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The endogenously bursting pacemaker neuron R15 of Aplysia exhibits an inwardly rectifying K+ current (IR) that was shown previously to be enhanced by various neurotransmitters via the intracellular second messenger, cyclic AMP (Drummond et al., 1980; Benson and Levitan, 1983; Levitan et al., 1987). Here we present evidence that Ca2+ influx, either caused by spontaneous bursting activity or elicited by depolarizing voltage-clamp pulses, causes a large, long-lasting inactivation of IR. The ionic current inactivated by bursts is identified as IR by several criteria: it activates steeply at membrane potentials more negative than the K+ equilibrium potential, has very fast kinetics, is reduced by lowering external K+ from 10 to 2 mM, and is blocked by adding 1 mM Ba2+, 10 mM Cs+, or 5 mM Rb+ to the bathing medium. The peak inactivation of IR is delayed following a single burst of spikes in R15, such that IR decreases maximally by about 20% after 60–90 sec, and then recovers gradually over more than 10 min. The inactivation caused by many bursts of spikes can reduce IR to less than 50% of its initial amplitude. The delay in onset and slow time course of recovery from inactivation of IR suggest that a complex biochemical mechanism underlies the effect of Ca2+ on IR. The effect of depolarization on IR is due specifically to the influx and intracellular accumulation of Ca2+. Depolarizing voltage-clamp pulses are maximally effective at reducing IR when they elicit a large influx of Ca2+, while pulses approaching the Ca2+ equilibrium potential have little effect.(ABSTRACT TRUNCATED AT 250 WORDS)

Calcium-dependent inactivation of a potassium current in the Aplysia neuron R15