A calcium-dependent potassium current is increased by a single-gene mutation inParamecium

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Abstract
The membrane currents of wild typeParamecium tetraurelia and the behavioral mutantteaA were analyzed under voltage clamp. TheteaA mutant was shown to have a greatly increased outward current which was blocked completely by the combined use of internally delivered Cs+ and external TEA+. This, along with previous work (Satow, Y., Kung, C., 1976,J. Exp. Biol. 65:51–63) identified this as a K+ current. It was further found to be a calcium-activated K+ current since this increased outward K+ current cannot be elicited when the internal calcium is buffered with injected EGTA. The mutationpwB, which blocks the inward calcium current, also blocks this increased outward K+ current inteaA. This shows that this mutant current is activated by calcium through the normal depolarization-sensitive calcium channel. While tail current decay kinetic analysis showed that the apparent inactivation rates for this calcium-dependent K+ current are the same for mutant and wild type, theteaA current activates extremely rapidly. It is fully activated within 2 msec. This early activation of such a large outward current causes a characteristic reduction in the amplitude of the action potential of theteaA mutant. TheteaA mutation had no effect on any of the other electrophysiological parameters examined. The phenotype of theteaA mutant is therefore a general decrease in responsiveness to depolarizing stimuli because of a rapidly activating calcium-dependent K+ current which prematurely repolarizes the action potential.