iberiotoxin  (Alomone Labs)


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    Structured Review

    Alomone Labs iberiotoxin
    For patch clamp experiments, undissociated CBs were used . The setup (A) and the image of the CB (B) are shown. Examples of K current records and mean I – V relationships in the DBA/2J (C) and the A/J mouse (D) are presented. Whole current traces were evoked by voltage steps from −80 to +60 mV with 10 mV increments for 100 ms. To construct a current–voltage curve, the mean current measured between 93 and 97 ms from the start of each voltage step. Mean currents were plotted versus the test pulse. Bars represent SEM. No statistical differences were seen between the strains. (E) The effect of <t>iberiotoxin</t> (a BK channel blocker; 200 nM) on outward current in GCs. The outward current was evoked by a test pulse from −80 to +20 mV for 100 ms. Iberiotoxin significantly and reversibly decreased outward current in GCs of the DBA/2J mice. However, K current in the A/J mice was not significantly affected by iberiotoxin. *, Significantly different from control and recovery. The amplitudes of K current (control and recovery) were significantly larger in GCs of the DBA/2J mice. Cont, control; Ibx, iberiotoxin; Rec, recovery.
    Iberiotoxin, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Differential Expression of Large-Conductance Ca2+-Activated K Channels in the Carotid Body between DBA/2J and A/J Strains of Mice"

    Article Title: Differential Expression of Large-Conductance Ca2+-Activated K Channels in the Carotid Body between DBA/2J and A/J Strains of Mice

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2011.00019

    For patch clamp experiments, undissociated CBs were used . The setup (A) and the image of the CB (B) are shown. Examples of K current records and mean I – V relationships in the DBA/2J (C) and the A/J mouse (D) are presented. Whole current traces were evoked by voltage steps from −80 to +60 mV with 10 mV increments for 100 ms. To construct a current–voltage curve, the mean current measured between 93 and 97 ms from the start of each voltage step. Mean currents were plotted versus the test pulse. Bars represent SEM. No statistical differences were seen between the strains. (E) The effect of iberiotoxin (a BK channel blocker; 200 nM) on outward current in GCs. The outward current was evoked by a test pulse from −80 to +20 mV for 100 ms. Iberiotoxin significantly and reversibly decreased outward current in GCs of the DBA/2J mice. However, K current in the A/J mice was not significantly affected by iberiotoxin. *, Significantly different from control and recovery. The amplitudes of K current (control and recovery) were significantly larger in GCs of the DBA/2J mice. Cont, control; Ibx, iberiotoxin; Rec, recovery.
    Figure Legend Snippet: For patch clamp experiments, undissociated CBs were used . The setup (A) and the image of the CB (B) are shown. Examples of K current records and mean I – V relationships in the DBA/2J (C) and the A/J mouse (D) are presented. Whole current traces were evoked by voltage steps from −80 to +60 mV with 10 mV increments for 100 ms. To construct a current–voltage curve, the mean current measured between 93 and 97 ms from the start of each voltage step. Mean currents were plotted versus the test pulse. Bars represent SEM. No statistical differences were seen between the strains. (E) The effect of iberiotoxin (a BK channel blocker; 200 nM) on outward current in GCs. The outward current was evoked by a test pulse from −80 to +20 mV for 100 ms. Iberiotoxin significantly and reversibly decreased outward current in GCs of the DBA/2J mice. However, K current in the A/J mice was not significantly affected by iberiotoxin. *, Significantly different from control and recovery. The amplitudes of K current (control and recovery) were significantly larger in GCs of the DBA/2J mice. Cont, control; Ibx, iberiotoxin; Rec, recovery.

    Techniques Used: Patch Clamp, Construct, Mouse Assay

    2) Product Images from "Epoxyeicosatrienoic and dihydroxyeicosatrienoic acids dilate human coronary arterioles via BKCa channels: implications for soluble epoxide hydrolase inhibition"

    Article Title: Epoxyeicosatrienoic and dihydroxyeicosatrienoic acids dilate human coronary arterioles via BKCa channels: implications for soluble epoxide hydrolase inhibition

    Journal:

    doi: 10.1152/ajpheart.00927.2005

    Effect of large-conductance Ca 2+ -activated K + (BK Ca ) channel blockade on EET- and dihydroxyeicosatrienoic acids (DHET)-induced dilation of HCAs. A–C : dilation to 8,9-, 11,12-, and 14,15-EET is inhibited by iberiotoxin (100 nmol/l, n = 6, 7, and
    Figure Legend Snippet: Effect of large-conductance Ca 2+ -activated K + (BK Ca ) channel blockade on EET- and dihydroxyeicosatrienoic acids (DHET)-induced dilation of HCAs. A–C : dilation to 8,9-, 11,12-, and 14,15-EET is inhibited by iberiotoxin (100 nmol/l, n = 6, 7, and

    Techniques Used:

    3) Product Images from "Serum-induced changes in the physiology of mammalian retinal glial cells: role of lysophosphatidic acid"

    Article Title: Serum-induced changes in the physiology of mammalian retinal glial cells: role of lysophosphatidic acid

    Journal: The Journal of Physiology

    doi: 10.1111/j.1469-7793.1998.445bw.x

    Effects of charybdotoxin, iberiotoxin and margatoxin on Müller cell currents induced by serum A , top panel, I - V relationship under control conditions and in the presence of either 10% bovine serum, 100 nM charybdotoxin (ChTX) or serum plus ChTX. Bottom panel, plot of the difference between the I - V curves of the serum-induced currents in the absence and presence of ChTX. B , similar to A , with 50 nM iberiotoxin (IbTX) in place of ChTX. C , similar to A and B , with 1 nM margatoxin (MTX) in place of ChTX or IbTX. Freshly dissociated bovine Müller cells were monitored with perforated-patch recordings. The sensitivity of the serum-induced outwardly rectifying current to charybdotoxin and margatoxin, but not iberiotoxin, is consistent with the activation of K V 1.3 channels.
    Figure Legend Snippet: Effects of charybdotoxin, iberiotoxin and margatoxin on Müller cell currents induced by serum A , top panel, I - V relationship under control conditions and in the presence of either 10% bovine serum, 100 nM charybdotoxin (ChTX) or serum plus ChTX. Bottom panel, plot of the difference between the I - V curves of the serum-induced currents in the absence and presence of ChTX. B , similar to A , with 50 nM iberiotoxin (IbTX) in place of ChTX. C , similar to A and B , with 1 nM margatoxin (MTX) in place of ChTX or IbTX. Freshly dissociated bovine Müller cells were monitored with perforated-patch recordings. The sensitivity of the serum-induced outwardly rectifying current to charybdotoxin and margatoxin, but not iberiotoxin, is consistent with the activation of K V 1.3 channels.

    Techniques Used: Activation Assay

    4) Product Images from "BK channel overexpression on plasma membrane of fibroblasts from Hutchinson-Gilford progeria syndrome"

    Article Title: BK channel overexpression on plasma membrane of fibroblasts from Hutchinson-Gilford progeria syndrome

    Journal: Aging (Albany NY)

    doi: 10.18632/aging.101621

    Proliferation and adhesion rates without and with the BK Ca inhibitor IbTx. ( A ) Average number of hDF obtained from young healthy donors and patients affected by HGPS estimated at 48, 72 and 96 hours from seeding and normalized at 24 h (fold-change ± SEM). Healthy and HGPS hDF were allowed to proliferate untreated (Young n=54; HGPS n=36) and treated by 100 nM IbTx (Young n=53; HGPS n=36). Young vs. HGPS: **p
    Figure Legend Snippet: Proliferation and adhesion rates without and with the BK Ca inhibitor IbTx. ( A ) Average number of hDF obtained from young healthy donors and patients affected by HGPS estimated at 48, 72 and 96 hours from seeding and normalized at 24 h (fold-change ± SEM). Healthy and HGPS hDF were allowed to proliferate untreated (Young n=54; HGPS n=36) and treated by 100 nM IbTx (Young n=53; HGPS n=36). Young vs. HGPS: **p

    Techniques Used:

    Outward currents patch-clamp recorded in whole-cell configuration. ( A ) Representative examples of current traces recorded in hDF obtained from a young donor, an elderly, and a patient affected by HGPS. Current traces recorded after 100 nM IbTx application and a graphical representation of the pulse protocol (holding potential at 0 mV) are also shown. ( B ) Average ± SEM of current-voltage relationships (I–V) recorded in hDF obtained from healthy donors (Young, n=83; Elderly, n=16) and patients affected by HGPS (n=80). ( C ) Average ± SEM of current-voltage relationships (I–V) recorded in hDF obtained from young donors and patients affected by HGPS treated by 100 nM IbTx (n=6) and 10 mM TEA (n=4). Young vs. HGPS: *p
    Figure Legend Snippet: Outward currents patch-clamp recorded in whole-cell configuration. ( A ) Representative examples of current traces recorded in hDF obtained from a young donor, an elderly, and a patient affected by HGPS. Current traces recorded after 100 nM IbTx application and a graphical representation of the pulse protocol (holding potential at 0 mV) are also shown. ( B ) Average ± SEM of current-voltage relationships (I–V) recorded in hDF obtained from healthy donors (Young, n=83; Elderly, n=16) and patients affected by HGPS (n=80). ( C ) Average ± SEM of current-voltage relationships (I–V) recorded in hDF obtained from young donors and patients affected by HGPS treated by 100 nM IbTx (n=6) and 10 mM TEA (n=4). Young vs. HGPS: *p

    Techniques Used: Patch Clamp

    5) Product Images from "Characterisation of K+ Channels in Human Fetoplacental Vascular Smooth Muscle Cells"

    Article Title: Characterisation of K+ Channels in Human Fetoplacental Vascular Smooth Muscle Cells

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0057451

    Characterisation of Ca 2+ -activated K + channel isoforms in CPASMCs. Representative example of the inhibition of outward currents by the BK Ca and IK Ca blocker charybdotoxin (ChTx; n = 4; N = 2; 100 nM; A ), but not the specific IK Ca inhibitor TRAM-34 (n = 3, N = 2; 10µM; B ). The specific BK Ca blocker iberiotoxin (IbTx; 100 nM; C ) inhibited outward currents at depolarised potentials. Mean current-voltage relationships measured at the end of the 500 ms voltage step ranging from -70 mV to +80 mV were obtained in the absence (•) and presence (○) of IbTx ( D ; *P
    Figure Legend Snippet: Characterisation of Ca 2+ -activated K + channel isoforms in CPASMCs. Representative example of the inhibition of outward currents by the BK Ca and IK Ca blocker charybdotoxin (ChTx; n = 4; N = 2; 100 nM; A ), but not the specific IK Ca inhibitor TRAM-34 (n = 3, N = 2; 10µM; B ). The specific BK Ca blocker iberiotoxin (IbTx; 100 nM; C ) inhibited outward currents at depolarised potentials. Mean current-voltage relationships measured at the end of the 500 ms voltage step ranging from -70 mV to +80 mV were obtained in the absence (•) and presence (○) of IbTx ( D ; *P

    Techniques Used: Inhibition, Mass Spectrometry

    6) 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

    Effect of NGEN on whole-cell I K(Ca) in α -hSlo -expressing HEK293T cells. In these experiments, cells were bathed in normal Tyrode’s solution containing 1.8 mM CaCl 2 . (A) Current traces in response to membrane depolarization from 0 to +50 mV. The upper part indicates the voltage protocol used. a: control; b: 3 μM NGEN; c: 10 μM NGEN; and d: 30 μM NGEN. (B) Summary of the data showing effects of NGEN, NGEN plus verruculogen (Verr; 1 μM) and NGEN plus iberiotoxin (Iber; 200 nM) on I K(Ca) amplitude in these cells (mean ± SEM; n = 10-13 for each bar). * Significantly different from control. ** Significantly different from NGEN (30 μM) alone group.
    Figure Legend Snippet: Effect of NGEN on whole-cell I K(Ca) in α -hSlo -expressing HEK293T cells. In these experiments, cells were bathed in normal Tyrode’s solution containing 1.8 mM CaCl 2 . (A) Current traces in response to membrane depolarization from 0 to +50 mV. The upper part indicates the voltage protocol used. a: control; b: 3 μM NGEN; c: 10 μM NGEN; and d: 30 μM NGEN. (B) Summary of the data showing effects of NGEN, NGEN plus verruculogen (Verr; 1 μM) and NGEN plus iberiotoxin (Iber; 200 nM) on I K(Ca) amplitude in these cells (mean ± SEM; n = 10-13 for each bar). * Significantly different from control. ** Significantly different from NGEN (30 μM) alone group.

    Techniques Used: Expressing

    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

    7) Product Images from "Inhibition of vascular calcium-gated chloride currents by blockers of KCa1.1, but not by modulators of KCa2.1 or KCa2.3 channels"

    Article Title: Inhibition of vascular calcium-gated chloride currents by blockers of KCa1.1, but not by modulators of KCa2.1 or KCa2.3 channels

    Journal: British Journal of Pharmacology

    doi: 10.1111/j.1476-5381.2009.00332.x

    Modulation of spontaneous transient outward currents (STOCs) by anti-K Ca 1.1 antibody. (A–C) Representative recordings of STOCs at 0 mV under control conditions, after 5 min application of 10 nM iberiotoxin (B) or after 10 min intracellular dialysis
    Figure Legend Snippet: Modulation of spontaneous transient outward currents (STOCs) by anti-K Ca 1.1 antibody. (A–C) Representative recordings of STOCs at 0 mV under control conditions, after 5 min application of 10 nM iberiotoxin (B) or after 10 min intracellular dialysis

    Techniques Used:

    Effects of penitrem A and iberiotoxin on I ClCa . (A) The effect of 10 µM penitrem A (Pen) on I ClCa . (A)i shows representative currents recorded in the absence and presence of penitrem A (5 min, 1 µM). (A)ii and (A)iii show the effect of
    Figure Legend Snippet: Effects of penitrem A and iberiotoxin on I ClCa . (A) The effect of 10 µM penitrem A (Pen) on I ClCa . (A)i shows representative currents recorded in the absence and presence of penitrem A (5 min, 1 µM). (A)ii and (A)iii show the effect of

    Techniques Used:

    8) Product Images from "Activation of TRPV4 channels leads to a consistent tocolytic effect on human myometrial tissues"

    Article Title: Activation of TRPV4 channels leads to a consistent tocolytic effect on human myometrial tissues

    Journal: European Journal of Obstetrics & Gynecology and Reproductive Biology: X

    doi: 10.1016/j.eurox.2021.100124

    Tocolytic effects of 4αPDD and GSK1016790A were reversed by ruthenium red and IbTX. A: Tocolytic effect of 100 and 300 nM 4αPDD on the oxytocin-induced contractile activity. This effect was reversed by 5 μM Ruthenium Red. B: This recording demonstrates that the tocolytic effect of 100 nM GSK1016790A on the uterotonic-induced contractile activity (300 nM PGF 2α and 100 nM oxytocin) was reversed by 50 nM IbTX, a specific inhibitor of BKCa channels. C: This recording illustrates the difference of tocolytic mechanism between 100 nM GSK1016790A and 300 nM Nifedipine. The former results in the full inactivation of contractions, while the latter reduced the amplitude of the contractions, likely by blocking the L-type Ca 2+ channels.
    Figure Legend Snippet: Tocolytic effects of 4αPDD and GSK1016790A were reversed by ruthenium red and IbTX. A: Tocolytic effect of 100 and 300 nM 4αPDD on the oxytocin-induced contractile activity. This effect was reversed by 5 μM Ruthenium Red. B: This recording demonstrates that the tocolytic effect of 100 nM GSK1016790A on the uterotonic-induced contractile activity (300 nM PGF 2α and 100 nM oxytocin) was reversed by 50 nM IbTX, a specific inhibitor of BKCa channels. C: This recording illustrates the difference of tocolytic mechanism between 100 nM GSK1016790A and 300 nM Nifedipine. The former results in the full inactivation of contractions, while the latter reduced the amplitude of the contractions, likely by blocking the L-type Ca 2+ channels.

    Techniques Used: Activity Assay, Blocking Assay

    Graphic summary: Involvement of TRPV4 and BKCa activation results in a strong tocolytic effect on human myometrial strips. The TRPV4 agonist (GSK1016790A) may exert a tocolytic effect on human myometrial strips by activating the BKCa channels. This strong inhibitory effect is likely due to a localized Ca 2+ entry, which in turn activates BKCa channels. An increase in open state probability of BKCa channels results in membrane hyperpolarization and concomitant inactivation of Nifedipine-sensitive Ca 2+ channels, while either ruthenium red (a TRPV4 blocker), or iberiotoxin (IbTX) -a high-affinity BKCa blocker- reverses this tocolytic effect [ 17 ].
    Figure Legend Snippet: Graphic summary: Involvement of TRPV4 and BKCa activation results in a strong tocolytic effect on human myometrial strips. The TRPV4 agonist (GSK1016790A) may exert a tocolytic effect on human myometrial strips by activating the BKCa channels. This strong inhibitory effect is likely due to a localized Ca 2+ entry, which in turn activates BKCa channels. An increase in open state probability of BKCa channels results in membrane hyperpolarization and concomitant inactivation of Nifedipine-sensitive Ca 2+ channels, while either ruthenium red (a TRPV4 blocker), or iberiotoxin (IbTX) -a high-affinity BKCa blocker- reverses this tocolytic effect [ 17 ].

    Techniques Used: Activation Assay

    9) Product Images from "Modulation by simvastatin of iberiotoxin-sensitive, Ca2+-activated K+ channels of porcine coronary artery smooth muscle cells"

    Article Title: Modulation by simvastatin of iberiotoxin-sensitive, Ca2+-activated K+ channels of porcine coronary artery smooth muscle cells

    Journal:

    doi: 10.1038/sj.bjp.0707327

    Effect of ( a ) NS 1619 (10 μ M ), ( b ) isopimaric acid (10 μ M ) and ( c ) iberiotoxin (100 n M ) on the whole-cell, outward K + currents of pig coronary artery smooth muscle cells. Representative whole-cell, outward
    Figure Legend Snippet: Effect of ( a ) NS 1619 (10 μ M ), ( b ) isopimaric acid (10 μ M ) and ( c ) iberiotoxin (100 n M ) on the whole-cell, outward K + currents of pig coronary artery smooth muscle cells. Representative whole-cell, outward

    Techniques Used:

    Mechanism(s) responsible for simvastatin-mediated inhibition of iberiotoxin-sensitive BKCa channels
    Figure Legend Snippet: Mechanism(s) responsible for simvastatin-mediated inhibition of iberiotoxin-sensitive BKCa channels

    Techniques Used: Inhibition

    10) 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:

    11) Product Images from "Heterogeneity of intrinsic plasticity in cerebellar Purkinje cells linked with cortical molecular zones"

    Article Title: Heterogeneity of intrinsic plasticity in cerebellar Purkinje cells linked with cortical molecular zones

    Journal: iScience

    doi: 10.1016/j.isci.2021.103705

    Intrinsic plasticity examined under the administration of blockers of Ca-activated potassium channels in Z+ and Z- PC (A) Spike response to square current injection (300 pA and 500 ms) before and 20 s after giving the LTP-IE protocol in Z+ and Z- PCs under apamin (100 nM) administration. (B) The spike-current relationship before and 20 s after giving the LTP-IE protocol in Z+ and Z- PCs under apamin. The thick gray line is the spike-count relationship before the LTP-IE protocol without apamin (as shown in Figure 3 C) for comparison. (C) Spike count change calculated from the measurements with 300-pA current injection before and 20 min after the LTP-IE protocol in the control condition ( Figure 3 C), and under apamin. (D and E) Change in fAHP (D) and mAHP (E) in the LTP-IE protocol under apamin. Amplitudes of the fAHP (D) and mAHP (E) in individual PCs (dashed lines) and the average (solid line) were compared before and 20 min after the LTP-IE protocol in 9 Z+ (left graph in each panel) and 9 Z- (right graph in each panel) PCs. Pale gray lines indicate the average change under the control condition (as shown in Figures 3 E and 3F). (F) AHP amplitude change obtained for each PC by subtracting the AHP amplitude under baseline from the AHP amplitude 20 min after the LTP-IE protocol. (G) Spike response to square current injection (300 pA and 500 ms) before and 20 s after giving the LTP-IE protocol in Z+ and Z- PCs under iberiotoxin (50 nM) administration. (H) The spike-current relationship before and 20 s after giving the LTP-IE protocol in Z+ and Z- PCs under iberiotoxin. The thick gray line is the spike-count relationship before the LTP-IE protocol without iberiotoxin (as shown in Figure 3 C) for comparison. (I) Spike count change calculated from the measurements with 300-pA current injection before and 20 min after the LTP-IE protocol in the control condition ( Figure 3 C), and under iberiotoxin. (J and K) Change in fAHP (J) and mAHP (K) in the LTP-IE protocol under iberiotoxin. Amplitudes of the fAHP (J) and mAHP (K) in individual PCs (dashed lines) and the average (solid line) were compared before and 20 min after the LTP-IE protocol in 9 Z+ (left graph in each panel) and 9 Z- (right graph in each panel) PCs. Pale gray lines indicate the average change under the control condition ( Figures 3 E and 3F). (L) AHP amplitude change obtained for each PC by subtracting the AHP amplitude under baseline from the AHP amplitude 20 min after the LTP-IE protocol. Data are represented as mean ± standard in (B, D, E, H, J, and K) and Tukey method box and whisker graphs in (C, F, I, and L). The significant difference was tested with two-way ANOVA with repeated measures (B, Z+, F(1,96) = 9, p = 0.003, n = 9, 9; Z-, F(1,96) = 0.04 p = 0.85, n = 9, 9; H, Z+, F(1,96) = 7.18, p = 0.0087, n = 9, 9; Z-, F(1,96) = 29.17, p = 0.0005, n = 9, 9), paired Student's t test (D, Z+, t(8) = 3.14, p = 0.014, n = 9; Z-, t(8) = 0.183, p = 0.859, n = 9; E, Z+, t(8) = -2.13, p = 0.065, n = 9; Z-, t(8) = -0.425, p = 0.682, n = 9; J, Z+, t(8) = 2.074, n = 9, p = 0.072; Z-, t(8) = 1.690, p = 0.151, n = 9; K, Z+, t(8) = -3.942, p = 0.004, n = 9; Z-, t(8) = 1.845, p = 0.102, n = 9), and unpaired Student's t test (C, control Z+/Z-, t(24) = -2.33, p = 0.029, n13, 13; apamin Z+/Z-, t(16) = 3.56, p = 0.003, n = 9, 9; Z+ control/apamin, t(20) = 1.19, p = 0.248, n = 13, 9; Z-control/apamin, t(20) = -8.46, p = 0.0000, n = 13, 9; D, baseline Z+/Z-, t(16) = 0.520, p = 0.610, n = 9, 9; E, baseline Z+/Z-, t(16) = 1.410, p = 0.178, n = 9, 9; F, fAHP/Z+, t(20) = 1.924, p = 0.068, n = 13, 9, fAHP/Z-, t(20) = -0.418, p = 0.681, n = 13, 9, mAHP/Z+, t(20) = -0.331, p = 0.744, n = 13, 9, mAHP/Z-, t(20) = -2.51, p = 0.021, n = 13, 9; I, iberiotoxin Z+/Z-, t(16) = -2.76, p = 0.014, n = 9, 9; Z+ control/iberiotoxin, t(20) = 1.45, p = 0.164, n = 13, 9; Z-control/iberiotoxin, t(20) = 0.350, p = 0.730, n = 13, 9; J, baseline Z+/Z-, t(16) = 1.095, p = 0.290, n = 9, 9; K, baseline Z+/Z-, t(16) = -1.013, p = 0.326, n = 9, 9; L, fAHP/Z+, t(20) = -0.249, p = 0.806, n = 13, 9, fAHP/Z-, t(20) = 1.044, p = 0.309, n = 13, 9, mAHP/Z+, t(20) = -0.034, p = 0.973, n = 13, 9, mAHP/Z-, t(20) = -0.415, p = 0.682, n = 13, 9). ∗∗∗p
    Figure Legend Snippet: Intrinsic plasticity examined under the administration of blockers of Ca-activated potassium channels in Z+ and Z- PC (A) Spike response to square current injection (300 pA and 500 ms) before and 20 s after giving the LTP-IE protocol in Z+ and Z- PCs under apamin (100 nM) administration. (B) The spike-current relationship before and 20 s after giving the LTP-IE protocol in Z+ and Z- PCs under apamin. The thick gray line is the spike-count relationship before the LTP-IE protocol without apamin (as shown in Figure 3 C) for comparison. (C) Spike count change calculated from the measurements with 300-pA current injection before and 20 min after the LTP-IE protocol in the control condition ( Figure 3 C), and under apamin. (D and E) Change in fAHP (D) and mAHP (E) in the LTP-IE protocol under apamin. Amplitudes of the fAHP (D) and mAHP (E) in individual PCs (dashed lines) and the average (solid line) were compared before and 20 min after the LTP-IE protocol in 9 Z+ (left graph in each panel) and 9 Z- (right graph in each panel) PCs. Pale gray lines indicate the average change under the control condition (as shown in Figures 3 E and 3F). (F) AHP amplitude change obtained for each PC by subtracting the AHP amplitude under baseline from the AHP amplitude 20 min after the LTP-IE protocol. (G) Spike response to square current injection (300 pA and 500 ms) before and 20 s after giving the LTP-IE protocol in Z+ and Z- PCs under iberiotoxin (50 nM) administration. (H) The spike-current relationship before and 20 s after giving the LTP-IE protocol in Z+ and Z- PCs under iberiotoxin. The thick gray line is the spike-count relationship before the LTP-IE protocol without iberiotoxin (as shown in Figure 3 C) for comparison. (I) Spike count change calculated from the measurements with 300-pA current injection before and 20 min after the LTP-IE protocol in the control condition ( Figure 3 C), and under iberiotoxin. (J and K) Change in fAHP (J) and mAHP (K) in the LTP-IE protocol under iberiotoxin. Amplitudes of the fAHP (J) and mAHP (K) in individual PCs (dashed lines) and the average (solid line) were compared before and 20 min after the LTP-IE protocol in 9 Z+ (left graph in each panel) and 9 Z- (right graph in each panel) PCs. Pale gray lines indicate the average change under the control condition ( Figures 3 E and 3F). (L) AHP amplitude change obtained for each PC by subtracting the AHP amplitude under baseline from the AHP amplitude 20 min after the LTP-IE protocol. Data are represented as mean ± standard in (B, D, E, H, J, and K) and Tukey method box and whisker graphs in (C, F, I, and L). The significant difference was tested with two-way ANOVA with repeated measures (B, Z+, F(1,96) = 9, p = 0.003, n = 9, 9; Z-, F(1,96) = 0.04 p = 0.85, n = 9, 9; H, Z+, F(1,96) = 7.18, p = 0.0087, n = 9, 9; Z-, F(1,96) = 29.17, p = 0.0005, n = 9, 9), paired Student's t test (D, Z+, t(8) = 3.14, p = 0.014, n = 9; Z-, t(8) = 0.183, p = 0.859, n = 9; E, Z+, t(8) = -2.13, p = 0.065, n = 9; Z-, t(8) = -0.425, p = 0.682, n = 9; J, Z+, t(8) = 2.074, n = 9, p = 0.072; Z-, t(8) = 1.690, p = 0.151, n = 9; K, Z+, t(8) = -3.942, p = 0.004, n = 9; Z-, t(8) = 1.845, p = 0.102, n = 9), and unpaired Student's t test (C, control Z+/Z-, t(24) = -2.33, p = 0.029, n13, 13; apamin Z+/Z-, t(16) = 3.56, p = 0.003, n = 9, 9; Z+ control/apamin, t(20) = 1.19, p = 0.248, n = 13, 9; Z-control/apamin, t(20) = -8.46, p = 0.0000, n = 13, 9; D, baseline Z+/Z-, t(16) = 0.520, p = 0.610, n = 9, 9; E, baseline Z+/Z-, t(16) = 1.410, p = 0.178, n = 9, 9; F, fAHP/Z+, t(20) = 1.924, p = 0.068, n = 13, 9, fAHP/Z-, t(20) = -0.418, p = 0.681, n = 13, 9, mAHP/Z+, t(20) = -0.331, p = 0.744, n = 13, 9, mAHP/Z-, t(20) = -2.51, p = 0.021, n = 13, 9; I, iberiotoxin Z+/Z-, t(16) = -2.76, p = 0.014, n = 9, 9; Z+ control/iberiotoxin, t(20) = 1.45, p = 0.164, n = 13, 9; Z-control/iberiotoxin, t(20) = 0.350, p = 0.730, n = 13, 9; J, baseline Z+/Z-, t(16) = 1.095, p = 0.290, n = 9, 9; K, baseline Z+/Z-, t(16) = -1.013, p = 0.326, n = 9, 9; L, fAHP/Z+, t(20) = -0.249, p = 0.806, n = 13, 9, fAHP/Z-, t(20) = 1.044, p = 0.309, n = 13, 9, mAHP/Z+, t(20) = -0.034, p = 0.973, n = 13, 9, mAHP/Z-, t(20) = -0.415, p = 0.682, n = 13, 9). ∗∗∗p

    Techniques Used: Injection, Whisker Assay

    12) Product Images from "Neuronal Atrophy Early in Degenerative Ataxia Is a Compensatory Mechanism to Regulate Membrane Excitability"

    Article Title: Neuronal Atrophy Early in Degenerative Ataxia Is a Compensatory Mechanism to Regulate Membrane Excitability

    Journal: The Journal of Neuroscience

    doi: 10.1523/JNEUROSCI.1357-15.2015

    BK channel function is maintained in atrophic 15-week-old ATXN1[82Q] Purkinje neurons despite reduced BK channel gene expression. A , The amplitude of the AHP is similar in 15-week-old wild-type and ATXN1[82Q] Purkinje neurons, summarized in B . The iberiotoxin-sensitive
    Figure Legend Snippet: BK channel function is maintained in atrophic 15-week-old ATXN1[82Q] Purkinje neurons despite reduced BK channel gene expression. A , The amplitude of the AHP is similar in 15-week-old wild-type and ATXN1[82Q] Purkinje neurons, summarized in B . The iberiotoxin-sensitive

    Techniques Used: Expressing

    13) Product Images from "Differential Expression of Large-Conductance Ca2+-Activated K Channels in the Carotid Body between DBA/2J and A/J Strains of Mice"

    Article Title: Differential Expression of Large-Conductance Ca2+-Activated K Channels in the Carotid Body between DBA/2J and A/J Strains of Mice

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2011.00019

    For patch clamp experiments, undissociated CBs were used . The setup (A) and the image of the CB (B) are shown. Examples of K current records and mean I – V relationships in the DBA/2J (C) and the A/J mouse (D) are presented. Whole current traces were evoked by voltage steps from −80 to +60 mV with 10 mV increments for 100 ms. To construct a current–voltage curve, the mean current measured between 93 and 97 ms from the start of each voltage step. Mean currents were plotted versus the test pulse. Bars represent SEM. No statistical differences were seen between the strains. (E) The effect of iberiotoxin (a BK channel blocker; 200 nM) on outward current in GCs. The outward current was evoked by a test pulse from −80 to +20 mV for 100 ms. Iberiotoxin significantly and reversibly decreased outward current in GCs of the DBA/2J mice. However, K current in the A/J mice was not significantly affected by iberiotoxin. *, Significantly different from control and recovery. The amplitudes of K current (control and recovery) were significantly larger in GCs of the DBA/2J mice. Cont, control; Ibx, iberiotoxin; Rec, recovery.
    Figure Legend Snippet: For patch clamp experiments, undissociated CBs were used . The setup (A) and the image of the CB (B) are shown. Examples of K current records and mean I – V relationships in the DBA/2J (C) and the A/J mouse (D) are presented. Whole current traces were evoked by voltage steps from −80 to +60 mV with 10 mV increments for 100 ms. To construct a current–voltage curve, the mean current measured between 93 and 97 ms from the start of each voltage step. Mean currents were plotted versus the test pulse. Bars represent SEM. No statistical differences were seen between the strains. (E) The effect of iberiotoxin (a BK channel blocker; 200 nM) on outward current in GCs. The outward current was evoked by a test pulse from −80 to +20 mV for 100 ms. Iberiotoxin significantly and reversibly decreased outward current in GCs of the DBA/2J mice. However, K current in the A/J mice was not significantly affected by iberiotoxin. *, Significantly different from control and recovery. The amplitudes of K current (control and recovery) were significantly larger in GCs of the DBA/2J mice. Cont, control; Ibx, iberiotoxin; Rec, recovery.

    Techniques Used: Patch Clamp, Construct, Mouse Assay

    14) Product Images from "Molecular basis of ancestral vertebrate electroreception"

    Article Title: Molecular basis of ancestral vertebrate electroreception

    Journal: Nature

    doi: 10.1038/nature21401

    BK agonist NS11021 modulates skate BK channels a. In representative records from outside-out patches expressing sBK the BK agonist NS11021 (NS, 10 μM) increased the Po and open-state dwell time of sBK channels and this effect was blocked by iberotoxin (IbTx, 100 nM). Scale bar: 5pA, 100ms. Associated all-points histograms demonstrate the increase in open time. P o : basal = 0.0024 ± 0.00068, NS: 0.16 ± 0.041, NS + IbTx = 0.00036 ± 0.00025, p
    Figure Legend Snippet: BK agonist NS11021 modulates skate BK channels a. In representative records from outside-out patches expressing sBK the BK agonist NS11021 (NS, 10 μM) increased the Po and open-state dwell time of sBK channels and this effect was blocked by iberotoxin (IbTx, 100 nM). Scale bar: 5pA, 100ms. Associated all-points histograms demonstrate the increase in open time. P o : basal = 0.0024 ± 0.00068, NS: 0.16 ± 0.041, NS + IbTx = 0.00036 ± 0.00025, p

    Techniques Used: Expressing

    15) Product Images from "Mechanism of resveratrol-induced relaxation in the human gallbladder"

    Article Title: Mechanism of resveratrol-induced relaxation in the human gallbladder

    Journal: BMC Complementary and Alternative Medicine

    doi: 10.1186/s12906-017-1752-x

    The effects of tetraethylammonium (TEA), charybdotoxin, apamine, iberiotoxin, and glibenclamide on resveratrol-induced relaxation in the human gallbladder. TEA (1 mM), apamine (100 nM), and charybdotoxin (100 nM) had no significant effect on resveratrol-induced relaxation of human gallbladder muscle strips ( p > 0.05, n ≥ 4). In contrast, iberiotoxin (200 nM) and glibenclamide (10 μM) significantly inhibited resveratrol-induced relaxation of human gallbladder muscle strips ( p
    Figure Legend Snippet: The effects of tetraethylammonium (TEA), charybdotoxin, apamine, iberiotoxin, and glibenclamide on resveratrol-induced relaxation in the human gallbladder. TEA (1 mM), apamine (100 nM), and charybdotoxin (100 nM) had no significant effect on resveratrol-induced relaxation of human gallbladder muscle strips ( p > 0.05, n ≥ 4). In contrast, iberiotoxin (200 nM) and glibenclamide (10 μM) significantly inhibited resveratrol-induced relaxation of human gallbladder muscle strips ( p

    Techniques Used:

    16) Product Images from "High Capability of Pentagalloylglucose (PGG) in Inhibiting Multiple Types of Membrane Ionic Currents"

    Article Title: High Capability of Pentagalloylglucose (PGG) in Inhibiting Multiple Types of Membrane Ionic Currents

    Journal: International Journal of Molecular Sciences

    doi: 10.3390/ijms21249369

    Concentration-dependent inhibitory effect of PGG on I PAC density ( A , B ) and comparisons in effects of PGG, chlorotoxin, hesperetin, kaempferol, morin, hydroxychloroquine and iberiotoxin on I PAC density ( C ). In these experiments, cells were kept immersed in acidic (i.e., pH 4.0) and Ca 2+ -free Tyrode’s solution, and the electrode was filled up with Cs + -containing solution. ( A ) Representative I PAC density taken in the control (i.e., in the absence of PGG, but still exposed to acidic extracellular solution with pH 4.0) and during cell exposure to 3 μM PGG (b) or 10 μM PGG (c), but still in the presence of acidic solution. ( B ) Concentration–response relationship for the PGG-induced inhibition of I PAC density measured at the end of the 500-msec square potential command to +50 mV from a holding potential of −50 mV (mean ± SEM; n = 8–9 for each point). A smooth sigmoidal line is drawn according to the three-parameter logistic model (i.e., modified Hill equation) as described in the Materials and Methods. A vertical dashed line indicates the IC 50 value of this compound needed for its inhibition of I PAC density. ( C ) Comparison between the effect of PGG and those of chlorotoxin, hesperetin, kaempferol, morin, hydroxychloroquine (HCQ), 4-[(2-butyl-6,7-dichloro-2-cyclopentyl-2,3-dihydro-1-oxo-1H-inden-5yl)oxy] butanoic acid (DCPIB) and iberiotoxin (mean ± SEM; n = 7 for each bar). The examined cell was held at −50 mV, and the command voltage pulses to +50 mV were applied. Current density was measured at the end of each depolarizing voltage-clamp pulse. The statistical analyses were done by ANOVA-1, p
    Figure Legend Snippet: Concentration-dependent inhibitory effect of PGG on I PAC density ( A , B ) and comparisons in effects of PGG, chlorotoxin, hesperetin, kaempferol, morin, hydroxychloroquine and iberiotoxin on I PAC density ( C ). In these experiments, cells were kept immersed in acidic (i.e., pH 4.0) and Ca 2+ -free Tyrode’s solution, and the electrode was filled up with Cs + -containing solution. ( A ) Representative I PAC density taken in the control (i.e., in the absence of PGG, but still exposed to acidic extracellular solution with pH 4.0) and during cell exposure to 3 μM PGG (b) or 10 μM PGG (c), but still in the presence of acidic solution. ( B ) Concentration–response relationship for the PGG-induced inhibition of I PAC density measured at the end of the 500-msec square potential command to +50 mV from a holding potential of −50 mV (mean ± SEM; n = 8–9 for each point). A smooth sigmoidal line is drawn according to the three-parameter logistic model (i.e., modified Hill equation) as described in the Materials and Methods. A vertical dashed line indicates the IC 50 value of this compound needed for its inhibition of I PAC density. ( C ) Comparison between the effect of PGG and those of chlorotoxin, hesperetin, kaempferol, morin, hydroxychloroquine (HCQ), 4-[(2-butyl-6,7-dichloro-2-cyclopentyl-2,3-dihydro-1-oxo-1H-inden-5yl)oxy] butanoic acid (DCPIB) and iberiotoxin (mean ± SEM; n = 7 for each bar). The examined cell was held at −50 mV, and the command voltage pulses to +50 mV were applied. Current density was measured at the end of each depolarizing voltage-clamp pulse. The statistical analyses were done by ANOVA-1, p

    Techniques Used: Concentration Assay, Inhibition, Modification

    17) Product Images from "Dynamic coupling between TRPV4 and Ca2+-activated SK1/3 and IK1 K+ channels plays a critical role in regulating the K+-secretory BK channel in kidney collecting duct cells"

    Article Title: Dynamic coupling between TRPV4 and Ca2+-activated SK1/3 and IK1 K+ channels plays a critical role in regulating the K+-secretory BK channel in kidney collecting duct cells

    Journal: American Journal of Physiology - Renal Physiology

    doi: 10.1152/ajprenal.00037.2017

    Electrophysiological examination of SK1/3 and IK1 dependence of BK channel activity during TRPV4 stimulation. A : representative V m trace showing that TRPV4 activation by GSK101 (arrow 1) led to V m depolarization (occasionally, this is preceded by an initial transient hyperpolarization as in the example shown) in mCCDcl1 cells, demonstrating that the depolarizing effect (upward deflection) of TRPV4 dominates over the hyperpolarizing effect (downward deflection) associated with activation of the KCa. Subsequent inhibition of BK by IbTX (100 nM; arrow 2) caused a further V m depolarization (maximal depolarization indicated by arrow 3), indicating the involvement of BK channels to counter the depolarizing effect of TRPV4. B : representative V m trace showing that the pretreatment with SK1/3 and IK1 blockers (apamin + TRAM-34) resulted in a much stronger V m depolarization on TRPV4 activation, consistent with TRPV4 mediating the activation of SK1/3 and IK1. In the continued presence of apamin and TRAM-34, the application of IbTX (arrow 2) did not lead to further depolarization in this example, indicating that BK was not very active when SK1/3 and IK1 were inhibited. Arrow 3 reflects the apparent maximum depolarization observed in the presence of IbTX. C : summary data for A and B showing that in the absence of apamin and TRAM-34, GSK101 evoked a depolarization of 5.5 ± 1.0 mV (100 ± 17.2%, n = 17) from a resting V m of −30.4 ± 1.2 mV, whereas in the presence of apamin and TRAM-34, the GSK101-evoked V m depolarization was much larger, averaging 12.4 ± 1.9 mV (223 ± 35.0%, n = 13; ** P
    Figure Legend Snippet: Electrophysiological examination of SK1/3 and IK1 dependence of BK channel activity during TRPV4 stimulation. A : representative V m trace showing that TRPV4 activation by GSK101 (arrow 1) led to V m depolarization (occasionally, this is preceded by an initial transient hyperpolarization as in the example shown) in mCCDcl1 cells, demonstrating that the depolarizing effect (upward deflection) of TRPV4 dominates over the hyperpolarizing effect (downward deflection) associated with activation of the KCa. Subsequent inhibition of BK by IbTX (100 nM; arrow 2) caused a further V m depolarization (maximal depolarization indicated by arrow 3), indicating the involvement of BK channels to counter the depolarizing effect of TRPV4. B : representative V m trace showing that the pretreatment with SK1/3 and IK1 blockers (apamin + TRAM-34) resulted in a much stronger V m depolarization on TRPV4 activation, consistent with TRPV4 mediating the activation of SK1/3 and IK1. In the continued presence of apamin and TRAM-34, the application of IbTX (arrow 2) did not lead to further depolarization in this example, indicating that BK was not very active when SK1/3 and IK1 were inhibited. Arrow 3 reflects the apparent maximum depolarization observed in the presence of IbTX. C : summary data for A and B showing that in the absence of apamin and TRAM-34, GSK101 evoked a depolarization of 5.5 ± 1.0 mV (100 ± 17.2%, n = 17) from a resting V m of −30.4 ± 1.2 mV, whereas in the presence of apamin and TRAM-34, the GSK101-evoked V m depolarization was much larger, averaging 12.4 ± 1.9 mV (223 ± 35.0%, n = 13; ** P

    Techniques Used: Activity Assay, Activation Assay, Inhibition

    The initial [Ca 2+ ] i attained by TRPV4 activation is directly correlated with BK activation. A : pooled data from individual cells showing that the IbTX-sensitive [Ca 2+ ] i , −Δ[Ca 2+ ] i due to addition of IbTX, was directly proportional to the Initial [Ca 2+ ] i (pseudoplateau) following TRPV4 activation (6 nM GSK101) in the absence of IbTX. Linear regression (LR) analysis showed a strong correlation ( r = 0.8494, n = 72; P
    Figure Legend Snippet: The initial [Ca 2+ ] i attained by TRPV4 activation is directly correlated with BK activation. A : pooled data from individual cells showing that the IbTX-sensitive [Ca 2+ ] i , −Δ[Ca 2+ ] i due to addition of IbTX, was directly proportional to the Initial [Ca 2+ ] i (pseudoplateau) following TRPV4 activation (6 nM GSK101) in the absence of IbTX. Linear regression (LR) analysis showed a strong correlation ( r = 0.8494, n = 72; P

    Techniques Used: Activation Assay

    SK1/3 and IK1 KCa play a dominant role in controlling [Ca 2+ ] i rise and BK channel activation in response to TRPV4 activation. All studies were done on a paired basis where a coverslip of mCCDcl1 cells grown to confluency was split in half with 1 part used for control (untreated) and the other part treated with apamin + TRAM-34. A : example showing GSK101-evoked [Ca 2+ ] i increase through activation of TRPV4 in control cells, with the expected IbTX-sensitive component indicating BK activation. B : example showing that prior blocking of SK1/3 (apamin) and IK1 (TRAM-34) channels markedly reduced the GSK101-induced [Ca 2+ ] i increase and the IbTX-sensitive component reflecting BK activity was nearly abolished. C : summary analysis showing that in the presence of apamin and TRAM-34, the GSK101-induced peak [Ca 2+ ] i , or the observed maximum [Ca 2+ ] i , was reduced from control values of 766 ± 25 nM ( n = 30) to 348 ± 40 nM ( n = 30) in the presence of apamin and TRAM-34. D : the initial rate of GSK101-induced [Ca 2+ ] i rise was also markedly reduced in the presence of apamin and TRAM-34, as shown by the dashed line in A and B , being reduced from 215 ± 14 nmol·l −1 ·min −1 ( n = 30) in the control to only 31 ± 6 nmol·l −1 ·min −1 with apamin + TRAM-34 treatment ( n = 30). E : summary data showing that the IbTX-induced reduction in [Ca 2+ ] i in GSK101-treated cells (−Δ[Ca 2+ ] i )was significantly reduced from 384 ± 29 to 90 ± 27 nM ( n = 30) in the presence of apamin and TRAM-34 ( n = 30). *** P
    Figure Legend Snippet: SK1/3 and IK1 KCa play a dominant role in controlling [Ca 2+ ] i rise and BK channel activation in response to TRPV4 activation. All studies were done on a paired basis where a coverslip of mCCDcl1 cells grown to confluency was split in half with 1 part used for control (untreated) and the other part treated with apamin + TRAM-34. A : example showing GSK101-evoked [Ca 2+ ] i increase through activation of TRPV4 in control cells, with the expected IbTX-sensitive component indicating BK activation. B : example showing that prior blocking of SK1/3 (apamin) and IK1 (TRAM-34) channels markedly reduced the GSK101-induced [Ca 2+ ] i increase and the IbTX-sensitive component reflecting BK activity was nearly abolished. C : summary analysis showing that in the presence of apamin and TRAM-34, the GSK101-induced peak [Ca 2+ ] i , or the observed maximum [Ca 2+ ] i , was reduced from control values of 766 ± 25 nM ( n = 30) to 348 ± 40 nM ( n = 30) in the presence of apamin and TRAM-34. D : the initial rate of GSK101-induced [Ca 2+ ] i rise was also markedly reduced in the presence of apamin and TRAM-34, as shown by the dashed line in A and B , being reduced from 215 ± 14 nmol·l −1 ·min −1 ( n = 30) in the control to only 31 ± 6 nmol·l −1 ·min −1 with apamin + TRAM-34 treatment ( n = 30). E : summary data showing that the IbTX-induced reduction in [Ca 2+ ] i in GSK101-treated cells (−Δ[Ca 2+ ] i )was significantly reduced from 384 ± 29 to 90 ± 27 nM ( n = 30) in the presence of apamin and TRAM-34 ( n = 30). *** P

    Techniques Used: Activation Assay, Blocking Assay, Activity Assay

    18) Product Images from "Altered Capicua expression drives regional Purkinje neuron vulnerability through ion channel gene dysregulation in Spinocerebellar ataxia type 1"

    Article Title: Altered Capicua expression drives regional Purkinje neuron vulnerability through ion channel gene dysregulation in Spinocerebellar ataxia type 1

    Journal: bioRxiv

    doi: 10.1101/2020.05.21.104976

    Regionally-dysregulated ion channel genes form a functional module critical for Purkinje neuron pacemaking (A) The distribution of regularly firing, irregularly firing, and non-firing cells was recorded for Purkinje neurons in the anterior cerebellum and nodular zone. (B) Representative trace from a tonic firing wild-type and non-firing ATXN1[82Q] Purkinje neuron in the anterior cerebellum at P35. (C) Representative trace from wild-type and ATXN1[82Q] Purkinje neurons in the nodular zone at P35. (D) Quantification of the afterhyperpolarization (AHP) and ISI of wild-type and ATXN1[82Q] Purkinje neurons in the anterior cerebellum at P35. (E) Similar to (D), quantification of the AHP and ISI of wild-type and ATXN1[82Q] Purkinje neurons in the nodular zone at P35. (F) Representative traces of wild-type Purkinje neurons in the anterior cerebellum at P35. Traces are shown at baseline (left), after perfusion of 200 nM iberiotoxin (middle), and after perfusion of 200 nM iberiotoxin + 4 µM mibefradil. (G and H) Summary distribution of regularly firing, irregularly firing, and non-firing Purkinje neurons before and after perfusion of 200 nM iberiotoxin (G) and after 200 nM iberiotoxin + 4 µM mibefradil (H). ** denotes p
    Figure Legend Snippet: Regionally-dysregulated ion channel genes form a functional module critical for Purkinje neuron pacemaking (A) The distribution of regularly firing, irregularly firing, and non-firing cells was recorded for Purkinje neurons in the anterior cerebellum and nodular zone. (B) Representative trace from a tonic firing wild-type and non-firing ATXN1[82Q] Purkinje neuron in the anterior cerebellum at P35. (C) Representative trace from wild-type and ATXN1[82Q] Purkinje neurons in the nodular zone at P35. (D) Quantification of the afterhyperpolarization (AHP) and ISI of wild-type and ATXN1[82Q] Purkinje neurons in the anterior cerebellum at P35. (E) Similar to (D), quantification of the AHP and ISI of wild-type and ATXN1[82Q] Purkinje neurons in the nodular zone at P35. (F) Representative traces of wild-type Purkinje neurons in the anterior cerebellum at P35. Traces are shown at baseline (left), after perfusion of 200 nM iberiotoxin (middle), and after perfusion of 200 nM iberiotoxin + 4 µM mibefradil. (G and H) Summary distribution of regularly firing, irregularly firing, and non-firing Purkinje neurons before and after perfusion of 200 nM iberiotoxin (G) and after 200 nM iberiotoxin + 4 µM mibefradil (H). ** denotes p

    Techniques Used: Functional Assay

    19) Product Images from "Ryanodine-induced vasoconstriction of the gerbil spiral modiolar artery depends on the Ca2+ sensitivity but not on Ca2+ sparks or BK channels"

    Article Title: Ryanodine-induced vasoconstriction of the gerbil spiral modiolar artery depends on the Ca2+ sensitivity but not on Ca2+ sparks or BK channels

    Journal: BMC Physiology

    doi: 10.1186/s12899-016-0026-z

    Inhibition of BK channels in the presence of high K + does not increase the global [Ca 2+ ] i or constrict the SMA. a Representative recordings of [Ca 2+ ] i changes from single smooth muscle cells from a pressurized (40 cmH 2 O) SMA in the presence of PSS containing 30 mM K + and 100 nM Ibtx. b Average of normalized traces of [Ca 2+ ] i changes in the presence of PSS containing 30 mM K + and Ibtx (36 cells). Traces in a and b were normalized as described in Methods. c Average trace of corresponding changes in vascular diameter (6 arteries). Diameter changes were normalized to the average of values recorded between 30 – 60 s (value indicated by ‘a’ was set to 1). [Ca 2+ ] i and diameter data were simultaneously acquired at 1 s intervals, however, for clarity, error bars (sem) are plotted only every 10 s
    Figure Legend Snippet: Inhibition of BK channels in the presence of high K + does not increase the global [Ca 2+ ] i or constrict the SMA. a Representative recordings of [Ca 2+ ] i changes from single smooth muscle cells from a pressurized (40 cmH 2 O) SMA in the presence of PSS containing 30 mM K + and 100 nM Ibtx. b Average of normalized traces of [Ca 2+ ] i changes in the presence of PSS containing 30 mM K + and Ibtx (36 cells). Traces in a and b were normalized as described in Methods. c Average trace of corresponding changes in vascular diameter (6 arteries). Diameter changes were normalized to the average of values recorded between 30 – 60 s (value indicated by ‘a’ was set to 1). [Ca 2+ ] i and diameter data were simultaneously acquired at 1 s intervals, however, for clarity, error bars (sem) are plotted only every 10 s

    Techniques Used: Inhibition

    Inhibition of BK channels with iberiotoxin or inhibition of Ca 2+ sparks with tetracaine does not increase the global [Ca 2+ ] i or constrict the SMA at 40 cmH 2 O. a Representative recordings of [Ca 2+ ] i changes from single smooth muscle cells from a pressurized (40 cmH 2 O) SMA in response to 100 nM Ibtx. b Average of normalized traces of [Ca 2+ ] i changes in the presence of Ibtx (65 cells). Traces in a and b were normalized as described in Methods. c Average trace of corresponding changes in vascular diameter in the presence of Ibtx (8 arteries). d Representative recordings of [Ca 2+ ] i changes from single smooth muscle cells from a pressurized (40 cmH 2 O) SMA in response to 100 μM Tet and 1 μM nifedipine (Nif). e Average of normalized traces of [Ca 2+ ] i changes at 40 cmH 2 O (26 cells). Traces in d and e were normalized as described in Methods. f Average trace of corresponding changes in vascular diameter (5 arteries) in the presence of Tet and Nif. Diameter changes were normalized to the average of values recorded between 30–60s (value indicated by ‘a’ was set to 1). [Ca 2+ ] i and diameter data were simultaneously acquired at 1 s intervals, however, for clarity, error bars (sem) are plotted only every 10s
    Figure Legend Snippet: Inhibition of BK channels with iberiotoxin or inhibition of Ca 2+ sparks with tetracaine does not increase the global [Ca 2+ ] i or constrict the SMA at 40 cmH 2 O. a Representative recordings of [Ca 2+ ] i changes from single smooth muscle cells from a pressurized (40 cmH 2 O) SMA in response to 100 nM Ibtx. b Average of normalized traces of [Ca 2+ ] i changes in the presence of Ibtx (65 cells). Traces in a and b were normalized as described in Methods. c Average trace of corresponding changes in vascular diameter in the presence of Ibtx (8 arteries). d Representative recordings of [Ca 2+ ] i changes from single smooth muscle cells from a pressurized (40 cmH 2 O) SMA in response to 100 μM Tet and 1 μM nifedipine (Nif). e Average of normalized traces of [Ca 2+ ] i changes at 40 cmH 2 O (26 cells). Traces in d and e were normalized as described in Methods. f Average trace of corresponding changes in vascular diameter (5 arteries) in the presence of Tet and Nif. Diameter changes were normalized to the average of values recorded between 30–60s (value indicated by ‘a’ was set to 1). [Ca 2+ ] i and diameter data were simultaneously acquired at 1 s intervals, however, for clarity, error bars (sem) are plotted only every 10s

    Techniques Used: Inhibition

    20) Product Images from "Mitochondrial monoamine oxidase-A-mediated hydrogen peroxide generation enhances 5-hydroxytryptamine-induced contraction of rat basilar artery"

    Article Title: Mitochondrial monoamine oxidase-A-mediated hydrogen peroxide generation enhances 5-hydroxytryptamine-induced contraction of rat basilar artery

    Journal: British Journal of Pharmacology

    doi: 10.1111/j.1476-5381.2010.00941.x

    Time course of the inhibitory effects of 5-HT (1 µM, top panel) and H 2 O 2 (100 µM, middle panel) on iberiotoxin-sensitive, large-conductance Ca 2+ -activated K + (BK Ca ) amplitude of single basilar artery myocytes of SHR and WKY rats. The BK
    Figure Legend Snippet: Time course of the inhibitory effects of 5-HT (1 µM, top panel) and H 2 O 2 (100 µM, middle panel) on iberiotoxin-sensitive, large-conductance Ca 2+ -activated K + (BK Ca ) amplitude of single basilar artery myocytes of SHR and WKY rats. The BK

    Techniques Used:

    21) Product Images from "Smooth muscle and neural mechanisms contributing to the downregulation of neonatal rat spontaneous bladder contractions during postnatal development"

    Article Title: Smooth muscle and neural mechanisms contributing to the downregulation of neonatal rat spontaneous bladder contractions during postnatal development

    Journal: American journal of physiology. Regulatory, integrative and comparative physiology

    doi: 10.1152/ajpregu.00779.2006

    Effects of K Ca channel blockers on spontaneous contractions. Both iberiotoxin (IBTX) and apamin were used at 100 nM concentrations. Values are expressed as means (SD). A : IBTX increased the amplitude in 2 wk-old bladders, whereas apamin increased the amplitude in 6-wk-old bladders. B : IBTX increased the frequency in 2-wk-old bladders, whereas apamin did not affect frequency at any time. C : IBTX increased AUC in the 2- to 3-wk-old bladders, whereas apamin did not affect AUC at any time. Values are expressed as means (SD). ** P
    Figure Legend Snippet: Effects of K Ca channel blockers on spontaneous contractions. Both iberiotoxin (IBTX) and apamin were used at 100 nM concentrations. Values are expressed as means (SD). A : IBTX increased the amplitude in 2 wk-old bladders, whereas apamin increased the amplitude in 6-wk-old bladders. B : IBTX increased the frequency in 2-wk-old bladders, whereas apamin did not affect frequency at any time. C : IBTX increased AUC in the 2- to 3-wk-old bladders, whereas apamin did not affect AUC at any time. Values are expressed as means (SD). ** P

    Techniques Used:

    Combined small-conductance K Ca (SK) and large-conductance K Ca (BK) blockade. Both IBTX and apamin were used at 100 nM concentrations. A : effect of apamin followed by IBTX on spontaneous contractions in the 3-day-old bladder, then the effects of IBTX followed by apamin. B : effect of apamin followed by IBTX on spontaneous contractions in the 1-wk-old bladder, then the effects of IBTX followed by apamin. C : apamin followed by iberiotoxin results in a significantly larger AUC at 2 and 3 wk of life compared with apamin alone. ** P
    Figure Legend Snippet: Combined small-conductance K Ca (SK) and large-conductance K Ca (BK) blockade. Both IBTX and apamin were used at 100 nM concentrations. A : effect of apamin followed by IBTX on spontaneous contractions in the 3-day-old bladder, then the effects of IBTX followed by apamin. B : effect of apamin followed by IBTX on spontaneous contractions in the 1-wk-old bladder, then the effects of IBTX followed by apamin. C : apamin followed by iberiotoxin results in a significantly larger AUC at 2 and 3 wk of life compared with apamin alone. ** P

    Techniques Used:

    22) Product Images from "Effect of knockout of α2δ-1 on action potentials in mouse sensory neurons"

    Article Title: Effect of knockout of α2δ-1 on action potentials in mouse sensory neurons

    Journal: Philosophical Transactions of the Royal Society B: Biological Sciences

    doi: 10.1098/rstb.2015.0430

    Effect of BK and SK channel blockers and reduced intracellular Ca 2+ chelation on AP duration. ( a , b ) Duration of 100% AP height in WT (black bars, n = 11 at −60 mV and n = 10 at −70 mV) and α 2 δ-1 KO (red bars, n = 10 for both HPs) DRG neurons, and lack of effect of iberiotoxin (0.1 µM, hatched bars), from HP of −60 mV ( a ) and −70 mV ( b ). ( c , d ) Comparison of AP duration between WT ( n = 21, 24; black squares) and α 2 δ-1 KO ( n = 10, 10; red circles) DRG neurons using the low intracellular Ca 2+ -buffering intracellular solution, at −60 mV ( c ) and −70 mV ( d ) HP. * p
    Figure Legend Snippet: Effect of BK and SK channel blockers and reduced intracellular Ca 2+ chelation on AP duration. ( a , b ) Duration of 100% AP height in WT (black bars, n = 11 at −60 mV and n = 10 at −70 mV) and α 2 δ-1 KO (red bars, n = 10 for both HPs) DRG neurons, and lack of effect of iberiotoxin (0.1 µM, hatched bars), from HP of −60 mV ( a ) and −70 mV ( b ). ( c , d ) Comparison of AP duration between WT ( n = 21, 24; black squares) and α 2 δ-1 KO ( n = 10, 10; red circles) DRG neurons using the low intracellular Ca 2+ -buffering intracellular solution, at −60 mV ( c ) and −70 mV ( d ) HP. * p

    Techniques Used:

    23) Product Images from "Characterization of Perturbing Actions by Verteporfin, a Benzoporphyrin Photosensitizer, on Membrane Ionic Currents"

    Article Title: Characterization of Perturbing Actions by Verteporfin, a Benzoporphyrin Photosensitizer, on Membrane Ionic Currents

    Journal: Frontiers in Chemistry

    doi: 10.3389/fchem.2019.00566

    Concentration-dependent effect of VP on I K(Ca) and the effects of different related compounds on VP-stimulated I K(Ca) in GH 3 cells. The experiments were conducted in cells bathed in normal Tyrode's solution and the depolarizing pulse from 0 to +50 mV [indicated in the upper part of (A) ] was delivered to the cell examined. (A) Superimposed I K(Ca) taken during step depolarization. a: control; b:1 μM VP; c: 3 μM VP; d: 10 μM VP. Arrowhead is the zero-current level and calibration bar refers to all traces. (B) Concentration-dependent effect of VP on I K(Ca) amplitude [mean ± SEM; n = 10–14 for each point (□)]. The examined cell was depolarized from 0 to +50 mV and current amplitude at the end of each depolarizing step was measured. As cells were exposed to 100 μM VP, I K(Ca) amplitude was taken to be 100%, and those at different VP concentrations were then compared. The values for EC 50 and the Hill coefficient were 2.4 μM and 1.1, respectively. Non-linear smooth line was least-squares fitted to a modified Hill function described in Materials and Methods . (C) Summary bar graph showing the effect of VP, VP plus tolbutamide, VP plus TRAM-39, VP plus paxilline, VP plus iberiotoxin, and VP plus dithiothreitol. Each bar showing I K(Ca) amplitude at the level of +60 mV indicates the mean ± SEM ( n = 11–14). *Significantly different from control ( P
    Figure Legend Snippet: Concentration-dependent effect of VP on I K(Ca) and the effects of different related compounds on VP-stimulated I K(Ca) in GH 3 cells. The experiments were conducted in cells bathed in normal Tyrode's solution and the depolarizing pulse from 0 to +50 mV [indicated in the upper part of (A) ] was delivered to the cell examined. (A) Superimposed I K(Ca) taken during step depolarization. a: control; b:1 μM VP; c: 3 μM VP; d: 10 μM VP. Arrowhead is the zero-current level and calibration bar refers to all traces. (B) Concentration-dependent effect of VP on I K(Ca) amplitude [mean ± SEM; n = 10–14 for each point (□)]. The examined cell was depolarized from 0 to +50 mV and current amplitude at the end of each depolarizing step was measured. As cells were exposed to 100 μM VP, I K(Ca) amplitude was taken to be 100%, and those at different VP concentrations were then compared. The values for EC 50 and the Hill coefficient were 2.4 μM and 1.1, respectively. Non-linear smooth line was least-squares fitted to a modified Hill function described in Materials and Methods . (C) Summary bar graph showing the effect of VP, VP plus tolbutamide, VP plus TRAM-39, VP plus paxilline, VP plus iberiotoxin, and VP plus dithiothreitol. Each bar showing I K(Ca) amplitude at the level of +60 mV indicates the mean ± SEM ( n = 11–14). *Significantly different from control ( P

    Techniques Used: Concentration Assay, Modification

    24) Product Images from "The Functional Availability of Arterial Kv7 Channels Is Suppressed Considerably by Large-Conductance Calcium-Activated Potassium Channels in 2- to 3-Month Old but Not in 10- to 15-Day Old Rats"

    Article Title: The Functional Availability of Arterial Kv7 Channels Is Suppressed Considerably by Large-Conductance Calcium-Activated Potassium Channels in 2- to 3-Month Old but Not in 10- to 15-Day Old Rats

    Journal: Frontiers in Physiology

    doi: 10.3389/fphys.2020.597395

    Effect of Retigabine, XE991, NS19504 and IBTX on methoxamine-induced contractions of the saphenous artery of young rats. (A) Normalized tension of saphenous arteries at different methoxamine concentrations in the absence of Kv7 channel active agents (Control), in the presence of XE991 (XE991 3*10 –6 M), in the presence of retigabine (Retigabine 3*10 –5 M). (B) Normalized tension of saphenous arteries with different methoxamine concentrations in the presence of IBTX (IBTX 10 –7 M), in the combined presence of IBTX and XE991 (IBTX + XE991), and in the combined presence of IBTX and retigabine (IBTX + Retigabine). (C) Normalized tension of saphenous arteries with different methoxamine concentrations in the presence of NS19504 (NS19504 6*10 –6 M), in the combined presence of NS19504 and XE991 (NS19504 + XE991) and in the combined presence of NS19504 and retigabine (NS19504 + Retigabine). *** p
    Figure Legend Snippet: Effect of Retigabine, XE991, NS19504 and IBTX on methoxamine-induced contractions of the saphenous artery of young rats. (A) Normalized tension of saphenous arteries at different methoxamine concentrations in the absence of Kv7 channel active agents (Control), in the presence of XE991 (XE991 3*10 –6 M), in the presence of retigabine (Retigabine 3*10 –5 M). (B) Normalized tension of saphenous arteries with different methoxamine concentrations in the presence of IBTX (IBTX 10 –7 M), in the combined presence of IBTX and XE991 (IBTX + XE991), and in the combined presence of IBTX and retigabine (IBTX + Retigabine). (C) Normalized tension of saphenous arteries with different methoxamine concentrations in the presence of NS19504 (NS19504 6*10 –6 M), in the combined presence of NS19504 and XE991 (NS19504 + XE991) and in the combined presence of NS19504 and retigabine (NS19504 + Retigabine). *** p

    Techniques Used:

    Effect of retigabine and IBTX on methoxamine-induced contractions of the saphenous artery. (A1,A2) Normalized tension of saphenous arteries with different methoxamine concentrations in the absence of potassium channel active agents (Control), in the presence of IBTX (IBTX 10 –7 M), in the presence of retigabine ( A1 : Retigabine 3*10 –6 M; A2 : Retigabine 10 –5 M) and in the combined presence of retigabine and IBTX (Retigabine + IBTX). (B1,B2) Retigabine anti-contractile effect in the absence of (Control) and presence of IBTX (IBTX 10 –7 M). (C1,C2) IBTX contractile effect in the absence of (Control) and presence of retigabine ( C1 : Retigabine 3*10 –6 M, C2 : Retigabine 10 –5 M). n1 = 9, n2 = 9; * p
    Figure Legend Snippet: Effect of retigabine and IBTX on methoxamine-induced contractions of the saphenous artery. (A1,A2) Normalized tension of saphenous arteries with different methoxamine concentrations in the absence of potassium channel active agents (Control), in the presence of IBTX (IBTX 10 –7 M), in the presence of retigabine ( A1 : Retigabine 3*10 –6 M; A2 : Retigabine 10 –5 M) and in the combined presence of retigabine and IBTX (Retigabine + IBTX). (B1,B2) Retigabine anti-contractile effect in the absence of (Control) and presence of IBTX (IBTX 10 –7 M). (C1,C2) IBTX contractile effect in the absence of (Control) and presence of retigabine ( C1 : Retigabine 3*10 –6 M, C2 : Retigabine 10 –5 M). n1 = 9, n2 = 9; * p

    Techniques Used:

    Effect of XE991 and IBTX on methoxamine-induced contractions of the saphenous artery of young rats. (A) Normalized tension of saphenous arteries with different methoxamine concentrations in the absence of potassium channel active agents (Control), in the presence of IBTX (IBTX 10 –7 M), in the presence of XE991 (XE991 3*10 –6 M) and in the combined presence of XE991 and IBTX (XE991 + IBTX). (B) XE991 contractile effect in the absence (Control) and presence of IBTX (IBTX 10 –7 M). (C) IBTX contractile effect in the absence (Control) and presence of XE991 (XE991 3*10 –6 M). n = 11; * p
    Figure Legend Snippet: Effect of XE991 and IBTX on methoxamine-induced contractions of the saphenous artery of young rats. (A) Normalized tension of saphenous arteries with different methoxamine concentrations in the absence of potassium channel active agents (Control), in the presence of IBTX (IBTX 10 –7 M), in the presence of XE991 (XE991 3*10 –6 M) and in the combined presence of XE991 and IBTX (XE991 + IBTX). (B) XE991 contractile effect in the absence (Control) and presence of IBTX (IBTX 10 –7 M). (C) IBTX contractile effect in the absence (Control) and presence of XE991 (XE991 3*10 –6 M). n = 11; * p

    Techniques Used:

    Effect of retigabine and IBTX on methoxamine-induced contractions of the saphenous artery of young rats. (A) Normalized tension of saphenous arteries with different methoxamine concentrations in the absence of potassium channel active agents (Control), in the presence of IBTX (IBTX 10 –7 M), in the presence of retigabine (Retigabine 10 –5 M) and in the combined presence of retigabine and IBTX (Retigabine + IBTX). (B) Retigabine anti-contractile effect in the absence of (Control) and presence of IBTX (IBTX 10 –7 M). C) IBTX contractile effect in the absence of (Control) and presence of retigabine (Retigabine 10 –5 M). n = 11; * p
    Figure Legend Snippet: Effect of retigabine and IBTX on methoxamine-induced contractions of the saphenous artery of young rats. (A) Normalized tension of saphenous arteries with different methoxamine concentrations in the absence of potassium channel active agents (Control), in the presence of IBTX (IBTX 10 –7 M), in the presence of retigabine (Retigabine 10 –5 M) and in the combined presence of retigabine and IBTX (Retigabine + IBTX). (B) Retigabine anti-contractile effect in the absence of (Control) and presence of IBTX (IBTX 10 –7 M). C) IBTX contractile effect in the absence of (Control) and presence of retigabine (Retigabine 10 –5 M). n = 11; * p

    Techniques Used:

    Effect of Retigabine, XE991, NS19504 and IBTX on methoxamine-induced contractions of the saphenous artery of adult rats. (A) Normalized tension of saphenous arteries at different methoxamine concentrations in the absence of Kv7 channel active agents (Control), in the presence of XE991 (XE991 3*10 –6 M), in the presence of retigabine (Retigabine 3*10 –5 M). (B) Normalized tension of saphenous arteries with different methoxamine concentrations in the presence of IBTX (IBTX 10 –7 M), in the combined presence of IBTX and XE991 (IBTX + XE991), and in the combined presence of IBTX and retigabine (IBTX + Retigabine). (C) Normalized tension of saphenous arteries with different methoxamine concentrations in the presence of NS19504 (NS19504 6*10 –6 M), in the combined presence of NS19504 and XE991 (NS19504 + XE991) and in the combined presence of NS19504 and retigabine (NS19504 + Retigabine). * p
    Figure Legend Snippet: Effect of Retigabine, XE991, NS19504 and IBTX on methoxamine-induced contractions of the saphenous artery of adult rats. (A) Normalized tension of saphenous arteries at different methoxamine concentrations in the absence of Kv7 channel active agents (Control), in the presence of XE991 (XE991 3*10 –6 M), in the presence of retigabine (Retigabine 3*10 –5 M). (B) Normalized tension of saphenous arteries with different methoxamine concentrations in the presence of IBTX (IBTX 10 –7 M), in the combined presence of IBTX and XE991 (IBTX + XE991), and in the combined presence of IBTX and retigabine (IBTX + Retigabine). (C) Normalized tension of saphenous arteries with different methoxamine concentrations in the presence of NS19504 (NS19504 6*10 –6 M), in the combined presence of NS19504 and XE991 (NS19504 + XE991) and in the combined presence of NS19504 and retigabine (NS19504 + Retigabine). * p

    Techniques Used:

    Effect of XE991 and IBTX on methoxamine-induced contractions of the saphenous artery. (A) Normalized tension of saphenous arteries with different methoxamine concentrations in the absence of potassium channel active agents (Control), in the presence of IBTX (IBTX 10 –7 M), in the presence of XE991 (XE991 3*10 –6 M) and in the combined presence of XE991 and IBTX (XE991 + IBTX). (B) XE991 contractile effect in the absence (Control) and presence of IBTX (IBTX 10 –7 M). (C) IBTX contractile effect in the absence (Control) and presence of XE991 (XE991 3*10 –6 M). n = 12; * p
    Figure Legend Snippet: Effect of XE991 and IBTX on methoxamine-induced contractions of the saphenous artery. (A) Normalized tension of saphenous arteries with different methoxamine concentrations in the absence of potassium channel active agents (Control), in the presence of IBTX (IBTX 10 –7 M), in the presence of XE991 (XE991 3*10 –6 M) and in the combined presence of XE991 and IBTX (XE991 + IBTX). (B) XE991 contractile effect in the absence (Control) and presence of IBTX (IBTX 10 –7 M). (C) IBTX contractile effect in the absence (Control) and presence of XE991 (XE991 3*10 –6 M). n = 12; * p

    Techniques Used:

    Effect of NS19504, IBTX, Retigabine and XE991 on methoxamine-induced contractions of the saphenous artery in adult and young rats. (A) Normalized tension of adult saphenous arteries with different methoxamine concentrations in the absence of BK channel active agents (Control), in the presence of IBTX (IBTX 10 –7 M) and in the presence of NS19504 (NS19504 6*10 –6 M). (B) Normalized tension of adult saphenous arteries at different methoxamine concentrations in the absence of Kv7 channel active agents (Control), in the presence of XE991 (XE991 3*10 –6 M), in the presence of retigabine (Retigabine 3*10 –5 M). (C) Normalized tension of young saphenous arteries with different methoxamine concentrations in the absence of BK channel active agents (Control), in the presence of IBTX (IBTX 10 –7 M) and in the presence of NS19504 (NS19504 6*10 –6 M). (D) Normalized tension of young saphenous arteries at different methoxamine concentrations in the absence of Kv7 channel active agents (Control), in the presence of XE991 (XE991 3*10 –6 M), in the presence of retigabine (Retigabine 3*10 –5 M).
    Figure Legend Snippet: Effect of NS19504, IBTX, Retigabine and XE991 on methoxamine-induced contractions of the saphenous artery in adult and young rats. (A) Normalized tension of adult saphenous arteries with different methoxamine concentrations in the absence of BK channel active agents (Control), in the presence of IBTX (IBTX 10 –7 M) and in the presence of NS19504 (NS19504 6*10 –6 M). (B) Normalized tension of adult saphenous arteries at different methoxamine concentrations in the absence of Kv7 channel active agents (Control), in the presence of XE991 (XE991 3*10 –6 M), in the presence of retigabine (Retigabine 3*10 –5 M). (C) Normalized tension of young saphenous arteries with different methoxamine concentrations in the absence of BK channel active agents (Control), in the presence of IBTX (IBTX 10 –7 M) and in the presence of NS19504 (NS19504 6*10 –6 M). (D) Normalized tension of young saphenous arteries at different methoxamine concentrations in the absence of Kv7 channel active agents (Control), in the presence of XE991 (XE991 3*10 –6 M), in the presence of retigabine (Retigabine 3*10 –5 M).

    Techniques Used:

    25) Product Images from "Senescence‐induced immunophenotype, gene expression and electrophysiology changes in human amniocytes, et al. Senescence‐induced immunophenotype, gene expression and electrophysiology changes in human amniocytes"

    Article Title: Senescence‐induced immunophenotype, gene expression and electrophysiology changes in human amniocytes, et al. Senescence‐induced immunophenotype, gene expression and electrophysiology changes in human amniocytes

    Journal: Journal of Cellular and Molecular Medicine

    doi: 10.1111/jcmm.14495

    Pharmacology assays in cryopreserved amniocytes via automated patch‐clamp. (A) Double‐ramp voltage‐clamp protocol with traces recorded before and during application of iberiotoxin 100 nmol/L that blocked big conductance Ca 2+ ‐dependent K + (BK) current fluctuations at positive potentials; (B) kinetics of BK channels block by iberiotoxin: SD of current fluctuations in a 6‐ms interval centred around the +80 mV peak in the double‐ramp protocol (values relative to the sweep before compound application, mean ± SD of n = 6 experiments). Fitting with a monoexponential function yielded a time constant τ = 13.3 s and a base (constant) of 0.29; (C) kinetics of use‐dependent I Na block by lidocaine 200 µmol/L (relative peak I Na amplitudes for five consecutive depolarizing pulses, mean ± SD of n = 3 experiments); (D) voltage‐clamp protocol for study of use‐dependent I Na block by lidocaine (only the first five of 40 consecutive pulses are shown). Applied voltage is shown below the current trace. I Na , voltage‐dependent Na + current
    Figure Legend Snippet: Pharmacology assays in cryopreserved amniocytes via automated patch‐clamp. (A) Double‐ramp voltage‐clamp protocol with traces recorded before and during application of iberiotoxin 100 nmol/L that blocked big conductance Ca 2+ ‐dependent K + (BK) current fluctuations at positive potentials; (B) kinetics of BK channels block by iberiotoxin: SD of current fluctuations in a 6‐ms interval centred around the +80 mV peak in the double‐ramp protocol (values relative to the sweep before compound application, mean ± SD of n = 6 experiments). Fitting with a monoexponential function yielded a time constant τ = 13.3 s and a base (constant) of 0.29; (C) kinetics of use‐dependent I Na block by lidocaine 200 µmol/L (relative peak I Na amplitudes for five consecutive depolarizing pulses, mean ± SD of n = 3 experiments); (D) voltage‐clamp protocol for study of use‐dependent I Na block by lidocaine (only the first five of 40 consecutive pulses are shown). Applied voltage is shown below the current trace. I Na , voltage‐dependent Na + current

    Techniques Used: Patch Clamp, Blocking Assay

    26) Product Images from "The Contribution of Resurgent Sodium Current to High-Frequency Firing in Purkinje Neurons: An Experimental and Modeling Study"

    Article Title: The Contribution of Resurgent Sodium Current to High-Frequency Firing in Purkinje Neurons: An Experimental and Modeling Study

    Journal: The Journal of Neuroscience

    doi: 10.1523/JNEUROSCI.23-12-04899.2003

    Iberiotoxin-sensitive K (Ca) currents in wild-type and med Purkinje neurons. A , A family of iberiotoxin-sensitive currents evoked from -60 mV in 10 mV increments for a wild-type (left) and a med ( right) neuron. Dashed line indicates 0 pA. The extent of inactivation was variable across cells of both phenotypes (see Results). B , Conductance–voltage curves for the currents in A .
    Figure Legend Snippet: Iberiotoxin-sensitive K (Ca) currents in wild-type and med Purkinje neurons. A , A family of iberiotoxin-sensitive currents evoked from -60 mV in 10 mV increments for a wild-type (left) and a med ( right) neuron. Dashed line indicates 0 pA. The extent of inactivation was variable across cells of both phenotypes (see Results). B , Conductance–voltage curves for the currents in A .

    Techniques Used:

    27) Product Images from "Cholinergic Modulation of Large-Conductance Calcium-Activated Potassium Channels Regulates Synaptic Strength and Spine Calcium in Cartwheel Cells of the Dorsal Cochlear Nucleus"

    Article Title: Cholinergic Modulation of Large-Conductance Calcium-Activated Potassium Channels Regulates Synaptic Strength and Spine Calcium in Cartwheel Cells of the Dorsal Cochlear Nucleus

    Journal: The Journal of Neuroscience

    doi: 10.1523/JNEUROSCI.3728-13.2014

    NMDAR activity is required for iberiotoxin (IbTx)-induced uEPSP and ΔCa spine increases. A , uEPSC (left), uEPSP (middle), and ΔG uEPSP /G sat (right) measured in the presence of d -APV (black) and d -APV plus iberiotoxin (red). B , uEPSC (left),
    Figure Legend Snippet: NMDAR activity is required for iberiotoxin (IbTx)-induced uEPSP and ΔCa spine increases. A , uEPSC (left), uEPSP (middle), and ΔG uEPSP /G sat (right) measured in the presence of d -APV (black) and d -APV plus iberiotoxin (red). B , uEPSC (left),

    Techniques Used: Activity Assay

    CWCs express rapidly inactivating BK channels. A , BK channel blockade using iberiotoxin reduced the afterhyperpolarization, increasing the tendency to fire complex spikes. B , Depolarizing voltage steps (from −90 to −30 mV, 200 ms) in a
    Figure Legend Snippet: CWCs express rapidly inactivating BK channels. A , BK channel blockade using iberiotoxin reduced the afterhyperpolarization, increasing the tendency to fire complex spikes. B , Depolarizing voltage steps (from −90 to −30 mV, 200 ms) in a

    Techniques Used: Mass Spectrometry

    Effects of mAChR activation on synaptic potentials and Ca influx are occluded by blocking BK channels. A , uEPSC, uEPSP, and ΔG uEPSP /G sat measured in the presence of the antagonists iberiotoxin (IbTx; black) and iberiotoxin plus Oxo-m (red). B
    Figure Legend Snippet: Effects of mAChR activation on synaptic potentials and Ca influx are occluded by blocking BK channels. A , uEPSC, uEPSP, and ΔG uEPSP /G sat measured in the presence of the antagonists iberiotoxin (IbTx; black) and iberiotoxin plus Oxo-m (red). B

    Techniques Used: Activation Assay, Blocking Assay

    BK channel blockade mimics the mAChR activation effects, whereas SK channels have no effect on uEPSP and Ca signal in CWC spines. A , B , uEPSC (left), uEPSP (middle), and ΔG uEPSP /G sat (right) measured in the presence of apamin ( A ) and iberiotoxin
    Figure Legend Snippet: BK channel blockade mimics the mAChR activation effects, whereas SK channels have no effect on uEPSP and Ca signal in CWC spines. A , B , uEPSC (left), uEPSP (middle), and ΔG uEPSP /G sat (right) measured in the presence of apamin ( A ) and iberiotoxin

    Techniques Used: Activation Assay

    28) Product Images from "BK current contributions to action potentials across the first postnatal week reflect age dependent changes in BK current kinetics in rat hippocampal neurons"

    Article Title: BK current contributions to action potentials across the first postnatal week reflect age dependent changes in BK current kinetics in rat hippocampal neurons

    Journal: bioRxiv

    doi: 10.1101/839233

    Iberiotoxin increases action potential duration to a greater extent in P1 neurons than in P7 neurons. (A) Representative traces comparing the effect of IbTx perfusion (control is in black, IbTx treatment is in red) on action potentials of P1 and P7 neurons. (B) Mean+SEM effect of IbTx on action potential duration. A single asterisk indicates significant difference from P1; a double asterisk indicates significant difference from P1 and P4. (one-way ANOVA on ranks, p=0.001, Dunn’s multiple comparisons, p
    Figure Legend Snippet: Iberiotoxin increases action potential duration to a greater extent in P1 neurons than in P7 neurons. (A) Representative traces comparing the effect of IbTx perfusion (control is in black, IbTx treatment is in red) on action potentials of P1 and P7 neurons. (B) Mean+SEM effect of IbTx on action potential duration. A single asterisk indicates significant difference from P1; a double asterisk indicates significant difference from P1 and P4. (one-way ANOVA on ranks, p=0.001, Dunn’s multiple comparisons, p

    Techniques Used:

    Iberiotoxin effects have different timing in P1 and P7 neurons (A) Representative traces of 1s action potential trains from P1 and P7 neurons before (black) and after IbTx perfusion (red). (B) Input-output curves for P1 (left) and P7 (right) without (black trace) and with IbTx (red trace) for 10-100 pA current injections. Asterisks at the end of the curves indicate a main effect of IbTx (two-way ANOVA, p
    Figure Legend Snippet: Iberiotoxin effects have different timing in P1 and P7 neurons (A) Representative traces of 1s action potential trains from P1 and P7 neurons before (black) and after IbTx perfusion (red). (B) Input-output curves for P1 (left) and P7 (right) without (black trace) and with IbTx (red trace) for 10-100 pA current injections. Asterisks at the end of the curves indicate a main effect of IbTx (two-way ANOVA, p

    Techniques Used:

    29) Product Images from "Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus"

    Article Title: Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2019.00027

    AP waveform properties from CA1 pyramidal neurons under pharmacological block of various ion channels [100 nM Iberiotoxin (IbTx) to block BK-channels, [100 nM Apamin to block SK-channels, 1 mM 4-Aminopyridine (4-AP) to block voltage-gated potassium channels]. (A) Quantification of the AP half-width. (B) Quantification of the fast after-hyperpolarization. n = 10–17 for all groups. (C,D) Quantification of the half-width (C) and fAHP (D) of the first six APs after a current injection of 200 pA and after application of potassium channel blockers ( C1 and D1 Apamin, C2 and D2 IbTx). (E) Firing frequency of current-step elicited APs in CA1 pyramidal neurons after application of potassium channel blockers ( E1 Apamin, E2 IbTx). All data shown as mean ± SEM or as min/max boxplot, with one-way ANOVA to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p
    Figure Legend Snippet: AP waveform properties from CA1 pyramidal neurons under pharmacological block of various ion channels [100 nM Iberiotoxin (IbTx) to block BK-channels, [100 nM Apamin to block SK-channels, 1 mM 4-Aminopyridine (4-AP) to block voltage-gated potassium channels]. (A) Quantification of the AP half-width. (B) Quantification of the fast after-hyperpolarization. n = 10–17 for all groups. (C,D) Quantification of the half-width (C) and fAHP (D) of the first six APs after a current injection of 200 pA and after application of potassium channel blockers ( C1 and D1 Apamin, C2 and D2 IbTx). (E) Firing frequency of current-step elicited APs in CA1 pyramidal neurons after application of potassium channel blockers ( E1 Apamin, E2 IbTx). All data shown as mean ± SEM or as min/max boxplot, with one-way ANOVA to probe for significance and Holm-Sidak to account for multiple comparisons (n.s. = not significant, * p

    Techniques Used: Blocking Assay, Injection

    30) Product Images from "The Unexpected Role of Calcium‐Activated Potassium Channels: Limitation of NO‐Induced Arterial Relaxation"

    Article Title: The Unexpected Role of Calcium‐Activated Potassium Channels: Limitation of NO‐Induced Arterial Relaxation

    Journal: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease

    doi: 10.1161/JAHA.117.007808

    Sodium nitroprusside ( SNP ) decreases the functional availability of the BK channel. Effect of SNP and iberiotoxin (Ib TX ) on methoxamine (MX)–induced contractions. Vessel tension in the absence of Ib TX and SNP ( CONTROL ), in the presence of Ib TX alone (Ib TX ), in the presence of SNP alone ( SNP ), and in the combined presence of Ib TX and SNP (Ib TX + SNP ) at, for example, 10 −7 mol/L (A) and 10 −5 mol/L (B) SNP . C, The functional availability of the BK channel represented as the area (marked in gray) between the MX ‐induced concentration‐response relationships obtained in the absence ( CONTROL ) and in the presence of Ib TX (Ib TX ) (*repeated‐measures ANOVA : n=9; P
    Figure Legend Snippet: Sodium nitroprusside ( SNP ) decreases the functional availability of the BK channel. Effect of SNP and iberiotoxin (Ib TX ) on methoxamine (MX)–induced contractions. Vessel tension in the absence of Ib TX and SNP ( CONTROL ), in the presence of Ib TX alone (Ib TX ), in the presence of SNP alone ( SNP ), and in the combined presence of Ib TX and SNP (Ib TX + SNP ) at, for example, 10 −7 mol/L (A) and 10 −5 mol/L (B) SNP . C, The functional availability of the BK channel represented as the area (marked in gray) between the MX ‐induced concentration‐response relationships obtained in the absence ( CONTROL ) and in the presence of Ib TX (Ib TX ) (*repeated‐measures ANOVA : n=9; P

    Techniques Used: Functional Assay, Concentration Assay

    The BK channel blocker IBTX increases the effect of SNP on intracellular calcium. A) Effect of SNP on MX‐induced [Ca 2+ ] i increase. F340/F380 ratio, a measure for the intracellular calcium concentration, in the absence (CONTROL) and presence of SNP (SNP 10 −7 M) (* ‐ repeated measures ANOVA: n=5, P
    Figure Legend Snippet: The BK channel blocker IBTX increases the effect of SNP on intracellular calcium. A) Effect of SNP on MX‐induced [Ca 2+ ] i increase. F340/F380 ratio, a measure for the intracellular calcium concentration, in the absence (CONTROL) and presence of SNP (SNP 10 −7 M) (* ‐ repeated measures ANOVA: n=5, P

    Techniques Used: Concentration Assay

    The BK channel blocker iberiotoxin (IbTX) increases the anticontractile effect of sodium nitroprusside (SNP). A, Effect of SNP on methoxamine (MX)‐induced contractions. Vessel tension in the absence ( CONTROL ) and presence of increasing concentrations of SNP ( SNP ) (repeated‐measures ANOVA : n=6, P =0.23 for SNP 10 −8 mol/L; *n=9, P
    Figure Legend Snippet: The BK channel blocker iberiotoxin (IbTX) increases the anticontractile effect of sodium nitroprusside (SNP). A, Effect of SNP on methoxamine (MX)‐induced contractions. Vessel tension in the absence ( CONTROL ) and presence of increasing concentrations of SNP ( SNP ) (repeated‐measures ANOVA : n=6, P =0.23 for SNP 10 −8 mol/L; *n=9, P

    Techniques Used:

    Contribution of the BK channel to the anticontractile effect of sodium nitroprusside (SNP) in tail arteries of β1‐deficient mice. Effect of SNP and iberiotoxin (Ib TX) on methoxamine‐induced contractions. Vessel tension in the absence of Ib TX and SNP ( CONTROL ), in the presence of Ib TX alone (Ib TX ), in the presence of SNP alone ( SNP ), and in the combined presence of Ib TX and SNP (Ib TX + SNP ) at 10 −7 mol/L (A) and 10 −6 mol/L (B) SNP . C, The anticontractile effect of SNP in the absence ( CONTROL ) and presence of Ib TX (2‐way ANOVA for effect of SNP : n=8; P
    Figure Legend Snippet: Contribution of the BK channel to the anticontractile effect of sodium nitroprusside (SNP) in tail arteries of β1‐deficient mice. Effect of SNP and iberiotoxin (Ib TX) on methoxamine‐induced contractions. Vessel tension in the absence of Ib TX and SNP ( CONTROL ), in the presence of Ib TX alone (Ib TX ), in the presence of SNP alone ( SNP ), and in the combined presence of Ib TX and SNP (Ib TX + SNP ) at 10 −7 mol/L (A) and 10 −6 mol/L (B) SNP . C, The anticontractile effect of SNP in the absence ( CONTROL ) and presence of Ib TX (2‐way ANOVA for effect of SNP : n=8; P

    Techniques Used: Mouse Assay

    Effect of the guanylyl cyclase inhibitor 1H‐[1,2,4]oxadiazolo[4,3‐a]quinoxalin‐1‐one (ODQ) and the protein kinase G inhibitor Rp‐8‐Br‐ PET ‐ cGMPS (Rp) on the anticontractile effect of sodium nitroprusside (SNP). A, Effect of SNP and iberiotoxin (Ib TX) on methoxamine (MX)–induced contractions in the presence of ODQ (10 −6 mol/L). Vessel tension in the absence of Ib TX and SNP ( CONTROL ), in the presence of Ib TX alone (Ib TX ), in the presence of SNP alone ( SNP ), and in the combined presence of Ib TX and SNP (Ib TX + SNP ) at 10 −7 mol/L SNP (repeated‐measures ANOVA : n=5, P =0.71 for CONTROL vs SNP and n=5, P =0.85 for Ib TX vs Ib TX + SNP ). B, The anticontractile effect of SNP in the absence ( CONTROL ) and presence of Ib TX ( t test: n=5, P =0.38). C, Functional availability of the BK channel in the absence ( CONTROL ) and presence of SNP ( SNP ) ( t test: n=5, P =0.53). D, Effect of SNP and Ib TX on MX ‐induced contractions in the presence of 10 −5 mol/L Rp. Vessel tension in the absence of Ib TX and SNP ( CONTROL ), in the presence of Ib TX alone (Ib TX ), in the presence of SNP alone ( SNP ), and in the combined presence of Ib TX and SNP (Ib TX + SNP ) at 10 −7 mol/L SNP (repeated‐measures ANOVA : n=8, P
    Figure Legend Snippet: Effect of the guanylyl cyclase inhibitor 1H‐[1,2,4]oxadiazolo[4,3‐a]quinoxalin‐1‐one (ODQ) and the protein kinase G inhibitor Rp‐8‐Br‐ PET ‐ cGMPS (Rp) on the anticontractile effect of sodium nitroprusside (SNP). A, Effect of SNP and iberiotoxin (Ib TX) on methoxamine (MX)–induced contractions in the presence of ODQ (10 −6 mol/L). Vessel tension in the absence of Ib TX and SNP ( CONTROL ), in the presence of Ib TX alone (Ib TX ), in the presence of SNP alone ( SNP ), and in the combined presence of Ib TX and SNP (Ib TX + SNP ) at 10 −7 mol/L SNP (repeated‐measures ANOVA : n=5, P =0.71 for CONTROL vs SNP and n=5, P =0.85 for Ib TX vs Ib TX + SNP ). B, The anticontractile effect of SNP in the absence ( CONTROL ) and presence of Ib TX ( t test: n=5, P =0.38). C, Functional availability of the BK channel in the absence ( CONTROL ) and presence of SNP ( SNP ) ( t test: n=5, P =0.53). D, Effect of SNP and Ib TX on MX ‐induced contractions in the presence of 10 −5 mol/L Rp. Vessel tension in the absence of Ib TX and SNP ( CONTROL ), in the presence of Ib TX alone (Ib TX ), in the presence of SNP alone ( SNP ), and in the combined presence of Ib TX and SNP (Ib TX + SNP ) at 10 −7 mol/L SNP (repeated‐measures ANOVA : n=8, P

    Techniques Used: Positron Emission Tomography, Functional Assay

    31) Product Images from "Molecular tuning of electroreception in sharks and skates"

    Article Title: Molecular tuning of electroreception in sharks and skates

    Journal: Nature

    doi: 10.1038/s41586-018-0160-9

    Shark BK properties a. mRNA expression of major K + channel α subunits (Kcna3, K V 1.3) and (Kcnma1, BK) in shark and skate electrosensory cells. b. Average K + current density, 4-AP-sensitive current (I KV ), and IbTx-sensitive current (I BK ) in shark and skate electrosensory cells. n = 5, p
    Figure Legend Snippet: Shark BK properties a. mRNA expression of major K + channel α subunits (Kcna3, K V 1.3) and (Kcnma1, BK) in shark and skate electrosensory cells. b. Average K + current density, 4-AP-sensitive current (I KV ), and IbTx-sensitive current (I BK ) in shark and skate electrosensory cells. n = 5, p

    Techniques Used: Expressing

    Shark electrosensory cell vesicular release characteristics a. ( Top ) Currents and capacitance changes in response to a 10ms −20mV voltage pulse in shark and skate electrosensory cells. Scale bars, 50pA, 200ms. ( Bottom ) Representative capacitance changes in response to the indicated durations of a −20mV voltage stimulus. Scale bars, 25fF, 200ms. b. −20mV voltage pulses of various durations induced similar integrated I CaV (Q Ca2+ ) in shark or skate electrosensory cells. n = 6. c. I CaV elicited by simulated voltage spikes in shark electrosensory cells and smaller voltage oscillations in skate cells. K + currents were blocked by intracellular Cs + , extracellular 4-AP and IbTx. d. Voltage-clamp protocols made to simulate shark electrosensory cell spiking induced the same amount of Q Ca2+ in shark or skate cells. Similarly, voltage protocols that simulated smaller skate electrosensory cell voltage oscillations induced the same amount of Q Ca2+ in shark or skate cells. Q Ca2+ elicited by simulated voltage spikes was larger than Q Ca2+ elicited by simulated oscillations. n = 10 for shark and 5 for skate. All data represented as mean ± s.e.m.
    Figure Legend Snippet: Shark electrosensory cell vesicular release characteristics a. ( Top ) Currents and capacitance changes in response to a 10ms −20mV voltage pulse in shark and skate electrosensory cells. Scale bars, 50pA, 200ms. ( Bottom ) Representative capacitance changes in response to the indicated durations of a −20mV voltage stimulus. Scale bars, 25fF, 200ms. b. −20mV voltage pulses of various durations induced similar integrated I CaV (Q Ca2+ ) in shark or skate electrosensory cells. n = 6. c. I CaV elicited by simulated voltage spikes in shark electrosensory cells and smaller voltage oscillations in skate cells. K + currents were blocked by intracellular Cs + , extracellular 4-AP and IbTx. d. Voltage-clamp protocols made to simulate shark electrosensory cell spiking induced the same amount of Q Ca2+ in shark or skate cells. Similarly, voltage protocols that simulated smaller skate electrosensory cell voltage oscillations induced the same amount of Q Ca2+ in shark or skate cells. Q Ca2+ elicited by simulated voltage spikes was larger than Q Ca2+ elicited by simulated oscillations. n = 10 for shark and 5 for skate. All data represented as mean ± s.e.m.

    Techniques Used:

    32) Product Images from "Altered Capicua expression drives regional Purkinje neuron vulnerability through ion channel gene dysregulation in spinocerebellar ataxia type 1"

    Article Title: Altered Capicua expression drives regional Purkinje neuron vulnerability through ion channel gene dysregulation in spinocerebellar ataxia type 1

    Journal: Human Molecular Genetics

    doi: 10.1093/hmg/ddaa212

    Regionally dysregulated ion channel genes form a functional module critical for Purkinje neuron pacemaking. ( A ) The distribution of regularly firing, irregularly firing and non-firing cells was recorded for Purkinje neurons in the anterior cerebellum and nodular zone. ( B ) Representative trace from a tonic firing wild-type and non-firing ATXN1[82Q] Purkinje neuron in the anterior cerebellum at P35. ( C ) Representative trace from wild-type and ATXN1[82Q] Purkinje neurons in the nodular zone at P35. ( D and E ) Membrane potential measurements during the AHP in wild-type Purkinje neurons (D) and ATXN1[82Q] Purkinje neurons (E) in the anterior cerebellum at P35. ( F ) Representative traces of wild-type Purkinje neurons in the anterior cerebellum at P35. Traces are shown at baseline (left), after perfusion of 200 nM iberiotoxin (middle) and after perfusion of 200 nM iberiotoxin +4 μM mibefradil. ( G and H ) Summary distribution of regularly firing, irregularly firing and non-firing Purkinje neurons before and after perfusion of 200 nM iberiotoxin (G) and after 200 nM iberiotoxin +4 μM mibefradil (H). **Denotes P
    Figure Legend Snippet: Regionally dysregulated ion channel genes form a functional module critical for Purkinje neuron pacemaking. ( A ) The distribution of regularly firing, irregularly firing and non-firing cells was recorded for Purkinje neurons in the anterior cerebellum and nodular zone. ( B ) Representative trace from a tonic firing wild-type and non-firing ATXN1[82Q] Purkinje neuron in the anterior cerebellum at P35. ( C ) Representative trace from wild-type and ATXN1[82Q] Purkinje neurons in the nodular zone at P35. ( D and E ) Membrane potential measurements during the AHP in wild-type Purkinje neurons (D) and ATXN1[82Q] Purkinje neurons (E) in the anterior cerebellum at P35. ( F ) Representative traces of wild-type Purkinje neurons in the anterior cerebellum at P35. Traces are shown at baseline (left), after perfusion of 200 nM iberiotoxin (middle) and after perfusion of 200 nM iberiotoxin +4 μM mibefradil. ( G and H ) Summary distribution of regularly firing, irregularly firing and non-firing Purkinje neurons before and after perfusion of 200 nM iberiotoxin (G) and after 200 nM iberiotoxin +4 μM mibefradil (H). **Denotes P

    Techniques Used: Functional Assay

    33) Product Images from "Regulation of the Mitochondrial BKCa Channel by the Citrus Flavonoid Naringenin as a Potential Means of Preventing Cell Damage"

    Article Title: Regulation of the Mitochondrial BKCa Channel by the Citrus Flavonoid Naringenin as a Potential Means of Preventing Cell Damage

    Journal: Molecules

    doi: 10.3390/molecules25133010

    Naringenin-induced changes in the ∆Ψ and respiratory rate of isolated endothelial mitochondria under nonphosphorylating conditions. The effect of different naringenin concentrations on ∆Ψ ( a ) and respiratory rate change ( b ) in the absence or presence of mitoBK Ca channel inhibitors (2 µM iberiotoxin (+IbTx) or 0.3 mM paxilline (+Pax)). The data represent at least five different mitochondrial preparations and are expressed as the means ± SD. *** p
    Figure Legend Snippet: Naringenin-induced changes in the ∆Ψ and respiratory rate of isolated endothelial mitochondria under nonphosphorylating conditions. The effect of different naringenin concentrations on ∆Ψ ( a ) and respiratory rate change ( b ) in the absence or presence of mitoBK Ca channel inhibitors (2 µM iberiotoxin (+IbTx) or 0.3 mM paxilline (+Pax)). The data represent at least five different mitochondrial preparations and are expressed as the means ± SD. *** p

    Techniques Used: Isolation

    Influence of naringenin on the oxygen consumption rate and ∆Ψ of isolated endothelial mitochondria under nonphosphorylating conditions. Effect of 10 µM naringenin on mitochondrial oxygen consumption rate ( a ) and ΔΨ ( b ) under control conditions (control) and in the absence or presence of 2 µM iberiotoxin (+IbTx). The Ca 2+ concentration was modulated by the addition of 1.5 mM ethylene glycol tetraacetic acid (EGTA) or 100 µM Ca 2+ to the incubation medium, as indicated. The data represent at least five different mitochondrial preparations and are expressed as the means ± SD. *** p
    Figure Legend Snippet: Influence of naringenin on the oxygen consumption rate and ∆Ψ of isolated endothelial mitochondria under nonphosphorylating conditions. Effect of 10 µM naringenin on mitochondrial oxygen consumption rate ( a ) and ΔΨ ( b ) under control conditions (control) and in the absence or presence of 2 µM iberiotoxin (+IbTx). The Ca 2+ concentration was modulated by the addition of 1.5 mM ethylene glycol tetraacetic acid (EGTA) or 100 µM Ca 2+ to the incubation medium, as indicated. The data represent at least five different mitochondrial preparations and are expressed as the means ± SD. *** p

    Techniques Used: Isolation, Concentration Assay, Incubation

    34) Product Images from "SK4 Ca2+ activated K+ channel is a critical player in cardiac pacemaker derived from human embryonic stem cells"

    Article Title: SK4 Ca2+ activated K+ channel is a critical player in cardiac pacemaker derived from human embryonic stem cells

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

    doi: 10.1073/pnas.1221022110

    Characterization of a Ca 2+ -activated K + current, IK Ca , and its impact on the pacemaker in early stage-derived hESC-CMs (11–21 d in vitro). ( A ) Iberiotoxin did not affect the AP beating rate ( n = 3). ( B ) Dequalinium (50 µM) significantly
    Figure Legend Snippet: Characterization of a Ca 2+ -activated K + current, IK Ca , and its impact on the pacemaker in early stage-derived hESC-CMs (11–21 d in vitro). ( A ) Iberiotoxin did not affect the AP beating rate ( n = 3). ( B ) Dequalinium (50 µM) significantly

    Techniques Used: Derivative Assay, In Vitro

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    Alomone Labs iberiotoxin
    For patch clamp experiments, undissociated CBs were used . The setup (A) and the image of the CB (B) are shown. Examples of K current records and mean I – V relationships in the DBA/2J (C) and the A/J mouse (D) are presented. Whole current traces were evoked by voltage steps from −80 to +60 mV with 10 mV increments for 100 ms. To construct a current–voltage curve, the mean current measured between 93 and 97 ms from the start of each voltage step. Mean currents were plotted versus the test pulse. Bars represent SEM. No statistical differences were seen between the strains. (E) The effect of <t>iberiotoxin</t> (a BK channel blocker; 200 nM) on outward current in GCs. The outward current was evoked by a test pulse from −80 to +20 mV for 100 ms. Iberiotoxin significantly and reversibly decreased outward current in GCs of the DBA/2J mice. However, K current in the A/J mice was not significantly affected by iberiotoxin. *, Significantly different from control and recovery. The amplitudes of K current (control and recovery) were significantly larger in GCs of the DBA/2J mice. Cont, control; Ibx, iberiotoxin; Rec, recovery.
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    For patch clamp experiments, undissociated CBs were used . The setup (A) and the image of the CB (B) are shown. Examples of K current records and mean I – V relationships in the DBA/2J (C) and the A/J mouse (D) are presented. Whole current traces were evoked by voltage steps from −80 to +60 mV with 10 mV increments for 100 ms. To construct a current–voltage curve, the mean current measured between 93 and 97 ms from the start of each voltage step. Mean currents were plotted versus the test pulse. Bars represent SEM. No statistical differences were seen between the strains. (E) The effect of iberiotoxin (a BK channel blocker; 200 nM) on outward current in GCs. The outward current was evoked by a test pulse from −80 to +20 mV for 100 ms. Iberiotoxin significantly and reversibly decreased outward current in GCs of the DBA/2J mice. However, K current in the A/J mice was not significantly affected by iberiotoxin. *, Significantly different from control and recovery. The amplitudes of K current (control and recovery) were significantly larger in GCs of the DBA/2J mice. Cont, control; Ibx, iberiotoxin; Rec, recovery.

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Differential Expression of Large-Conductance Ca2+-Activated K Channels in the Carotid Body between DBA/2J and A/J Strains of Mice

    doi: 10.3389/fncel.2011.00019

    Figure Lengend Snippet: For patch clamp experiments, undissociated CBs were used . The setup (A) and the image of the CB (B) are shown. Examples of K current records and mean I – V relationships in the DBA/2J (C) and the A/J mouse (D) are presented. Whole current traces were evoked by voltage steps from −80 to +60 mV with 10 mV increments for 100 ms. To construct a current–voltage curve, the mean current measured between 93 and 97 ms from the start of each voltage step. Mean currents were plotted versus the test pulse. Bars represent SEM. No statistical differences were seen between the strains. (E) The effect of iberiotoxin (a BK channel blocker; 200 nM) on outward current in GCs. The outward current was evoked by a test pulse from −80 to +20 mV for 100 ms. Iberiotoxin significantly and reversibly decreased outward current in GCs of the DBA/2J mice. However, K current in the A/J mice was not significantly affected by iberiotoxin. *, Significantly different from control and recovery. The amplitudes of K current (control and recovery) were significantly larger in GCs of the DBA/2J mice. Cont, control; Ibx, iberiotoxin; Rec, recovery.

    Article Snippet: To examine the BK channel component, a single step protocol was applied with or without iberiotoxin (200 nM; Alomone Laboratories), a selective blocker for BK channels.

    Techniques: Patch Clamp, Construct, Mouse Assay

    Proliferation and adhesion rates without and with the BK Ca inhibitor IbTx. ( A ) Average number of hDF obtained from young healthy donors and patients affected by HGPS estimated at 48, 72 and 96 hours from seeding and normalized at 24 h (fold-change ± SEM). Healthy and HGPS hDF were allowed to proliferate untreated (Young n=54; HGPS n=36) and treated by 100 nM IbTx (Young n=53; HGPS n=36). Young vs. HGPS: **p

    Journal: Aging (Albany NY)

    Article Title: BK channel overexpression on plasma membrane of fibroblasts from Hutchinson-Gilford progeria syndrome

    doi: 10.18632/aging.101621

    Figure Lengend Snippet: Proliferation and adhesion rates without and with the BK Ca inhibitor IbTx. ( A ) Average number of hDF obtained from young healthy donors and patients affected by HGPS estimated at 48, 72 and 96 hours from seeding and normalized at 24 h (fold-change ± SEM). Healthy and HGPS hDF were allowed to proliferate untreated (Young n=54; HGPS n=36) and treated by 100 nM IbTx (Young n=53; HGPS n=36). Young vs. HGPS: **p

    Article Snippet: Stock solution of Iberiotoxin (Alomone Labs, Jerusalem) in MilliQ water were added to the bath solution at the final saturating concentration of 100 nM.

    Techniques:

    Outward currents patch-clamp recorded in whole-cell configuration. ( A ) Representative examples of current traces recorded in hDF obtained from a young donor, an elderly, and a patient affected by HGPS. Current traces recorded after 100 nM IbTx application and a graphical representation of the pulse protocol (holding potential at 0 mV) are also shown. ( B ) Average ± SEM of current-voltage relationships (I–V) recorded in hDF obtained from healthy donors (Young, n=83; Elderly, n=16) and patients affected by HGPS (n=80). ( C ) Average ± SEM of current-voltage relationships (I–V) recorded in hDF obtained from young donors and patients affected by HGPS treated by 100 nM IbTx (n=6) and 10 mM TEA (n=4). Young vs. HGPS: *p

    Journal: Aging (Albany NY)

    Article Title: BK channel overexpression on plasma membrane of fibroblasts from Hutchinson-Gilford progeria syndrome

    doi: 10.18632/aging.101621

    Figure Lengend Snippet: Outward currents patch-clamp recorded in whole-cell configuration. ( A ) Representative examples of current traces recorded in hDF obtained from a young donor, an elderly, and a patient affected by HGPS. Current traces recorded after 100 nM IbTx application and a graphical representation of the pulse protocol (holding potential at 0 mV) are also shown. ( B ) Average ± SEM of current-voltage relationships (I–V) recorded in hDF obtained from healthy donors (Young, n=83; Elderly, n=16) and patients affected by HGPS (n=80). ( C ) Average ± SEM of current-voltage relationships (I–V) recorded in hDF obtained from young donors and patients affected by HGPS treated by 100 nM IbTx (n=6) and 10 mM TEA (n=4). Young vs. HGPS: *p

    Article Snippet: Stock solution of Iberiotoxin (Alomone Labs, Jerusalem) in MilliQ water were added to the bath solution at the final saturating concentration of 100 nM.

    Techniques: Patch Clamp

    Effects of TEA on the complex spike are mediated by block of Kv3 channels. Specific blockers of the non-Kv3 TEA-sensitive ion channels were bath applied to determine contributions of these channels to the effects of TEA on the complex spike. IbTx at 100 nM ( A ), which blocks BK channels, and 100 nM DTX-K ( B ), which blocks channels containing Kv1.1 subunits, mildly affected the complex spike waveform, typically increasing duration of the complex spike and yielding an additional spikelet (green arrows). C , Linopirdine at 10 μ M, blocker of KCNQ channels, had no effect on the complex spike waveform. Unlike the effects of 1 mM TEA, none of these blockers eliminated spikelet expression or considerably affected rate of repolarization of the first spike (right traces). D , DTX-I at 100 nM, which blocks Kv1.1, Kv1.2, and Kv1.6 subunits, did not affect repolarization of the first spike but compromised repetitive spikelet expression and dramatically extended the duration of the complex spike. E , Complex spike recordings from PCs in Kv3.3 KO mice show disrupted spikelet generation and affected repolarization of the first spike. Right traces are overlaid recordings from three Kv3.3 KO and two wild-type PCs at expanded timescales and normalized amplitudes.

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

    Article Title: Kv3.3 Channels at the Purkinje Cell Soma Are Necessary for Generation of the Classical Complex Spike Waveform

    doi: 10.1523/JNEUROSCI.4358-07.2008

    Figure Lengend Snippet: Effects of TEA on the complex spike are mediated by block of Kv3 channels. Specific blockers of the non-Kv3 TEA-sensitive ion channels were bath applied to determine contributions of these channels to the effects of TEA on the complex spike. IbTx at 100 nM ( A ), which blocks BK channels, and 100 nM DTX-K ( B ), which blocks channels containing Kv1.1 subunits, mildly affected the complex spike waveform, typically increasing duration of the complex spike and yielding an additional spikelet (green arrows). C , Linopirdine at 10 μ M, blocker of KCNQ channels, had no effect on the complex spike waveform. Unlike the effects of 1 mM TEA, none of these blockers eliminated spikelet expression or considerably affected rate of repolarization of the first spike (right traces). D , DTX-I at 100 nM, which blocks Kv1.1, Kv1.2, and Kv1.6 subunits, did not affect repolarization of the first spike but compromised repetitive spikelet expression and dramatically extended the duration of the complex spike. E , Complex spike recordings from PCs in Kv3.3 KO mice show disrupted spikelet generation and affected repolarization of the first spike. Right traces are overlaid recordings from three Kv3.3 KO and two wild-type PCs at expanded timescales and normalized amplitudes.

    Article Snippet: Iberiotoxin (IbTx), dendrotoxin-K (DTX-K), and dendrotoxin-I (DTX-I) were purchased from Alomone Labs (Jerusalem, Israel), linopirdine and CNQX were from Tocris Bioscience (Ellisville, MO), and all other salts and reagents were from Sigma (St. Louis, MO).

    Techniques: Blocking Assay, Expressing, Mouse Assay

    Effect of large-conductance Ca 2+ -activated K + (BK Ca ) channel blockade on EET- and dihydroxyeicosatrienoic acids (DHET)-induced dilation of HCAs. A–C : dilation to 8,9-, 11,12-, and 14,15-EET is inhibited by iberiotoxin (100 nmol/l, n = 6, 7, and

    Journal:

    Article Title: Epoxyeicosatrienoic and dihydroxyeicosatrienoic acids dilate human coronary arterioles via BKCa channels: implications for soluble epoxide hydrolase inhibition

    doi: 10.1152/ajpheart.00927.2005

    Figure Lengend Snippet: Effect of large-conductance Ca 2+ -activated K + (BK Ca ) channel blockade on EET- and dihydroxyeicosatrienoic acids (DHET)-induced dilation of HCAs. A–C : dilation to 8,9-, 11,12-, and 14,15-EET is inhibited by iberiotoxin (100 nmol/l, n = 6, 7, and

    Article Snippet: Iberiotoxin was obtained from Alomone Labs.

    Techniques: