Fig. 4. Shifts of Na+current inactivation curves to lower potentials by ketamine. To examine voltage-dependent inactivation, neurons (n = 6) were conditioned (2 s) at voltages from −110 to 0 mV before applying a test command pulse to 0 mV (A ). Test pulses to 0 mV were applied to open Na+channels not inactivated by the previous conditioning pulse (note broken time axes). Compared with control conditions, ketamine (10 μm–1 mm) depressed (P < 0.05) peak Na+currents after submaximal, inactivating conditioning voltages. Currents were normalized to the value of the peak mean current in control (B ). Ketamine shifted the inactivation curves to the left and thus to more hyperpolarized potentials. Ketamine significantly shifted the conditioning voltages, IV20and IV50, which are the conditioning voltages required to inactivate 20% and 50% of the peak currents, respectively, at concentrations of 100 μm and 1 mm (table 1). *P < 0.05 versus  control. **P < 0.01 versus  control.

Fig. 4. Shifts of Na+current inactivation curves to lower potentials by ketamine. To examine voltage-dependent inactivation, neurons (n = 6) were conditioned (2 s) at voltages from −110 to 0 mV before applying a test command pulse to 0 mV (A ). Test pulses to 0 mV were applied to open Na+channels not inactivated by the previous conditioning pulse (note broken time axes). Compared with control conditions, ketamine (10 μm–1 mm) depressed (P < 0.05) peak Na+currents after submaximal, inactivating conditioning voltages. Currents were normalized to the value of the peak mean current in control (B ). Ketamine shifted the inactivation curves to the left and thus to more hyperpolarized potentials. Ketamine significantly shifted the conditioning voltages, IV20and IV50, which are the conditioning voltages required to inactivate 20% and 50% of the peak currents, respectively, at concentrations of 100 μm and 1 mm (table 1). *P < 0.05 versus  control. **P < 0.01 versus  control.

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