Fig. 1. (  A ) Original current traces of human KCNQ2/Q3 channels transiently expressed in CHO cells channels ranging from −80 mV to 0 mV in 10-mV steps measured under control conditions and during the application of retigabine (10 μm). (  B ) The shift of the activation curve under the influence of retigabine (10 μm), control, and washout. The activation midpoint was shifted by −21 ± 3 mV compared with the mean of control and washout (n = 5;  P < 0.01). (  C ) Original current traces elicited with the ramp pulse protocol. The effects of retigabine on KCNQ2/Q3 currents were concentration-dependent and reversible on washout. (  D ) The effects of retigabine were normalized to control values. The diagram shows the retigabine effects compared to the respective mean of control and washout. Retigabine (300 nm, 1 μm, and 10 μm) increased the charge transfer by 1.07 ± 0.04 (n = 7;  P < 0.05); 1.46 ± 0.12 (n = 8;  P < 0.01); 2.28 ± 0.43 (n = 8;  P < 0.01) .

Fig. 1. (  A ) Original current traces of human KCNQ2/Q3 channels transiently expressed in CHO cells channels ranging from −80 mV to 0 mV in 10-mV steps measured under control conditions and during the application of retigabine (10 μm). (  B ) The shift of the activation curve under the influence of retigabine (10 μm), control, and washout. The activation midpoint was shifted by −21 ± 3 mV compared with the mean of control and washout (n = 5;  P < 0.01). (  C ) Original current traces elicited with the ramp pulse protocol. The effects of retigabine on KCNQ2/Q3 currents were concentration-dependent and reversible on washout. (  D ) The effects of retigabine were normalized to control values. The diagram shows the retigabine effects compared to the respective mean of control and washout. Retigabine (300 nm, 1 μm, and 10 μm) increased the charge transfer by 1.07 ± 0.04 (n = 7;  P < 0.05); 1.46 ± 0.12 (n = 8;  P < 0.01); 2.28 ± 0.43 (n = 8;  P < 0.01) .

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