TK (agatoxin, Alomone Labs, Jerusalem, Israel), ω-conotoxin GVIA (ω-CgTx, Bachem, Torrance, CA, USA), ω-conotoxin MVIIC (Alomone Labs), nifedipine (Sigma), tetraethylammonium chloride (TEA, Aldrich) and tetrodotoxin (TTX, Sigma).

    Techniques: Inhibition

    Composition of the HVA currents in Xenopus spinal neurons Aa, HVA Ca 2+ current elicited by a test pulse to +20 mV from a holding potential of −50 mV in control, agatoxin (200 nM), ω-CgTx (1 μM) and nifedipine (10 μM). b, time course of block measured at the points indicated in a. B, summary showing that agatoxin blocked 21.8 ± 0.9 % of total HVA current ( n = 24, P/Q-type), ω-CgTx blocked 66.3 ± 1.1 % of total HVA current ( n = 21, N-type), and nifedipine blocked 4.2 ± 0.8 % ( n = 5, L-type).

    Journal: The Journal of Physiology

    Article Title: Differential inhibition of N and P/Q Ca2+ currents by 5-HT1A and 5-HT1D receptors in spinal neurons of Xenopus larvae

    doi: 10.1111/j.1469-7793.1998.103bz.x

    Figure Lengend Snippet: Composition of the HVA currents in Xenopus spinal neurons Aa, HVA Ca 2+ current elicited by a test pulse to +20 mV from a holding potential of −50 mV in control, agatoxin (200 nM), ω-CgTx (1 μM) and nifedipine (10 μM). b, time course of block measured at the points indicated in a. B, summary showing that agatoxin blocked 21.8 ± 0.9 % of total HVA current ( n = 24, P/Q-type), ω-CgTx blocked 66.3 ± 1.1 % of total HVA current ( n = 21, N-type), and nifedipine blocked 4.2 ± 0.8 % ( n = 5, L-type).

    Article Snippet: The ion channel blockers used were: ω-agatoxin-IVA and ω-agatoxin-TK (agatoxin, Alomone Labs, Jerusalem, Israel), ω-conotoxin GVIA (ω-CgTx, Bachem, Torrance, CA, USA), ω-conotoxin MVIIC (Alomone Labs), nifedipine (Sigma), tetraethylammonium chloride (TEA, Aldrich) and tetrodotoxin (TTX, Sigma).

    Techniques: Blocking Assay

    P/Q-type Ca 2+ currents are reduced only through voltage-independent mechanisms A, agatoxin occluded the voltage-dependent block by 5-HT. Example traces of an experiment are shown in a and the time course measurements at 5 (•) and 70 ms (○) are shown in b. In agatoxin (100 nM), 5-HT caused a ‘pure’ voltage-dependent reduction which almost totally reversed at the end of the test pulse. Ba, a prepulse to +120 mV partially reversed the 5-HT inhibition in control (*, prepulse). b, agatoxin blocked around 20 % of the total HVA current, and in the presence of agatoxin, the prepulse relieved almost the same amount of current (*). However, some voltage-independent inhibition remained. Ca, in Ca 2+ currents elicited by a test pulse to +10 mV from a holding potential of −50 mV, the reduction of Ca 2+ currents by 8-OH-DPAT was not changed by a prepulse (*), suggesting voltage-independent inhibition. b, in the presence of agatoxin (100 nM), 8-OH-DPAT (1 μM) did not produce further inhibition in the same cell.

    Journal: The Journal of Physiology

    Article Title: Differential inhibition of N and P/Q Ca2+ currents by 5-HT1A and 5-HT1D receptors in spinal neurons of Xenopus larvae

    doi: 10.1111/j.1469-7793.1998.103bz.x

    Figure Lengend Snippet: P/Q-type Ca 2+ currents are reduced only through voltage-independent mechanisms A, agatoxin occluded the voltage-dependent block by 5-HT. Example traces of an experiment are shown in a and the time course measurements at 5 (•) and 70 ms (○) are shown in b. In agatoxin (100 nM), 5-HT caused a ‘pure’ voltage-dependent reduction which almost totally reversed at the end of the test pulse. Ba, a prepulse to +120 mV partially reversed the 5-HT inhibition in control (*, prepulse). b, agatoxin blocked around 20 % of the total HVA current, and in the presence of agatoxin, the prepulse relieved almost the same amount of current (*). However, some voltage-independent inhibition remained. Ca, in Ca 2+ currents elicited by a test pulse to +10 mV from a holding potential of −50 mV, the reduction of Ca 2+ currents by 8-OH-DPAT was not changed by a prepulse (*), suggesting voltage-independent inhibition. b, in the presence of agatoxin (100 nM), 8-OH-DPAT (1 μM) did not produce further inhibition in the same cell.

    Article Snippet: The ion channel blockers used were: ω-agatoxin-IVA and ω-agatoxin-TK (agatoxin, Alomone Labs, Jerusalem, Israel), ω-conotoxin GVIA (ω-CgTx, Bachem, Torrance, CA, USA), ω-conotoxin MVIIC (Alomone Labs), nifedipine (Sigma), tetraethylammonium chloride (TEA, Aldrich) and tetrodotoxin (TTX, Sigma).

    Techniques: Blocking Assay, Mass Spectrometry, Inhibition

    The effects of nifedipine, ω-conotoxin GVIA, ω-conotoxin MVIIC with ω-agatoxin TK and CdCl 2 on Ba 2+ currents In panels A , B , C and D left plots present data from the newborn and right plots from the adult animals. A , Ba 2+ currents were evoked during 30 ms voltage steps from −80 mV to +60 mV. All recordings were obtained after preincubation (2 min) with different VACC blockers as indicated. B , current densities from the same cells were plotted to obtain the Ba 2+ current I–V relationship. C , the effect of VACC blockers on the Ba 2+ current I–V relationship obtained from 300 ms voltage ramps. D , the time course of the effect of nifedipine (1), GVIA (2), MVIIC/TK (3) and CdCl 2 (4) on Ba 2+ currents. LVA currents in adults are shown as red triangles and the HVA are shown as black triangles. Note that current values were normalized to the peak amplitude of both VACC components. Nifedipine blocked about 50% of the LVA component; however, other toxins than Cd 2+ did not affect the LVA component.

    Journal: The Journal of Physiology

    Article Title: Voltage-activated Ca2+ channels and their role in the endocrine function of the pituitary gland in newborn and adult mice

    doi: 10.1113/jphysiol.2003.058271

    Figure Lengend Snippet: The effects of nifedipine, ω-conotoxin GVIA, ω-conotoxin MVIIC with ω-agatoxin TK and CdCl 2 on Ba 2+ currents In panels A , B , C and D left plots present data from the newborn and right plots from the adult animals. A , Ba 2+ currents were evoked during 30 ms voltage steps from −80 mV to +60 mV. All recordings were obtained after preincubation (2 min) with different VACC blockers as indicated. B , current densities from the same cells were plotted to obtain the Ba 2+ current I–V relationship. C , the effect of VACC blockers on the Ba 2+ current I–V relationship obtained from 300 ms voltage ramps. D , the time course of the effect of nifedipine (1), GVIA (2), MVIIC/TK (3) and CdCl 2 (4) on Ba 2+ currents. LVA currents in adults are shown as red triangles and the HVA are shown as black triangles. Note that current values were normalized to the peak amplitude of both VACC components. Nifedipine blocked about 50% of the LVA component; however, other toxins than Cd 2+ did not affect the LVA component.

    Article Snippet: Purified ω-conotoxin GVIA (GVIA), ω-conotoxin MVIIC (MVIIC), ω-agatoxin TK (TK) and SNX-482 were purchased from Alomone Laboratories (Jerusalem, Israel) and dissolved in distilled water to obtain stock solutions at concentrations of 100 μ m , 10 μ m , 1 μ m and 1 μ m , respectively.

    Techniques: Mass Spectrometry