Effect of the nonspecific K⁺ channel blocker TEA on light-triggered APs in Xenopus oocytes. Recordings were performed on a single oocyte expressing Na_v1.4, β1-ChR2, and K_v2.1. Duration of the light pulse was 25 ms. (A) Current-clamp recording in the absence and presence of 50 mM TEA. TEA reduced the upstroke velocity, which was due to a partial block of Na_v1.4 channels, and caused a deceleration of AP repolarization, which was due to a reduction of the K_v2.1 current. The early depolarization phase to nearly −55 mV remained unchanged, because β1-ChR2 currents were not affected by TEA. Corresponding light-triggered current values were as follows: I_peak = 581 ± 212 nA, I_plateau = 279 ± 95 nA (without TEA), and I_peak = 605 ± 224 nA, I_plateau = 307 ± 109 nA (50 mM TEA; P > 0.2 with n = 10). (B) Corresponding Na_v1.4 currents. The test pulse was −10 mV. At 50 mM TEA, Na_v1.4 was partially blocked (red). (C) Corresponding K_v2.1 currents. At 50 mM TEA, >75% of K_v2.1 channels were blocked, causing the pronounced AP prolongation seen in A.