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Fig. 4 | BMC Pharmacology and Toxicology

Fig. 4

From: Safinamide, an inhibitor of monoamine oxidase, modulates the magnitude, gating, and hysteresis of sodium ion current

Fig. 4

Mean current–voltage (I-V) or conductance-voltage relationship of INa(T) in GH3 cells. The measurements were performed as described in the legend of Fig. 1. Because we used the whole-cell mode, the test cells were maintained at −80 mV and subjected to a series of command voltages ranging from −100 to +30 mV in 10-mV increments. (A) Current traces during the control period (upper) and during the exposure to 3 μM SAF. The voltage-clamp protocol used is indicated atop the current traces. (B) Mean I–V relationship of INa(T) in the absence (blue filled squares) and with cell exposure to 3 μM SAF (red open circles) or 10 μM SAF (brown open triangles) (mean ± standard error of the mean; n = 8 for each point). INa(T) amplitude was measured at the beginning of each voltage pulse. Notably, the I–V relationship of INa(T) (or peak INa) induced by 30-ms voltage pulses was shifted to more negative potentials upon SAF (3 or 10 μM) exposure. (C) Mean conductance versus voltage (G-V) of INa(T) in the absence (blue filled squares) and with cell exposure to 3 μM SAF (red open circles) or 10 μM (brown open triangles) (mean ± standard error of the mean; n = 8 for each point). The conductance-voltage relationship of INa(T) was shifted to more negative potentials during exposure to SAF. (D) Effect of SAF (10 μM) on the steady-state inactivation curve of INa(T) (mean ± standard error of the mean; n = 7 for each point). In these experiments, the conditioning voltage pulse with a duration of 30 ms to various membrane potentials between −100 and +10 mV was applied from a holding potential of −80 mV. Following each conditioning potential, a test pulse to −10 mV for a duration of 30 ms was given to activate INa. The normalized amplitude of INa (I/Imax) was constructed against the conditioning potential

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