Abstract
Outward currents were recorded from voltage-clamped NG108-15 mouse neuroblastoma × rat glioma hybrid cells, differentiated with prostaglandin E1. Depolarising voltage steps from −70 mV, evoked a transient outward current from a threshold of −30 mV. The outward current showed complete inactivation at potentials positive to -10 mV. Inactivation was removed by hyperpolarisation with half-inactivation at −53 mV. The time course of the inactivation could be best fitted by two exponentials with mean time constants of 280 ms and 1.6 s at + 80 mV. Tail current measurements showed a shift in the reversal potential with changes in external K+ concentration, consistent with K+ as the current-carrying ion. The outward current amplitude was reversibly reduced by 4-aminopyridine, and the time course of inactivation modified. In the presence of other K+ channel blockers (tetraethylammonium, barium and tetrahydroaminoacridine) the amplitude of the outward current was also reversibly reduced, but with a negliglible effect on its time course. The current was unaffected by dendrotoxin, d-tubocurarine, apamin, Cd2+ and Ni2+, and by replacing external Ca2+ with Co2+ or Mg2+. In current clamp, action potential duration was greatly increased by 4-aminopyridine. The findings show that the NG108-15 cell line displays a transient outward current that resembles IK(A) but with a higher than usual threshold and relatively slow inactivation, and that this current is likely to be important for action potential repolarisation.