Fig. 2: BIL enhanced VGSC currents and accelerated their activation. | Cell Death & Disease

Fig. 2: BIL enhanced VGSC currents and accelerated their activation.

From: Ca2+-dependent recruitment of voltage-gated sodium channels underlies bilirubin-induced overexcitation and neurotoxicity

Fig. 2: BIL enhanced VGSC currents and accelerated their activation.The alternative text for this image may have been generated using AI.

a An example of raw current trace mediated by VGSCs in response to the voltage-step protocol (below) showing a good alignment of the peak of individual currents as a result of space clamp. b Contrast two recording traces of maximal VGSC currents in control and BIL (3 μM), showing that BIL enlarged the amplitude and shifted the maximal activation voltage by –10 mV. c The current–voltage relationships (IV) of VGSCs in control and BIL groups, showing that the current density (pA/pF) was significantly increased, while the voltage for maximal activation was hyperpolarized. df The overlaid activation curves of control and BIL groups are shown, as well as the pooled results of their activation V0.5 and slope factor. The BIL group showed steeper voltage dependence for activation than the control as reflected by a more negative V0.5 and a lowered slope factor. g Raw current traces of steady-state inactivation of VGSC currents evoked by a single test pulse to −20 mV following preconditioning voltage steps ranging from −120 to + 20 mV for 100 ms (below). h Example current traces showing that BIL enhanced the amplitude of VGSC current evoked by the same test pulse from −120 to −20 mV. i The inactivation curves of the control group and the BIL group, showing that BIL had little effects on VGSCs. j, k Pooled data showing no significant difference between control and BIL groups in inactivation V0.5 or the slope factor. **p < 0.01, ***p < 0.001, NS not significant, independent-samples t-test.

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