GABA B agonists modulate a transient potassium current in cultured mammalian hippocampal neurons

Abstract

Depolarization of voltage-clamped cultured rat hippocampal neurons from holding potentials more negative than −60 mV produced a transient outward current with the characteristics of an A-current: it was 50% inactivated at a holding potential of −85 mV and blocked by 4-aminopyridine (1 mM). In the presence of GABA or baclofen (50–200 μM), with or without bicuculline, inactivation of this current was shifted to more positive potentials so that there was little inactivation at −70 mV. Activation of the A-current was also shifted to more positive potentials by these agonists, but the voltage dependence of activation of the sodium current was unaffected. If A-currents with similar properties can influence the time course of action potentials in presynaptic terminals, GABA B agonists could make action potentials briefer by potentiating the A-current and hence depress transmitter release.