Dataset of electrophysiological patch-clamp recordings of the effect of the compounds deltamethrin, ATx-II and β4-peptide on human cardiac Nav1.5 sodium channel gating properties

Figures

• 

  Fig. 1. Nav1.5 channels display resurgent-like currents induced by 10 µM deltamethrin (a) Representative current traces evoked by the indicated voltage protocol in human Nav1.5 channels expressed in HEK293 cells. Cells were treated with vehicle or 10 µM deltamethrin. Representative trace of tail current in vehicle recordings (black) and resurgent-like current at −120 mV of 10 µM deltamethrin (orange) in magnified sections, respectively. Resurgent-like currents were determined as maximal current, elicited after repolarization, subtracted from a baseline. (b) Resurgent-like currents were normalized to maximum inward current of the depolarizing pre-pulse. Maximum resurgent-like currents were obtained at −110 mV: 10 µM deltamethrin 0.90% ± 0.42% (yellow, n = 12), 1 µM deltamethrin 0.77% ± 0.13% (red, n = 15) and vehicle 0.19% ± 0.03% (black, n = 15).(For interpretation of the references to color in this figure legend, the reader is referred to the web version of this article.)

• 

  Fig. 2. Time course of fast inactivation and deactivationin deltamethrin unbound Nav1.5 channels (a) Representative voltage protocol and traces of fast inactivation and deactivation kinetics during vehicle (gray) and 1 µM deltamethrin (black) recordings. Time constants of deactivation and fast inactivation were obtained by a double-exponential fit to the current decay, starting very briefly after inward current peak (fit highlighted in red). It should be noted that these fits mainly described the fast component of current decay and thus presumably the fraction of channels that did not bind deltamethrin. (b) Mean ± SEM values of the fast time constant (τfast) and slow time constant (τslow) of the decay of fast inactivation and deactivation during 1 µM deltamethrin (red) or vehicle (black). Deactivation was depicted from −120 mV to −80 mV, i.e. before the onset of persistent current (see Fig. 4d). For statistical comparison, the area under the curve (AUC) was calculated for each condition: τfast of 1 µM deltamethrin (unfilled red, n = 20, median AUC 0.874×10–9 Vs) and vehicle (unfilled black, n = 13, median AUC 0.898×10–9 Vs, p > 0.99, actual difference between the medians = 0.024×10–9 Vs,…

• 

  Fig. 3. Effect of ATx-II, deltamethrin and β4-peptide on the gating properties of Nav1.5 channels. (a) Representative voltage protocol and current traces of activating sodium currents during 1 µM deltamethrin and 0.5 nM ATx-II +1 µM deltamethrin recordings of Nav1.5 in HEK293 cells. (b) Conductance-voltage relationship of Nav1.5 in vehicle, 1 µM deltamethrin or 0.5 nM ATx-II + 1 µM deltamethrin recordings. Conductance was analyzed with leak and zero offset subtraction and normalized to the maximum conductance of each individual cell. Values for half maximal voltage-dependent activation (V1/2) were obtained from Boltzmann fits: vehicle −49.2 mV ± 2.4 mV (black, n = 14); 1 µM deltamethrin −56.2 mV ± 1.9 mV (red, n = 14, p = 0.03, difference between means = −7.0 mV ± 2.6 mV, 95% CI −13.6 mV to −0.5 mV, t-ratio = 2.7 vs. Vehicle; p = 0.2, difference between means = −5.3 mV ± 2.7 mV, 95% CI −12.1 mV to 1.5 mV, t-ratio = 2.0 vs. 0.5 nM ATx-II + 1 µM deltamethrin); 0.5 nM ATx-II + 1 µM deltamethrin −50.9 mV ± 0.8 mV (blue, n = 12, p > 0.99, difference between means = 3.4 mV ± 2.7 mV, 95% CI −5.1 mV to 8.5 mV, t-ratio = 0.6 vs. vehicle, one-way ANOVA with a Bonferroni's post-hoc analysis).…