Potassium currents contributing to action potential repolarization in dissociated cultured rat superior cervical sympathetic neurones.

Pharmacological blocking agents were used to assess the contributions of different K(+)-currents to spike-repolarization and early spike-afterhyperpolarization recorded in dissociated, tissue-cultured rat superior cervical sympathetic neurones using both patch-clamp and impalement microelectrode techniques. Effects of 4-aminopyridine (4-AP) and tetraethylammonium (TEA), in concentrations which selectively reduced the delayed rectifier current IK(DR) and Ca(2+)-activated K(+)-current IK(Ca, fast), respectively, indicated that IK(DR) made a significant contribution to both spike repolarization and spike afterhyperpolarization under all recording conditions, whereas the contribution of IK(Ca,fast) depended on the level of intracellular Ca(2+)-buffering. No evidence for a significant role for the transient current IK(A) could be adduced in these experiments.