Effects of linopirdine and XE991 onI_K and I_Acurrents in sympathetic neurons. A, The outward delayed rectifier I_K was not affected by 5 μm linopirdine and 3 μm XE991 added into the medium for up to 20 min. I_K was partly depressed by 20 μm linopirdine (27 ± 5% inhibition; n = 8; p < 0.05) and by 10 μm XE991 (18 ± 2% block;n = 8; p < 0.05). Similar inhibitory effects were seen in neurons deprived of NGF for 7–10 hr (n = 5 for each test).I_K was triggered by a voltage step from the holding potential of −70 to +40 mV for 300 msec; steady-state current was measured for the drug effect. *p < 0.05 indicates significant difference from the control current recorded before drug application. B, Linopirdine (20 μm) and XE991 (10 μm) showed no significant effect on the A-type K⁺ current triggered by a voltage step from −110 to −20 mV. The I_A peak current was measured for the drug effect (n = 8 for each group).C, The A-type K⁺ channel blocker 4-AP (0.1 and 1.0 mm) showed no protection against the NGF deprivation-induced cell death; 4-AP at tested concentrations was not toxic to SCG neurons. *p < 0.05 indicates significant difference from controls with NGF.