apamin  (Alomone Labs)


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    Structured Review

    Alomone Labs apamin
    Sustained small-conductance Ca 2+ -activated K + or large-conductance Ca 2+ -activated K + channel inhibition decreases α-cell cytosolic Ca 2+ (Ca 2+ c ) within whole islets. Representative α-GCaMP3 islet α-cell responses following a 30-min pretreatment with vehicle (H 2 O; A ) or <t>apamin</t> ( B ) at 1 mM glucose. Representative α-GCaMP3 islet α-cell responses following a 30-min pretreatment with vehicle ( C ) or apamin ( D ) at 11 mM glucose. Area under the curve (AUC; E ) and ( F ) maximum amplitude of α-GCaMP3 islet α-cell apamin responses relative to vehicle-treated controls at 1 mM glucose ( n ≥ 39 cells from 3 mice). Representative α-GCaMP3 islet α-cell responses following a 30-min pretreatment with vehicle (H 2 O; G ) or iberiotoxin <t>(IbTx;</t> H ) at 1 mM glucose. Representative α-GCaMP3 islet α-cell responses following a 30-min pretreatment with vehicle ( I ) or IbTx ( J ) at 11 mM glucose. AUC ( K ) and maximum amplitude ( L ) of α-GCaMP3 islet α-cell IbTx responses relative to vehicle-treated controls at 1 mM glucose ( n ≥ 59 cells from 6 mice). Statistical analysis was conducted using one-way ANOVA, and uncertainty is expressed as SE (* P
    Apamin, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Glucose-mediated inhibition of calcium-activated potassium channels limits α-cell calcium influx and glucagon secretion"

    Article Title: Glucose-mediated inhibition of calcium-activated potassium channels limits α-cell calcium influx and glucagon secretion

    Journal: American Journal of Physiology - Endocrinology and Metabolism

    doi: 10.1152/ajpendo.00342.2018

    Sustained small-conductance Ca 2+ -activated K + or large-conductance Ca 2+ -activated K + channel inhibition decreases α-cell cytosolic Ca 2+ (Ca 2+ c ) within whole islets. Representative α-GCaMP3 islet α-cell responses following a 30-min pretreatment with vehicle (H 2 O; A ) or apamin ( B ) at 1 mM glucose. Representative α-GCaMP3 islet α-cell responses following a 30-min pretreatment with vehicle ( C ) or apamin ( D ) at 11 mM glucose. Area under the curve (AUC; E ) and ( F ) maximum amplitude of α-GCaMP3 islet α-cell apamin responses relative to vehicle-treated controls at 1 mM glucose ( n ≥ 39 cells from 3 mice). Representative α-GCaMP3 islet α-cell responses following a 30-min pretreatment with vehicle (H 2 O; G ) or iberiotoxin (IbTx; H ) at 1 mM glucose. Representative α-GCaMP3 islet α-cell responses following a 30-min pretreatment with vehicle ( I ) or IbTx ( J ) at 11 mM glucose. AUC ( K ) and maximum amplitude ( L ) of α-GCaMP3 islet α-cell IbTx responses relative to vehicle-treated controls at 1 mM glucose ( n ≥ 59 cells from 6 mice). Statistical analysis was conducted using one-way ANOVA, and uncertainty is expressed as SE (* P
    Figure Legend Snippet: Sustained small-conductance Ca 2+ -activated K + or large-conductance Ca 2+ -activated K + channel inhibition decreases α-cell cytosolic Ca 2+ (Ca 2+ c ) within whole islets. Representative α-GCaMP3 islet α-cell responses following a 30-min pretreatment with vehicle (H 2 O; A ) or apamin ( B ) at 1 mM glucose. Representative α-GCaMP3 islet α-cell responses following a 30-min pretreatment with vehicle ( C ) or apamin ( D ) at 11 mM glucose. Area under the curve (AUC; E ) and ( F ) maximum amplitude of α-GCaMP3 islet α-cell apamin responses relative to vehicle-treated controls at 1 mM glucose ( n ≥ 39 cells from 3 mice). Representative α-GCaMP3 islet α-cell responses following a 30-min pretreatment with vehicle (H 2 O; G ) or iberiotoxin (IbTx; H ) at 1 mM glucose. Representative α-GCaMP3 islet α-cell responses following a 30-min pretreatment with vehicle ( I ) or IbTx ( J ) at 11 mM glucose. AUC ( K ) and maximum amplitude ( L ) of α-GCaMP3 islet α-cell IbTx responses relative to vehicle-treated controls at 1 mM glucose ( n ≥ 59 cells from 6 mice). Statistical analysis was conducted using one-way ANOVA, and uncertainty is expressed as SE (* P

    Techniques Used: Inhibition, Mouse Assay

    α-Cell Ca 2+ -activated K + (K slow ) currents are activated by Ca 2+ waves generated by repeated membrane potential depolarization. A : overview of pulse train K slow protocol ( top ) and a representative K slow current recorded from a single red fluorescent protein-expressing (α-RFP) α-cell ( bottom ). Inset shows a magnification of the K slow tail current. B : average α-cell K slow currents ( n ≥ 12 cells from 3 mice) with (red) and without (blue) extracellular Ca 2+ (2 mM). C : area under the curve (AUC) of α-cell K slow currents from B . Fast phase (0–2 τ f s), slow phase (2–3 τ s s), and total (0–3 s). D : average α-cell K slow currents ( n ≥ 15 cells from 3 mice) with vehicle (red) or agatoxin (100 nM; blue). E : AUC of α-cell K slow currents from D . F : average α-cell K slow currents ( n ≥ 16 cells from 3 mice) with vehicle (red) or nifedipine (50 μM; blue). G : AUC of α-cell K slow currents from F . H : average α-cell K slow currents ( n ≥ 13 cells from 3 mice) with vehicle (red) or thapsigargin (Tg; 2 μM; blue) at 1 mM glucose. I : AUC of α-cell K slow currents from H . J : average α-cell K slow currents ( n ≥ 10 cells from 3 mice) with vehicle (red) or Tg (blue) at 11 mM glucose. K : AUC of α-cell K slow currents from J . L : average α-cell K slow currents ( n ≥ 17 cells from 3 mice) with vehicle (red) or apamin (100 nM; blue). M : AUC of α-cell K slow currents from L . N : average α-cell K slow currents ( n ≥ 18 cells from 3 mice) with vehicle (red) or iberiotoxin (IbTx; 100 nM; blue). O : AUC of α-cell K slow currents from N : average K slow tail currents were fit to a model of two-phase decay. Statistical analysis was conducted using unpaired two-tailed t -tests, and uncertainty is expressed as SE (* P
    Figure Legend Snippet: α-Cell Ca 2+ -activated K + (K slow ) currents are activated by Ca 2+ waves generated by repeated membrane potential depolarization. A : overview of pulse train K slow protocol ( top ) and a representative K slow current recorded from a single red fluorescent protein-expressing (α-RFP) α-cell ( bottom ). Inset shows a magnification of the K slow tail current. B : average α-cell K slow currents ( n ≥ 12 cells from 3 mice) with (red) and without (blue) extracellular Ca 2+ (2 mM). C : area under the curve (AUC) of α-cell K slow currents from B . Fast phase (0–2 τ f s), slow phase (2–3 τ s s), and total (0–3 s). D : average α-cell K slow currents ( n ≥ 15 cells from 3 mice) with vehicle (red) or agatoxin (100 nM; blue). E : AUC of α-cell K slow currents from D . F : average α-cell K slow currents ( n ≥ 16 cells from 3 mice) with vehicle (red) or nifedipine (50 μM; blue). G : AUC of α-cell K slow currents from F . H : average α-cell K slow currents ( n ≥ 13 cells from 3 mice) with vehicle (red) or thapsigargin (Tg; 2 μM; blue) at 1 mM glucose. I : AUC of α-cell K slow currents from H . J : average α-cell K slow currents ( n ≥ 10 cells from 3 mice) with vehicle (red) or Tg (blue) at 11 mM glucose. K : AUC of α-cell K slow currents from J . L : average α-cell K slow currents ( n ≥ 17 cells from 3 mice) with vehicle (red) or apamin (100 nM; blue). M : AUC of α-cell K slow currents from L . N : average α-cell K slow currents ( n ≥ 18 cells from 3 mice) with vehicle (red) or iberiotoxin (IbTx; 100 nM; blue). O : AUC of α-cell K slow currents from N : average K slow tail currents were fit to a model of two-phase decay. Statistical analysis was conducted using unpaired two-tailed t -tests, and uncertainty is expressed as SE (* P

    Techniques Used: Generated, Expressing, Mouse Assay, Two Tailed Test

    A : average ( n ≥ 60 cells from 3 mice) Fura-2 acetoxymethyl ester (AM) responses (F 340 /F 380 ) of dispersed red fluorescent protein-expressing (α-RFP) α-cells to apamin (100 nM) at 1 mM ( top ) and 11 mM ( bottom ) glucose. The bars above the traces denote when stimuli are present. B : area under the curve (AUC) of mouse α-cell Fura-2 AM responses before (black) and after (white) the addition of apamin. C : average ( n ≥ 99 cells from 3 mice) Fura-2 AM responses (F 340 /F 380 ) of dispersed α-RFP α-cells to iberiotoxin (IbTx; 100 nM) at 1 mM ( top ) and 11 mM ( bottom ) glucose. D : AUC of mouse α-cell Fura-2 AM responses before (black) and after (white) the addition of IbTx. E : representative Fura-2 AM response (F 340 /F 380 ) of dispersed human α-cells to apamin at 1 mM glucose. F : AUC ( left ) and average Fura-2 AM response ( right ) of human α-cells before (black) and after (white) the addition of apamin (n ≥ 56 cells from 4 donors). Human islet cells were fixed with 4% paraformaldehyde, and α-cells were identified by glucagon staining. Statistical analysis was conducted using paired two-tailed t -tests, and uncertainty is expressed as SE (* P
    Figure Legend Snippet: A : average ( n ≥ 60 cells from 3 mice) Fura-2 acetoxymethyl ester (AM) responses (F 340 /F 380 ) of dispersed red fluorescent protein-expressing (α-RFP) α-cells to apamin (100 nM) at 1 mM ( top ) and 11 mM ( bottom ) glucose. The bars above the traces denote when stimuli are present. B : area under the curve (AUC) of mouse α-cell Fura-2 AM responses before (black) and after (white) the addition of apamin. C : average ( n ≥ 99 cells from 3 mice) Fura-2 AM responses (F 340 /F 380 ) of dispersed α-RFP α-cells to iberiotoxin (IbTx; 100 nM) at 1 mM ( top ) and 11 mM ( bottom ) glucose. D : AUC of mouse α-cell Fura-2 AM responses before (black) and after (white) the addition of IbTx. E : representative Fura-2 AM response (F 340 /F 380 ) of dispersed human α-cells to apamin at 1 mM glucose. F : AUC ( left ) and average Fura-2 AM response ( right ) of human α-cells before (black) and after (white) the addition of apamin (n ≥ 56 cells from 4 donors). Human islet cells were fixed with 4% paraformaldehyde, and α-cells were identified by glucagon staining. Statistical analysis was conducted using paired two-tailed t -tests, and uncertainty is expressed as SE (* P

    Techniques Used: Mouse Assay, Expressing, Staining, Two Tailed Test

    2) Product Images from "Nitric Oxide Regulates Neuronal Activity via Calcium-Activated Potassium Channels"

    Article Title: Nitric Oxide Regulates Neuronal Activity via Calcium-Activated Potassium Channels

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0078727

    Proposed model of ion channel targets through which NO results in a prolonged depolarization. Elevation of NO by NO donors, such as NOC7 or DEA/NO, inhibits two types of Ca 2+ -activated K + channels in Helisoma B19 neurons. Apamin-sensitive SK channels contribute to part of the initial effect of NO and are fully responsible for its long-lasting effect on membrane depolarization, whereas IbTX-sensitive BK channels only partially contribute to the initial depolarization. Voltage-gated Ca 2+ channels do not participate in the depolarizing effect of extrinsically applied NO. The mechanism(s) by which NO inhibits these ion channels is presently unknown (indicated by dotted lines). Inhibitors used are indicated in gray.
    Figure Legend Snippet: Proposed model of ion channel targets through which NO results in a prolonged depolarization. Elevation of NO by NO donors, such as NOC7 or DEA/NO, inhibits two types of Ca 2+ -activated K + channels in Helisoma B19 neurons. Apamin-sensitive SK channels contribute to part of the initial effect of NO and are fully responsible for its long-lasting effect on membrane depolarization, whereas IbTX-sensitive BK channels only partially contribute to the initial depolarization. Voltage-gated Ca 2+ channels do not participate in the depolarizing effect of extrinsically applied NO. The mechanism(s) by which NO inhibits these ion channels is presently unknown (indicated by dotted lines). Inhibitors used are indicated in gray.

    Techniques Used:

    3) Product Images from "Effects of inhibitors of small- and intermediate-conductance calcium-activated potassium channels, inwardly-rectifying potassium channels and Na+/K+ ATPase on EDHF relaxations in the rat hepatic artery"

    Article Title: Effects of inhibitors of small- and intermediate-conductance calcium-activated potassium channels, inwardly-rectifying potassium channels and Na+/K+ ATPase on EDHF relaxations in the rat hepatic artery

    Journal: British Journal of Pharmacology

    doi: 10.1038/sj.bjp.0703226

    Effects of K + channel inhibitors on calcium ionophore stimulated 86 Rb + influx in human erythrocytes. The K + channel inhibitors iberiotoxin (IbTx), apamin (Apa), charybdotoxin (ChTx), ciclazindol (Cz), clotrimazole (CLT) and 2-chlorophenyl-bisphenyl-methanol (C23) and the cytochrome P450 mono-oxygenase inhibitor ketoconazole (KEC) were present 85 min before erythrocytes were stimulated for 5 min by A23187 and Ca 2+ . Data are expressed as percentage of 86 Rb + influx in the absence of test drugs (control) and are presented as means±s.e.mean of six experiments (all from different individuals). Asterisks denote a statistically significant difference from control values ( P
    Figure Legend Snippet: Effects of K + channel inhibitors on calcium ionophore stimulated 86 Rb + influx in human erythrocytes. The K + channel inhibitors iberiotoxin (IbTx), apamin (Apa), charybdotoxin (ChTx), ciclazindol (Cz), clotrimazole (CLT) and 2-chlorophenyl-bisphenyl-methanol (C23) and the cytochrome P450 mono-oxygenase inhibitor ketoconazole (KEC) were present 85 min before erythrocytes were stimulated for 5 min by A23187 and Ca 2+ . Data are expressed as percentage of 86 Rb + influx in the absence of test drugs (control) and are presented as means±s.e.mean of six experiments (all from different individuals). Asterisks denote a statistically significant difference from control values ( P

    Techniques Used:

    4) Product Images from "α-Synuclein oligomers mediate the aberrant form of spike-induced calcium release from IP3 receptor"

    Article Title: α-Synuclein oligomers mediate the aberrant form of spike-induced calcium release from IP3 receptor

    Journal: Scientific Reports

    doi: 10.1038/s41598-019-52135-3

    α-Synuclein oligomers prolonged AHP by spike-induced Ca 2+ release from IP 3 receptor coupled with L-VDCC and SK channel. (a ) Specimen recordings of action potentials during positive current pulses (300 ms, 0.3 nA) in neurons with αSN or αSNo under the application of the L-VDCC blocker nifedipine (10 μM), the SK channel blocker apamin (100 nM) and the IP 3 R blocker heparin. These blockers canceled αSNo-mediated reduction of spike frequency. Scale bars, 100 ms and 10 mV. ( b ) Mean spike frequencies during 0.3 nA positive current steps under the application of various blockers of channels or receptors controlling intracellular Ca 2+ dynamics. * p
    Figure Legend Snippet: α-Synuclein oligomers prolonged AHP by spike-induced Ca 2+ release from IP 3 receptor coupled with L-VDCC and SK channel. (a ) Specimen recordings of action potentials during positive current pulses (300 ms, 0.3 nA) in neurons with αSN or αSNo under the application of the L-VDCC blocker nifedipine (10 μM), the SK channel blocker apamin (100 nM) and the IP 3 R blocker heparin. These blockers canceled αSNo-mediated reduction of spike frequency. Scale bars, 100 ms and 10 mV. ( b ) Mean spike frequencies during 0.3 nA positive current steps under the application of various blockers of channels or receptors controlling intracellular Ca 2+ dynamics. * p

    Techniques Used: Mass Spectrometry

    5) Product Images from "Pioglitazone, a PPAR-γ Activator, Stimulates BKCa but Suppresses IKM in Hippocampal Neurons"

    Article Title: Pioglitazone, a PPAR-γ Activator, Stimulates BKCa but Suppresses IKM in Hippocampal Neurons

    Journal: Frontiers in Pharmacology

    doi: 10.3389/fphar.2018.00977

    Effect of PIO on whole-cell Ca 2+ -activated K + current ( I K(Ca) ) in mHippoE-14 hippocampal neurons. In these experiments, cells were bathed in normal Tyrode’s solution, the composition of which was described under Section “Materials and Methods.” The recording pipette was filled with K + -containing solution. (A) Superimposed I K(Ca) traces obtained in the control (middle part) and during cell exposure to 10 μM PIO (bottom part). The upper part indicates the voltage protocol applied, and arrowheads are zero current level. (B) Averaged I–V relationships of I K(Ca) obtained in the control ( ), during the exposure ( ) to 10 μM PIO and after washout ( ) of PIO (mean ± SEM; n = 11 for each point). ∗ Significantly different from control groups taken at the same level of voltage pulse. (C) Bar graph showing summary of the effect of PIO, PIO plus TRAM-39, PIO plus apamin, and PIO plus paxilline, and PIO plus tolbutamide on I K(Ca) amplitude (mean ± SEM; n = 10–12 for each bar). Current amplitude was measured at +50 mV. (a) Control; (b) 10 μM PIO; (c) 10 μM PIO plus 3 μM TRAM-39; (d) 10 μM PIO plus 200 nM apamin; (e) 10 μM PIO plus 1 μM paxilline; (f) 10 μM PIO plus 30 μM tolbutamide. ∗ Significantly different from control ( P
    Figure Legend Snippet: Effect of PIO on whole-cell Ca 2+ -activated K + current ( I K(Ca) ) in mHippoE-14 hippocampal neurons. In these experiments, cells were bathed in normal Tyrode’s solution, the composition of which was described under Section “Materials and Methods.” The recording pipette was filled with K + -containing solution. (A) Superimposed I K(Ca) traces obtained in the control (middle part) and during cell exposure to 10 μM PIO (bottom part). The upper part indicates the voltage protocol applied, and arrowheads are zero current level. (B) Averaged I–V relationships of I K(Ca) obtained in the control ( ), during the exposure ( ) to 10 μM PIO and after washout ( ) of PIO (mean ± SEM; n = 11 for each point). ∗ Significantly different from control groups taken at the same level of voltage pulse. (C) Bar graph showing summary of the effect of PIO, PIO plus TRAM-39, PIO plus apamin, and PIO plus paxilline, and PIO plus tolbutamide on I K(Ca) amplitude (mean ± SEM; n = 10–12 for each bar). Current amplitude was measured at +50 mV. (a) Control; (b) 10 μM PIO; (c) 10 μM PIO plus 3 μM TRAM-39; (d) 10 μM PIO plus 200 nM apamin; (e) 10 μM PIO plus 1 μM paxilline; (f) 10 μM PIO plus 30 μM tolbutamide. ∗ Significantly different from control ( P

    Techniques Used: Transferring

    6) Product Images from "Duration differences of corticostriatal responses in striatal projection neurons depend on calcium activated potassium currents"

    Article Title: Duration differences of corticostriatal responses in striatal projection neurons depend on calcium activated potassium currents

    Journal: Frontiers in Systems Neuroscience

    doi: 10.3389/fnsys.2013.00063

    Ca 2+ -activated K + -currents control the propagation of autoregenerative potentials in iSPNs. (A) Green trace shows a control suprathreshold corticostriatal response in an iSPN. Addition of 100 nM apamin discloses an autoregenerative and propagated action potential whose main ionic component is Ca 2+ (purple trace; Bargas et al., 1991 ). Subsequent addition of 20 nM ChTx in the continuous presence of apamin further prolongs the duration of the regenerative event without increasing its amplitude, illustrating its all-or-none properties (black trace). (B) Green trace is a spontaneous regenerative event that sometimes appears in control suprathreshold responses in iSPNs (alternating with the initial burst of spikes). Addition of 2.5 μM NS 309 hindered the propagation of this event to the somatic area and accelerated the repolarization (orange trace). Clearly, fast spikes inactivate when calcium autoregenerative potentials propagate.
    Figure Legend Snippet: Ca 2+ -activated K + -currents control the propagation of autoregenerative potentials in iSPNs. (A) Green trace shows a control suprathreshold corticostriatal response in an iSPN. Addition of 100 nM apamin discloses an autoregenerative and propagated action potential whose main ionic component is Ca 2+ (purple trace; Bargas et al., 1991 ). Subsequent addition of 20 nM ChTx in the continuous presence of apamin further prolongs the duration of the regenerative event without increasing its amplitude, illustrating its all-or-none properties (black trace). (B) Green trace is a spontaneous regenerative event that sometimes appears in control suprathreshold responses in iSPNs (alternating with the initial burst of spikes). Addition of 2.5 μM NS 309 hindered the propagation of this event to the somatic area and accelerated the repolarization (orange trace). Clearly, fast spikes inactivate when calcium autoregenerative potentials propagate.

    Techniques Used:

    Blockade of BK and SK channels depolarize and prolong corticostriatal responses in striatal projection neurons. (A) Three superimposed records from a dSPN were obtained without changing stimulus strength: they show a corticostriatal response in control conditions (red trace), the same response in the presence of the blocker of BK-channels, 20 nM charybdotoxin (ChTx, blue trace), and finally, the same response in the presence of both ChTx and the blocker of SK channels, 100 nM apamin (ChTx + apamin, black trace). Each blocker depolarized and prolonged the response, and also increased the number of action potentials that were fired. Digital subtractions at bottom illustrate the hyperpolarizing influence that Ca 2+ -activated K + -currents exerted over the corticostriatal responses and that were suppressed by the blockade of ChTx (blue) and apamin (black). Note that the hyperpolarizing influence of Ca 2+ -activated K + -currents rise slowly and last hundreds of milliseconds thus contributing to restrain the build up of the corticostriatal response. (B) Intensity-response (I-R) graphs obtained by plotting average half width (duration at 50% of the peak amplitude of the response) as a function of threshold intensity including: minimal, subthreshold (0.5×), threshold (1.0×) and suprathreshold responses (2.0×). A sigmoid function was fitted. Curves with the action of each blocker are plotted individually as well as the administration of both blockers together. Shadowed colored areas denote 95% confidence intervals, symbols depict average values of the samples for each stimulus strength ± s.e.m. (C) Tukey box plots illustrate the distributions of measurements for suprathreshold responses (half width at 2× threshold strength), in control, in the presence of each blocker, and in the presence of both blockers. Differences are significant: * P
    Figure Legend Snippet: Blockade of BK and SK channels depolarize and prolong corticostriatal responses in striatal projection neurons. (A) Three superimposed records from a dSPN were obtained without changing stimulus strength: they show a corticostriatal response in control conditions (red trace), the same response in the presence of the blocker of BK-channels, 20 nM charybdotoxin (ChTx, blue trace), and finally, the same response in the presence of both ChTx and the blocker of SK channels, 100 nM apamin (ChTx + apamin, black trace). Each blocker depolarized and prolonged the response, and also increased the number of action potentials that were fired. Digital subtractions at bottom illustrate the hyperpolarizing influence that Ca 2+ -activated K + -currents exerted over the corticostriatal responses and that were suppressed by the blockade of ChTx (blue) and apamin (black). Note that the hyperpolarizing influence of Ca 2+ -activated K + -currents rise slowly and last hundreds of milliseconds thus contributing to restrain the build up of the corticostriatal response. (B) Intensity-response (I-R) graphs obtained by plotting average half width (duration at 50% of the peak amplitude of the response) as a function of threshold intensity including: minimal, subthreshold (0.5×), threshold (1.0×) and suprathreshold responses (2.0×). A sigmoid function was fitted. Curves with the action of each blocker are plotted individually as well as the administration of both blockers together. Shadowed colored areas denote 95% confidence intervals, symbols depict average values of the samples for each stimulus strength ± s.e.m. (C) Tukey box plots illustrate the distributions of measurements for suprathreshold responses (half width at 2× threshold strength), in control, in the presence of each blocker, and in the presence of both blockers. Differences are significant: * P

    Techniques Used:

    Influence of Ca 2+ -activated K + -currents on subthreshold corticostriatal responses. (A) Subthreshold synaptic potentials recorded after cortical stimulation in a dSPN in control conditions (red), after addition of 100 nM apamin (purple) and after addition of 20 nM ChTx in the continuous presence of apamin (black). (B) The same experiment was performed on an iSPN (control condition is in green). Note that Ca 2+ -activated K + -currents appear to exert more influence on subthreshold synaptic events of iSPNs. (C) Subthreshold synaptic potentials recorded after cortical stimulation in a dSPN in control conditions (red), after addition of 2.5 μM NS 309 (orange), an enhancer of SK-channels, and after addition of 2.5 μM NS 1619, an enhancer of BK-channels, in the continuous presence of NS 309 (black). (D) The same experiment performed on an iSPN (control condition is in green). Enhancers of Ca 2+ -activated K + -currents also indicate more influence of these currents in subthreshold synaptic events of iSPNs.
    Figure Legend Snippet: Influence of Ca 2+ -activated K + -currents on subthreshold corticostriatal responses. (A) Subthreshold synaptic potentials recorded after cortical stimulation in a dSPN in control conditions (red), after addition of 100 nM apamin (purple) and after addition of 20 nM ChTx in the continuous presence of apamin (black). (B) The same experiment was performed on an iSPN (control condition is in green). Note that Ca 2+ -activated K + -currents appear to exert more influence on subthreshold synaptic events of iSPNs. (C) Subthreshold synaptic potentials recorded after cortical stimulation in a dSPN in control conditions (red), after addition of 2.5 μM NS 309 (orange), an enhancer of SK-channels, and after addition of 2.5 μM NS 1619, an enhancer of BK-channels, in the continuous presence of NS 309 (black). (D) The same experiment performed on an iSPN (control condition is in green). Enhancers of Ca 2+ -activated K + -currents also indicate more influence of these currents in subthreshold synaptic events of iSPNs.

    Techniques Used:

    7) Product Images from "Essential Role of Somatic Kv2 Channels in High-Frequency Firing in Cartwheel Cells of the Dorsal Cochlear Nucleus"

    Article Title: Essential Role of Somatic Kv2 Channels in High-Frequency Firing in Cartwheel Cells of the Dorsal Cochlear Nucleus

    Journal: eNeuro

    doi: 10.1523/ENEURO.0515-20.2021

    Biophysical properties of GxTX-sensitive Kv2 current in cartwheel cells. A , Outward current evoked by voltage steps. Pulse protocol is indicated at the bottom of A . The recordings were made at room temperature (23–24°C) using ACSF supplemented with NBQX, MK-801, strychnine, picrotoxin, TTX, apamin (a SK channel blocker), and penitrem A (a BK channel blocker). To remove inward current by voltage-gated calcium channels, CaCl 2 in the ACSF was excluded and replaced with equimolar MgCl 2 , and 0.25 m m EGTA-Na was added. GxTX-sensitive current was obtained by subtraction. B , The current–voltage relationship of the outward current in the absence (control) or presence of 100 n m GxTX (GxTX). The amplitude of steady-state was used for the plotting. Here and the following figures, error bars indicate SEM, numbers in parentheses indicate the number of replications (cells). Statistical significance was tested using two-way repeated measure ANOVA and Bonferroni post hoc tests (significance at p
    Figure Legend Snippet: Biophysical properties of GxTX-sensitive Kv2 current in cartwheel cells. A , Outward current evoked by voltage steps. Pulse protocol is indicated at the bottom of A . The recordings were made at room temperature (23–24°C) using ACSF supplemented with NBQX, MK-801, strychnine, picrotoxin, TTX, apamin (a SK channel blocker), and penitrem A (a BK channel blocker). To remove inward current by voltage-gated calcium channels, CaCl 2 in the ACSF was excluded and replaced with equimolar MgCl 2 , and 0.25 m m EGTA-Na was added. GxTX-sensitive current was obtained by subtraction. B , The current–voltage relationship of the outward current in the absence (control) or presence of 100 n m GxTX (GxTX). The amplitude of steady-state was used for the plotting. Here and the following figures, error bars indicate SEM, numbers in parentheses indicate the number of replications (cells). Statistical significance was tested using two-way repeated measure ANOVA and Bonferroni post hoc tests (significance at p

    Techniques Used:

    8) Product Images from "Hypotonicity-induced TRPV4 function in renal collecting duct cells: modulation by progressive cross-talk with Ca2+-activated K+ channels"

    Article Title: Hypotonicity-induced TRPV4 function in renal collecting duct cells: modulation by progressive cross-talk with Ca2+-activated K+ channels

    Journal: Cell Calcium

    doi: 10.1016/j.ceca.2011.11.011

    Effect of BK antagonist, IbTX, and SK3 antagonist, apamin, on [Ca 2+ ] i response to HYPO in M-1 cells. A. Representative trace showing the effect of HYPO on [Ca 2+ ] i followed by a repeat HYPO stimulation in the presence of IbTX (100 nM). B. Representative
    Figure Legend Snippet: Effect of BK antagonist, IbTX, and SK3 antagonist, apamin, on [Ca 2+ ] i response to HYPO in M-1 cells. A. Representative trace showing the effect of HYPO on [Ca 2+ ] i followed by a repeat HYPO stimulation in the presence of IbTX (100 nM). B. Representative

    Techniques Used:

    9) Product Images from "Ability of naringenin, a bioflavonoid, to activate M-type potassium current in motor neuron-like cells and to increase BKCa-channel activity in HEK293T cells transfected with α-hSlo subunit"

    Article Title: Ability of naringenin, a bioflavonoid, to activate M-type potassium current in motor neuron-like cells and to increase BKCa-channel activity in HEK293T cells transfected with α-hSlo subunit

    Journal: BMC Neuroscience

    doi: 10.1186/s12868-014-0135-1

    Effects of NGEN and other K + current blockers on the amplitude of I K(M) in NSC-34 cells. In these experiments, cells were bathed in Ca 2+ -free Tyrode's solution which contained 200 nM iberiotoxin, 200 nM apamin and 1 μM tetrodotoxin, and each cell was hyperpolarized from -20 to -50 mV with a duration of 2 sec. Current amplitude was measured at the end of voltage pulse. Each bar represents the mean ± SEM (n = 7-13). Flu: flupirtine; Iber: iberiotoxin; Aps: apamin; Lino: linopirdine. * Significantly different from control. ** Significantly different from NGEN (10 μM) alone group. Notably, further application of linopirdine reversed NGEN-stimulated I K(M) , while neither iberiotoxin nor apamin produced any effects on it.
    Figure Legend Snippet: Effects of NGEN and other K + current blockers on the amplitude of I K(M) in NSC-34 cells. In these experiments, cells were bathed in Ca 2+ -free Tyrode's solution which contained 200 nM iberiotoxin, 200 nM apamin and 1 μM tetrodotoxin, and each cell was hyperpolarized from -20 to -50 mV with a duration of 2 sec. Current amplitude was measured at the end of voltage pulse. Each bar represents the mean ± SEM (n = 7-13). Flu: flupirtine; Iber: iberiotoxin; Aps: apamin; Lino: linopirdine. * Significantly different from control. ** Significantly different from NGEN (10 μM) alone group. Notably, further application of linopirdine reversed NGEN-stimulated I K(M) , while neither iberiotoxin nor apamin produced any effects on it.

    Techniques Used: Produced

    Effects of NGEN on I K(M) recorded from motor neuron-like NSC-34 cells. In (A) , superimposed current traces obtained in the absence (left) and presence (right) of 10 μM NGEN. In these experiments, cells were bathed Ca 2+ -Tyrode’s solution which contained 200 nM iberiotoxin, 200 nM apamin and 1 μM tetrodotoxin. The I K(M) was elicited from -20 mV to different potentials which ranged from -50 to +10 mV with 10-mV increments. (B) Effect of NGEN on the averaged I-V relations of I K(M) in NSC-34 cells (mean ± SEM; n = 9-13 for each point). ■: control; □: 10 μM NGEN. Current amplitude was measured at end of each voltage pulse. (C) Voltage dependence of I K(M) conductance in the absence (■) and presence (□) of 10 μM NGEN (mean ± SEM; n = 8-12 for each point). Note that there is a leftward shift in the activation curve of I K(M) conductance during cell exposure to NGEN, although the slope factor remains unchanged.
    Figure Legend Snippet: Effects of NGEN on I K(M) recorded from motor neuron-like NSC-34 cells. In (A) , superimposed current traces obtained in the absence (left) and presence (right) of 10 μM NGEN. In these experiments, cells were bathed Ca 2+ -Tyrode’s solution which contained 200 nM iberiotoxin, 200 nM apamin and 1 μM tetrodotoxin. The I K(M) was elicited from -20 mV to different potentials which ranged from -50 to +10 mV with 10-mV increments. (B) Effect of NGEN on the averaged I-V relations of I K(M) in NSC-34 cells (mean ± SEM; n = 9-13 for each point). ■: control; □: 10 μM NGEN. Current amplitude was measured at end of each voltage pulse. (C) Voltage dependence of I K(M) conductance in the absence (■) and presence (□) of 10 μM NGEN (mean ± SEM; n = 8-12 for each point). Note that there is a leftward shift in the activation curve of I K(M) conductance during cell exposure to NGEN, although the slope factor remains unchanged.

    Techniques Used: Activation Assay

    Stimulatory effect of NGEN on the activity of K M channels recorded from NSC-34 cells. In (A) , cells were bathed in Ca 2+ -free Tyrode’s solution which contained iberiotoxin (200 nM), apamin (200 nM) and tetrodotoxin (1 μM). Cell-attached configuration was made as the cell attached was held at 0 mV relative to the bath. Channel activity was obtained in the control (left) and after addition of NGEN (10 μM) to the bath. Portion of tracing in the upper part of (A) is amplified in the lower part. Channel openings give a downward deflection in current. (B) Summary of the data showing effects of NGEN and flupirtine (Flu) on K M -channel activity in NSC-34 cells (mean ± SEM; n = 9-12 for each bar). * Significantly different from control.
    Figure Legend Snippet: Stimulatory effect of NGEN on the activity of K M channels recorded from NSC-34 cells. In (A) , cells were bathed in Ca 2+ -free Tyrode’s solution which contained iberiotoxin (200 nM), apamin (200 nM) and tetrodotoxin (1 μM). Cell-attached configuration was made as the cell attached was held at 0 mV relative to the bath. Channel activity was obtained in the control (left) and after addition of NGEN (10 μM) to the bath. Portion of tracing in the upper part of (A) is amplified in the lower part. Channel openings give a downward deflection in current. (B) Summary of the data showing effects of NGEN and flupirtine (Flu) on K M -channel activity in NSC-34 cells (mean ± SEM; n = 9-12 for each bar). * Significantly different from control.

    Techniques Used: Activity Assay, Amplification

    10) Product Images from "Dyshomeostatic modulation of Ca2+-activated K+ channels in a human neuronal model of KCNQ2 encephalopathy"

    Article Title: Dyshomeostatic modulation of Ca2+-activated K+ channels in a human neuronal model of KCNQ2 encephalopathy

    Journal: eLife

    doi: 10.7554/eLife.64434

    Effects of acute paxilline/apamin treatment on chronically XE991-treated control neurons. ( A ) Experimental protocol. On day 32, apamin (500 nM) and paxilline (20 µM) were added to MEAs after 5 min of baseline spontaneous recordings. The effect of drugs was measured after 10 min of continuous recording for 5 min. ( B ) The magnitude by which apamin and paxilline reduced ISI CoV, spikes/burst and burst % was significantly larger in chronically XE991-treated isoQ2-04 +/+ neurons compared to untreated isoQ2-04 +/+ neurons (t-test: **p=0.0019, **p=0.0011 and *p=0.0482, respectively). A dotted line is drawn through the mean baseline values measured for isoQ2-04 +/+ neurons before acute application of apamin and paxilline. Teal * indicate significant difference between chronically XE991-treated isoQ2-04 +/+ and untreated isoQ2-04 +/+ neurons. Values displayed are mean ± SEM.
    Figure Legend Snippet: Effects of acute paxilline/apamin treatment on chronically XE991-treated control neurons. ( A ) Experimental protocol. On day 32, apamin (500 nM) and paxilline (20 µM) were added to MEAs after 5 min of baseline spontaneous recordings. The effect of drugs was measured after 10 min of continuous recording for 5 min. ( B ) The magnitude by which apamin and paxilline reduced ISI CoV, spikes/burst and burst % was significantly larger in chronically XE991-treated isoQ2-04 +/+ neurons compared to untreated isoQ2-04 +/+ neurons (t-test: **p=0.0019, **p=0.0011 and *p=0.0482, respectively). A dotted line is drawn through the mean baseline values measured for isoQ2-04 +/+ neurons before acute application of apamin and paxilline. Teal * indicate significant difference between chronically XE991-treated isoQ2-04 +/+ and untreated isoQ2-04 +/+ neurons. Values displayed are mean ± SEM.

    Techniques Used: T-Test

    11) Product Images from "Effective Activation by Kynurenic Acid and Its Aminoalkylated Derivatives on M-Type K+ Current"

    Article Title: Effective Activation by Kynurenic Acid and Its Aminoalkylated Derivatives on M-Type K+ Current

    Journal: International Journal of Molecular Sciences

    doi: 10.3390/ijms22031300

    Effect of kynurenic acid (KYNA, 4-hydroxyquinoline-2-carboxylic acid) and N -(2-(dimethylamino)ethyl)-3-(morpholinomethyl)-4-oxo-1,4-dihydroquinoline-2-carboxamide (KYNA-A4) on spontaneous action potentials (APs) recorded from GH 3 cells. In this set of the experiments, cells were bathed in normal Tyrode’s solution, the electrode was filled with K + -containing solution, and the whole-cell current-clamp voltage recordings were performed. ( A ) Original potential traces obtained in the control (a) and during exposure to 10 μM KYNA (b) or 30 μM KYNA (c). In ( B ), ( Ba ) illustrates summary bar graph depicting effects of KYNA (10 or 30 μM), KYNA (30 μM) plus iberiotoxin (Iber, 200 nM), KYNA (30 μM) plus apamin (Apa, 200 nM), and KYNA (30 μM) plus linopirdine (Lino, 10 μM) on the frequency of spontaneous APs in GH 3 cells, while ( Bb ) shows those of KYNA-A4 (3 or 10 μM), KYNA-A4 (10 μM) plus Iber (200 nM), KYNA-A4 (10 μM) plus Apa (200 nM), and KYNA-A4 (10 μM) plus Lino (10 μM) on firing frequency. Each bar indicates the mean ± SEM ( n = 7). * indicates a significant difference from controls ( p
    Figure Legend Snippet: Effect of kynurenic acid (KYNA, 4-hydroxyquinoline-2-carboxylic acid) and N -(2-(dimethylamino)ethyl)-3-(morpholinomethyl)-4-oxo-1,4-dihydroquinoline-2-carboxamide (KYNA-A4) on spontaneous action potentials (APs) recorded from GH 3 cells. In this set of the experiments, cells were bathed in normal Tyrode’s solution, the electrode was filled with K + -containing solution, and the whole-cell current-clamp voltage recordings were performed. ( A ) Original potential traces obtained in the control (a) and during exposure to 10 μM KYNA (b) or 30 μM KYNA (c). In ( B ), ( Ba ) illustrates summary bar graph depicting effects of KYNA (10 or 30 μM), KYNA (30 μM) plus iberiotoxin (Iber, 200 nM), KYNA (30 μM) plus apamin (Apa, 200 nM), and KYNA (30 μM) plus linopirdine (Lino, 10 μM) on the frequency of spontaneous APs in GH 3 cells, while ( Bb ) shows those of KYNA-A4 (3 or 10 μM), KYNA-A4 (10 μM) plus Iber (200 nM), KYNA-A4 (10 μM) plus Apa (200 nM), and KYNA-A4 (10 μM) plus Lino (10 μM) on firing frequency. Each bar indicates the mean ± SEM ( n = 7). * indicates a significant difference from controls ( p

    Techniques Used:

    12) Product Images from "Pioglitazone, a PPAR-γ Activator, Stimulates BKCa but Suppresses IKM in Hippocampal Neurons"

    Article Title: Pioglitazone, a PPAR-γ Activator, Stimulates BKCa but Suppresses IKM in Hippocampal Neurons

    Journal: Frontiers in Pharmacology

    doi: 10.3389/fphar.2018.00977

    Effect of PIO on whole-cell Ca 2+ -activated K + current ( I K(Ca) ) in mHippoE-14 hippocampal neurons. In these experiments, cells were bathed in normal Tyrode’s solution, the composition of which was described under Section “Materials and Methods.” The recording pipette was filled with K + -containing solution. (A) Superimposed I K(Ca) traces obtained in the control (middle part) and during cell exposure to 10 μM PIO (bottom part). The upper part indicates the voltage protocol applied, and arrowheads are zero current level. (B) Averaged I–V relationships of I K(Ca) obtained in the control ( ), during the exposure ( ) to 10 μM PIO and after washout ( ) of PIO (mean ± SEM; n = 11 for each point). ∗ Significantly different from control groups taken at the same level of voltage pulse. (C) Bar graph showing summary of the effect of PIO, PIO plus TRAM-39, PIO plus apamin, and PIO plus paxilline, and PIO plus tolbutamide on I K(Ca) amplitude (mean ± SEM; n = 10–12 for each bar). Current amplitude was measured at +50 mV. (a) Control; (b) 10 μM PIO; (c) 10 μM PIO plus 3 μM TRAM-39; (d) 10 μM PIO plus 200 nM apamin; (e) 10 μM PIO plus 1 μM paxilline; (f) 10 μM PIO plus 30 μM tolbutamide. ∗ Significantly different from control ( P
    Figure Legend Snippet: Effect of PIO on whole-cell Ca 2+ -activated K + current ( I K(Ca) ) in mHippoE-14 hippocampal neurons. In these experiments, cells were bathed in normal Tyrode’s solution, the composition of which was described under Section “Materials and Methods.” The recording pipette was filled with K + -containing solution. (A) Superimposed I K(Ca) traces obtained in the control (middle part) and during cell exposure to 10 μM PIO (bottom part). The upper part indicates the voltage protocol applied, and arrowheads are zero current level. (B) Averaged I–V relationships of I K(Ca) obtained in the control ( ), during the exposure ( ) to 10 μM PIO and after washout ( ) of PIO (mean ± SEM; n = 11 for each point). ∗ Significantly different from control groups taken at the same level of voltage pulse. (C) Bar graph showing summary of the effect of PIO, PIO plus TRAM-39, PIO plus apamin, and PIO plus paxilline, and PIO plus tolbutamide on I K(Ca) amplitude (mean ± SEM; n = 10–12 for each bar). Current amplitude was measured at +50 mV. (a) Control; (b) 10 μM PIO; (c) 10 μM PIO plus 3 μM TRAM-39; (d) 10 μM PIO plus 200 nM apamin; (e) 10 μM PIO plus 1 μM paxilline; (f) 10 μM PIO plus 30 μM tolbutamide. ∗ Significantly different from control ( P

    Techniques Used: Transferring

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    Alomone Labs apamin apa
    <t>Apamin</t> prolongs action potentials in TAB rat VMs and TAB rat whole heart A , representative current clamp traces in TAB rat VMs under baseline (left) or ISO (100 nmol L –1 for 3 min) (right) before and after treatment with apamin (100 nmol L –1 for 3 min). Pooled mean ± SD APD 90 . n = 5–9, N = 4–7, * P = 0.04, # P = 0.03, Student's t test. B , representative APD maps before and after APA (10 nmol L –1 ) recorded under basal conditions and in the presence of β‐adrenergic agonist ISO (50 nmol L –1 ) and the corresponding APD profile. Right, Pooled data for APD 75 . * P
    Apamin Apa, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    95
    Alomone Labs ω agatoxin iva
    P/Q‐ and L‐type Ca v channels mediated Ca 2+ influx in response to glutamate input. (a) Glutamate‐induced Ca 2+ rise in a GCaMP6f + OL in the presence of Naspm, <t>agatoxin</t> (200 nM) and nifedipine (100 μM). (b) Summary of Ca 2+ responses after application of nifedipine or agatoxin, and combinations of agatoxin + nifedipine and agatoxin + CdCl 2 . (c) Ca v channel currents in the presence of 4‐AP (2 mM), TEA (10 mM), BaCl 2 (1 mM), and TTX (1 μM) in voltage‐clamp recording (holding at −65 mV), which were inhibited by CdCl 2 . Inset, step‐like depolarization protocol. (d) Current–voltage (I‐V) relationship of OL Ca 2+ current ( I Ca ). I Ca was partially inhibited by agatoxin and completely inhibited by CdCl 2 . (e) Ca 2+ rise in a GCaMP6f + OL when directly depolarized using a depolarizing pulse (diagram) during voltage‐clamp recording in the presence of agatoxin and nifedipine. The OL was brought from resting membrane potential at −65 mV to −40, −20, or 0 mV over the course of 100 ms, held at 0 mV for 100 ms, and brought back to resting membrane potential over a period of 2 s. (f) Summary of depolarization‐induced Ca 2+ rise in the presence of agatoxin and nifedipine. Data are represented as ± SEM . *** represents p
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    Apamin prolongs action potentials in TAB rat VMs and TAB rat whole heart A , representative current clamp traces in TAB rat VMs under baseline (left) or ISO (100 nmol L –1 for 3 min) (right) before and after treatment with apamin (100 nmol L –1 for 3 min). Pooled mean ± SD APD 90 . n = 5–9, N = 4–7, * P = 0.04, # P = 0.03, Student's t test. B , representative APD maps before and after APA (10 nmol L –1 ) recorded under basal conditions and in the presence of β‐adrenergic agonist ISO (50 nmol L –1 ) and the corresponding APD profile. Right, Pooled data for APD 75 . * P

    Journal: The Journal of Physiology

    Article Title: PKA phosphorylation underlies functional recruitment of sarcolemmal SK2 channels in ventricular myocytes from hypertrophic hearts

    doi: 10.1113/JP277618

    Figure Lengend Snippet: Apamin prolongs action potentials in TAB rat VMs and TAB rat whole heart A , representative current clamp traces in TAB rat VMs under baseline (left) or ISO (100 nmol L –1 for 3 min) (right) before and after treatment with apamin (100 nmol L –1 for 3 min). Pooled mean ± SD APD 90 . n = 5–9, N = 4–7, * P = 0.04, # P = 0.03, Student's t test. B , representative APD maps before and after APA (10 nmol L –1 ) recorded under basal conditions and in the presence of β‐adrenergic agonist ISO (50 nmol L –1 ) and the corresponding APD profile. Right, Pooled data for APD 75 . * P

    Article Snippet: Apamin (APA), a selective SK1, 2 and 3 polypeptide inhibitor (IC50 < 10 nmol L–1 ; Alomone Labs) was used to identify SK currents.

    Techniques:

    SK current in Sham rat VMs with application of ISO A , representative superimposed traces of I SK (blue), I Ca (black) and [Ca 2+ ] i transient (red) recorded in Sham VMs depolarized to −20 mV (left). I SK was obtained by application of 1 nmol L –1 APA. Pooled I – V and peak [Ca 2+ ]/ V relationships. B , representative inward current traces recorded in Sham VMs at 3, 6 and 8 min following application of 100 nmol L –1 ISO at −10 mV (HP −40 mV). Right: plot of normalized inward current amplitude vs . time after application of ISO. Mean ± SD, n = 5, N = 2. The normalized inward current after 6 min of ISO and 3 min of 100 nmol L –1 apamin is plotted in red. Mean ± SD, n = 8, N = 7, * P = 0.04 vs . ISO only, Student's t test.

    Journal: The Journal of Physiology

    Article Title: PKA phosphorylation underlies functional recruitment of sarcolemmal SK2 channels in ventricular myocytes from hypertrophic hearts

    doi: 10.1113/JP277618

    Figure Lengend Snippet: SK current in Sham rat VMs with application of ISO A , representative superimposed traces of I SK (blue), I Ca (black) and [Ca 2+ ] i transient (red) recorded in Sham VMs depolarized to −20 mV (left). I SK was obtained by application of 1 nmol L –1 APA. Pooled I – V and peak [Ca 2+ ]/ V relationships. B , representative inward current traces recorded in Sham VMs at 3, 6 and 8 min following application of 100 nmol L –1 ISO at −10 mV (HP −40 mV). Right: plot of normalized inward current amplitude vs . time after application of ISO. Mean ± SD, n = 5, N = 2. The normalized inward current after 6 min of ISO and 3 min of 100 nmol L –1 apamin is plotted in red. Mean ± SD, n = 8, N = 7, * P = 0.04 vs . ISO only, Student's t test.

    Article Snippet: Apamin (APA), a selective SK1, 2 and 3 polypeptide inhibitor (IC50 < 10 nmol L–1 ; Alomone Labs) was used to identify SK currents.

    Techniques:

    Sustained small-conductance Ca 2+ -activated K + or large-conductance Ca 2+ -activated K + channel inhibition decreases α-cell cytosolic Ca 2+ (Ca 2+ c ) within whole islets. Representative α-GCaMP3 islet α-cell responses following a 30-min pretreatment with vehicle (H 2 O; A ) or apamin ( B ) at 1 mM glucose. Representative α-GCaMP3 islet α-cell responses following a 30-min pretreatment with vehicle ( C ) or apamin ( D ) at 11 mM glucose. Area under the curve (AUC; E ) and ( F ) maximum amplitude of α-GCaMP3 islet α-cell apamin responses relative to vehicle-treated controls at 1 mM glucose ( n ≥ 39 cells from 3 mice). Representative α-GCaMP3 islet α-cell responses following a 30-min pretreatment with vehicle (H 2 O; G ) or iberiotoxin (IbTx; H ) at 1 mM glucose. Representative α-GCaMP3 islet α-cell responses following a 30-min pretreatment with vehicle ( I ) or IbTx ( J ) at 11 mM glucose. AUC ( K ) and maximum amplitude ( L ) of α-GCaMP3 islet α-cell IbTx responses relative to vehicle-treated controls at 1 mM glucose ( n ≥ 59 cells from 6 mice). Statistical analysis was conducted using one-way ANOVA, and uncertainty is expressed as SE (* P

    Journal: American Journal of Physiology - Endocrinology and Metabolism

    Article Title: Glucose-mediated inhibition of calcium-activated potassium channels limits α-cell calcium influx and glucagon secretion

    doi: 10.1152/ajpendo.00342.2018

    Figure Lengend Snippet: Sustained small-conductance Ca 2+ -activated K + or large-conductance Ca 2+ -activated K + channel inhibition decreases α-cell cytosolic Ca 2+ (Ca 2+ c ) within whole islets. Representative α-GCaMP3 islet α-cell responses following a 30-min pretreatment with vehicle (H 2 O; A ) or apamin ( B ) at 1 mM glucose. Representative α-GCaMP3 islet α-cell responses following a 30-min pretreatment with vehicle ( C ) or apamin ( D ) at 11 mM glucose. Area under the curve (AUC; E ) and ( F ) maximum amplitude of α-GCaMP3 islet α-cell apamin responses relative to vehicle-treated controls at 1 mM glucose ( n ≥ 39 cells from 3 mice). Representative α-GCaMP3 islet α-cell responses following a 30-min pretreatment with vehicle (H 2 O; G ) or iberiotoxin (IbTx; H ) at 1 mM glucose. Representative α-GCaMP3 islet α-cell responses following a 30-min pretreatment with vehicle ( I ) or IbTx ( J ) at 11 mM glucose. AUC ( K ) and maximum amplitude ( L ) of α-GCaMP3 islet α-cell IbTx responses relative to vehicle-treated controls at 1 mM glucose ( n ≥ 59 cells from 6 mice). Statistical analysis was conducted using one-way ANOVA, and uncertainty is expressed as SE (* P

    Article Snippet: Agatoxin, apamin, IbTx, isradipine, thapsigargin (Tg), and TRAM 34 were purchased from Alomone Laboratories (Jerusalem, Israel).

    Techniques: Inhibition, Mouse Assay

    α-Cell Ca 2+ -activated K + (K slow ) currents are activated by Ca 2+ waves generated by repeated membrane potential depolarization. A : overview of pulse train K slow protocol ( top ) and a representative K slow current recorded from a single red fluorescent protein-expressing (α-RFP) α-cell ( bottom ). Inset shows a magnification of the K slow tail current. B : average α-cell K slow currents ( n ≥ 12 cells from 3 mice) with (red) and without (blue) extracellular Ca 2+ (2 mM). C : area under the curve (AUC) of α-cell K slow currents from B . Fast phase (0–2 τ f s), slow phase (2–3 τ s s), and total (0–3 s). D : average α-cell K slow currents ( n ≥ 15 cells from 3 mice) with vehicle (red) or agatoxin (100 nM; blue). E : AUC of α-cell K slow currents from D . F : average α-cell K slow currents ( n ≥ 16 cells from 3 mice) with vehicle (red) or nifedipine (50 μM; blue). G : AUC of α-cell K slow currents from F . H : average α-cell K slow currents ( n ≥ 13 cells from 3 mice) with vehicle (red) or thapsigargin (Tg; 2 μM; blue) at 1 mM glucose. I : AUC of α-cell K slow currents from H . J : average α-cell K slow currents ( n ≥ 10 cells from 3 mice) with vehicle (red) or Tg (blue) at 11 mM glucose. K : AUC of α-cell K slow currents from J . L : average α-cell K slow currents ( n ≥ 17 cells from 3 mice) with vehicle (red) or apamin (100 nM; blue). M : AUC of α-cell K slow currents from L . N : average α-cell K slow currents ( n ≥ 18 cells from 3 mice) with vehicle (red) or iberiotoxin (IbTx; 100 nM; blue). O : AUC of α-cell K slow currents from N : average K slow tail currents were fit to a model of two-phase decay. Statistical analysis was conducted using unpaired two-tailed t -tests, and uncertainty is expressed as SE (* P

    Journal: American Journal of Physiology - Endocrinology and Metabolism

    Article Title: Glucose-mediated inhibition of calcium-activated potassium channels limits α-cell calcium influx and glucagon secretion

    doi: 10.1152/ajpendo.00342.2018

    Figure Lengend Snippet: α-Cell Ca 2+ -activated K + (K slow ) currents are activated by Ca 2+ waves generated by repeated membrane potential depolarization. A : overview of pulse train K slow protocol ( top ) and a representative K slow current recorded from a single red fluorescent protein-expressing (α-RFP) α-cell ( bottom ). Inset shows a magnification of the K slow tail current. B : average α-cell K slow currents ( n ≥ 12 cells from 3 mice) with (red) and without (blue) extracellular Ca 2+ (2 mM). C : area under the curve (AUC) of α-cell K slow currents from B . Fast phase (0–2 τ f s), slow phase (2–3 τ s s), and total (0–3 s). D : average α-cell K slow currents ( n ≥ 15 cells from 3 mice) with vehicle (red) or agatoxin (100 nM; blue). E : AUC of α-cell K slow currents from D . F : average α-cell K slow currents ( n ≥ 16 cells from 3 mice) with vehicle (red) or nifedipine (50 μM; blue). G : AUC of α-cell K slow currents from F . H : average α-cell K slow currents ( n ≥ 13 cells from 3 mice) with vehicle (red) or thapsigargin (Tg; 2 μM; blue) at 1 mM glucose. I : AUC of α-cell K slow currents from H . J : average α-cell K slow currents ( n ≥ 10 cells from 3 mice) with vehicle (red) or Tg (blue) at 11 mM glucose. K : AUC of α-cell K slow currents from J . L : average α-cell K slow currents ( n ≥ 17 cells from 3 mice) with vehicle (red) or apamin (100 nM; blue). M : AUC of α-cell K slow currents from L . N : average α-cell K slow currents ( n ≥ 18 cells from 3 mice) with vehicle (red) or iberiotoxin (IbTx; 100 nM; blue). O : AUC of α-cell K slow currents from N : average K slow tail currents were fit to a model of two-phase decay. Statistical analysis was conducted using unpaired two-tailed t -tests, and uncertainty is expressed as SE (* P

    Article Snippet: Agatoxin, apamin, IbTx, isradipine, thapsigargin (Tg), and TRAM 34 were purchased from Alomone Laboratories (Jerusalem, Israel).

    Techniques: Generated, Expressing, Mouse Assay, Two Tailed Test

    A : average ( n ≥ 60 cells from 3 mice) Fura-2 acetoxymethyl ester (AM) responses (F 340 /F 380 ) of dispersed red fluorescent protein-expressing (α-RFP) α-cells to apamin (100 nM) at 1 mM ( top ) and 11 mM ( bottom ) glucose. The bars above the traces denote when stimuli are present. B : area under the curve (AUC) of mouse α-cell Fura-2 AM responses before (black) and after (white) the addition of apamin. C : average ( n ≥ 99 cells from 3 mice) Fura-2 AM responses (F 340 /F 380 ) of dispersed α-RFP α-cells to iberiotoxin (IbTx; 100 nM) at 1 mM ( top ) and 11 mM ( bottom ) glucose. D : AUC of mouse α-cell Fura-2 AM responses before (black) and after (white) the addition of IbTx. E : representative Fura-2 AM response (F 340 /F 380 ) of dispersed human α-cells to apamin at 1 mM glucose. F : AUC ( left ) and average Fura-2 AM response ( right ) of human α-cells before (black) and after (white) the addition of apamin (n ≥ 56 cells from 4 donors). Human islet cells were fixed with 4% paraformaldehyde, and α-cells were identified by glucagon staining. Statistical analysis was conducted using paired two-tailed t -tests, and uncertainty is expressed as SE (* P

    Journal: American Journal of Physiology - Endocrinology and Metabolism

    Article Title: Glucose-mediated inhibition of calcium-activated potassium channels limits α-cell calcium influx and glucagon secretion

    doi: 10.1152/ajpendo.00342.2018

    Figure Lengend Snippet: A : average ( n ≥ 60 cells from 3 mice) Fura-2 acetoxymethyl ester (AM) responses (F 340 /F 380 ) of dispersed red fluorescent protein-expressing (α-RFP) α-cells to apamin (100 nM) at 1 mM ( top ) and 11 mM ( bottom ) glucose. The bars above the traces denote when stimuli are present. B : area under the curve (AUC) of mouse α-cell Fura-2 AM responses before (black) and after (white) the addition of apamin. C : average ( n ≥ 99 cells from 3 mice) Fura-2 AM responses (F 340 /F 380 ) of dispersed α-RFP α-cells to iberiotoxin (IbTx; 100 nM) at 1 mM ( top ) and 11 mM ( bottom ) glucose. D : AUC of mouse α-cell Fura-2 AM responses before (black) and after (white) the addition of IbTx. E : representative Fura-2 AM response (F 340 /F 380 ) of dispersed human α-cells to apamin at 1 mM glucose. F : AUC ( left ) and average Fura-2 AM response ( right ) of human α-cells before (black) and after (white) the addition of apamin (n ≥ 56 cells from 4 donors). Human islet cells were fixed with 4% paraformaldehyde, and α-cells were identified by glucagon staining. Statistical analysis was conducted using paired two-tailed t -tests, and uncertainty is expressed as SE (* P

    Article Snippet: Agatoxin, apamin, IbTx, isradipine, thapsigargin (Tg), and TRAM 34 were purchased from Alomone Laboratories (Jerusalem, Israel).

    Techniques: Mouse Assay, Expressing, Staining, Two Tailed Test

    Proposed model of ion channel targets through which NO results in a prolonged depolarization. Elevation of NO by NO donors, such as NOC7 or DEA/NO, inhibits two types of Ca 2+ -activated K + channels in Helisoma B19 neurons. Apamin-sensitive SK channels contribute to part of the initial effect of NO and are fully responsible for its long-lasting effect on membrane depolarization, whereas IbTX-sensitive BK channels only partially contribute to the initial depolarization. Voltage-gated Ca 2+ channels do not participate in the depolarizing effect of extrinsically applied NO. The mechanism(s) by which NO inhibits these ion channels is presently unknown (indicated by dotted lines). Inhibitors used are indicated in gray.

    Journal: PLoS ONE

    Article Title: Nitric Oxide Regulates Neuronal Activity via Calcium-Activated Potassium Channels

    doi: 10.1371/journal.pone.0078727

    Figure Lengend Snippet: Proposed model of ion channel targets through which NO results in a prolonged depolarization. Elevation of NO by NO donors, such as NOC7 or DEA/NO, inhibits two types of Ca 2+ -activated K + channels in Helisoma B19 neurons. Apamin-sensitive SK channels contribute to part of the initial effect of NO and are fully responsible for its long-lasting effect on membrane depolarization, whereas IbTX-sensitive BK channels only partially contribute to the initial depolarization. Voltage-gated Ca 2+ channels do not participate in the depolarizing effect of extrinsically applied NO. The mechanism(s) by which NO inhibits these ion channels is presently unknown (indicated by dotted lines). Inhibitors used are indicated in gray.

    Article Snippet: Diethylamine NONOate (DEA/NO, Calbiochem), cadmium chloride (CdCl2 , Sigma), iberiotoxin (IbTX, Sigma), apamin (Alomone labs), and NG-nitro-L-arginine methyl ester (L-NAME, Calbiochem), were dissolved in distilled H2 O to make 100 mM, 1 M, 200 µM, 1 mM, 1 M stock solutions, respectively.

    Techniques:

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

    Journal: Glia

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

    doi: 10.1002/glia.23670

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

    Article Snippet: 6‐cyano‐7‐nitroquinoxaline‐2,3‐dione (CNQX; 50 μM; Tocris, Bristol, UK), 1‐naphthyl acetyl spermine (Naspm; 50 μM; Tocris, Bristol, UK), D‐AP5 (50 μM; Tocris, Bristol, UK), dantrolene (20 μM; Tocris, Bristol, UK), CdCl2 (200 μM; Sigma St. Louis, MO, USA), 4‐aminopyridine (4‐AP; 2 mM; Sigma, St. Louis, MO, USA), tertraethylammonium (TEA; 10 mM; Sigma, St. Louis, MO, USA), BaCl2 (1 mM; Sigma, St. Louis, MO, USA), tetrodotoxin (TTX; 1 μM; Sigma, St. Louis, MO, USA), nifedipine (100 μM; Sigma, St. Louis, MO, USA), and ω‐agatoxin‐IVA (agatoxin; 200 nM; Alomone, Jerusalem, Israel) were bath‐applied.

    Techniques: