iberiotoxin  (Alomone Labs)


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    Structured Review

    Alomone Labs iberiotoxin
    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 <t>iberiotoxin</t> (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
    Iberiotoxin, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 93/100, based on 15 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 93 stars, based on 15 article reviews
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    iberiotoxin - by Bioz Stars, 2022-12
    93/100 stars

    Images

    1) 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

    2) 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

    3) 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:

    4) 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

    5) 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

    6) 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:

    7) 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

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    Alomone Labs kca 3 1
    Kca 3 1, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Stimulatory effect of QO-58 on the activity of BK Ca channels recorded from GH 3 cells. We conducted these inside-out current recordings in cells which were bathed in high-K + solution containing 0.1 μM Ca 2+ , and the recording pipette was then filled up with K + -containing solution. ( A ) Original BK Ca -channel currents obtained in the control period (left, black color) and after bath application of 3 μM QO-58 (right, red color). The detached patch was voltage-clamped at +60 mV. The lower part indicates the expanded records from the uppermost part. The opening event of the channel is indicated by the upward deflection. ( B ) Summary scatter graph showing effect of QO-58, QO-58 plus linopirdine (Lino), or QO-58 plus <t>verruculogen</t> <t>(Ver)</t> (mean ± SEM; n = 8 for each point). Under inside-out configuration, the channel open probability was measured at the level of +60 mV. * Significantly different from control ( p
    Verruculogen Ver, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Alomone Labs cleavage resistant prongf
    Stimulatory effect of QO-58 on the activity of BK Ca channels recorded from GH 3 cells. We conducted these inside-out current recordings in cells which were bathed in high-K + solution containing 0.1 μM Ca 2+ , and the recording pipette was then filled up with K + -containing solution. ( A ) Original BK Ca -channel currents obtained in the control period (left, black color) and after bath application of 3 μM QO-58 (right, red color). The detached patch was voltage-clamped at +60 mV. The lower part indicates the expanded records from the uppermost part. The opening event of the channel is indicated by the upward deflection. ( B ) Summary scatter graph showing effect of QO-58, QO-58 plus linopirdine (Lino), or QO-58 plus <t>verruculogen</t> <t>(Ver)</t> (mean ± SEM; n = 8 for each point). Under inside-out configuration, the channel open probability was measured at the level of +60 mV. * Significantly different from control ( p
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    Stimulatory effect of QO-58 on the activity of BK Ca channels recorded from GH 3 cells. We conducted these inside-out current recordings in cells which were bathed in high-K + solution containing 0.1 μM Ca 2+ , and the recording pipette was then filled up with K + -containing solution. ( A ) Original BK Ca -channel currents obtained in the control period (left, black color) and after bath application of 3 μM QO-58 (right, red color). The detached patch was voltage-clamped at +60 mV. The lower part indicates the expanded records from the uppermost part. The opening event of the channel is indicated by the upward deflection. ( B ) Summary scatter graph showing effect of QO-58, QO-58 plus linopirdine (Lino), or QO-58 plus verruculogen (Ver) (mean ± SEM; n = 8 for each point). Under inside-out configuration, the channel open probability was measured at the level of +60 mV. * Significantly different from control ( p

    Journal: International Journal of Molecular Sciences

    Article Title: Evidence for Dual Activation of IK(M) and IK(Ca) Caused by QO-58 (5-(2,6-Dichloro-5-fluoropyridin-3-yl)-3-phenyl-2-(trifluoromethyl)-1H-pyrazolol[1,5-a]pyrimidin-7-one)

    doi: 10.3390/ijms23137042

    Figure Lengend Snippet: Stimulatory effect of QO-58 on the activity of BK Ca channels recorded from GH 3 cells. We conducted these inside-out current recordings in cells which were bathed in high-K + solution containing 0.1 μM Ca 2+ , and the recording pipette was then filled up with K + -containing solution. ( A ) Original BK Ca -channel currents obtained in the control period (left, black color) and after bath application of 3 μM QO-58 (right, red color). The detached patch was voltage-clamped at +60 mV. The lower part indicates the expanded records from the uppermost part. The opening event of the channel is indicated by the upward deflection. ( B ) Summary scatter graph showing effect of QO-58, QO-58 plus linopirdine (Lino), or QO-58 plus verruculogen (Ver) (mean ± SEM; n = 8 for each point). Under inside-out configuration, the channel open probability was measured at the level of +60 mV. * Significantly different from control ( p

    Article Snippet: QO-58 (5-(2,6-dichloro-5-fluoropyridin-3-yl)-3-phenyl-2-(trifluoromethyl)-1H-pyrazolol[1,5-a]pyrimidin-7-one, 5-(2,6-dichloro-5-fluoro-3-pyridinyl)-3-phenyl-2-(trifluoromethyl)-pyrazolo[1,5-a]pyrimidin-7(4H )-one, C18 H8 Cl2 F4 N4 O) was supplied by Tocris (Union Biomed, Taipei, Taiwan), iberiotoxin and verruculogen (Ver) were by Alomone (Asia Bioscience, Taipei, Taiwan), while we acquired linopirdine, tetrodotoxin (TTX), and thyrotropin releasing hormone (TRH) from Sigma-Aldrich (Merck, Taipei, Taiwan).

    Techniques: Activity Assay, Transferring