The Ca2+-sensitive K+-currents underlying the slow afterhyperpolarization of bullfrog sympathetic neurones.

Ca2+-sensitive K+ currents involved in the slow afterhyperpolarization (a.h.p.) of an action potential of bullfrog sympathetic neurones were studied with a single-electrode voltage clamp method. The outward tail current (IAH) generated after the end of a depolarizing command pulse (from the holding potential of -60 mV to 0 mV, 5-20 ms in duration), mimicking an action potential, was separated into at least two exponential components (IAHf and IAHs). They were identified as K+ currents, since their reversal potentials were close to the K+ equilibrium potential and they were sensitive to external K+. The time constant of IAHf (tf; 44 ms at -60 mV) was decreased by membrane hyperpolarization from -40 to -80 mV, while that of IAHs (ts; 213 ms) remained constant. Removal of external Ca2+ or addition of Cd2+ significantly decreased the IAHs amplitude (As) and tf without a change in ts and the IAHf amplitude (Af). On the other hand, increasing Ca2+ influx by applying repetitive command pulses enhanced both Af and As with negligible effects on tf and ts, and produced a much slower component. Intracellular injection of EGTA reduced Af with no effect on tf, and increased As with a decreased ts. Both muscarine and (+/-)-tubocurarine, which reduced IAHs, hardly affected IAHf. These results indicate that a.h.p. is induced by the activation of two distinct Ca2+-dependent K+ channels, which differ in voltage sensitivity, Ca2+-dependence and pharmacology.