Origin of calcium ions involved in the generation of a slow afterhyperpolarization in bullfrog sympathetic neurones.

The origin of Ca2+ that activates the Ca2+-dependent K+ conductance which is responsible for the slow afterhyperpolarization (a.h.p.) following an action potential was studied in bullfrog sympathetic ganglia. The decay phase of the a.h.p. was a graded function of the extracellular Ca2+, and showed a voltage sensitivity opposite to that of the Ca2+-dependent K+-current reported previously (Pallotta et al. 1981), indicating that it reflected the time course of an increase in intracellular free Ca2+. An a.h.p. of longer duration was generated in cells which showed more pronounced rhythmic hyperpolarizations induced by intracellular Ca2+ release. The duration of the a.h.p. recorded with electrodes filled with K3-citrate [a.h.p. (citrate)], which favors Ca2+ release, was longer than the a.h.p. recorded with KCl-filled electrodes [a.h.p. (C1)]. D-600 (50-100 microM) drastically reduced the a.h.p. (C1), but had less effect on the a.h.p. (citrate). Caffeine which facilitates Ca2+ release prolonged the a.h.p. (C1), but had less effect on the a.h.p. (citrate). The a.h.p. (citrate) showed a greater sensitivity to a low temperature than the a.h.p. (C1). Mn2+ (1-3 mM) depressed both types of a.h.ps to the same extent. These results suggest that the origin of intracellular Ca2+ for a.h.p. (C1) is mainly Ca2+ influx during an action potential, while that for the a.h.p. (citrate) is both Ca2+ entry and intracellular Ca2+ release, although the effect of Mn2+ is difficult to explain fully.