Electrophysiological function of the delayed rectifier (IK) in bullfrog sympathetic ganglion neurones

Abstract

Neurones of the bullfrog sympathetic ganglion exhibit at least 5 distinct K+ currents. Two calcium-dependent K+ currents IC and IAHP, the delayed rectifier IK, the muscarinic-sensitive IM and the transient outward current IA. Each current plays a unique role in controlling the shapes and firing patterns of action potentials observed in these neurones. We have found that 3,4-diaminopyridine (DAP) (greater than 0.1 mM) will selectively block IK and IA. Concentrations as high as 2 mM have no effect on IC, IAHP or IM. Since IA is mostly inactivated at resting potentials in these cells, DAP can be used to explore the electrophysiological function of IK. Under normal conditions DAP has no effect on action potential duration or no patterns of repetitive activity. This indicates that IK is normally not involved in modulating these parameters. When IC and IAHP are blocked by removing extracellular calcium, however, inhibition of IK prolongs action potential duration, reduces a fast afterhypolarization and enhances spike frequency adaptation. When IM and IAHP are reduced by barium (1 mM), inhibition of IK by DAP has smaller effects on action potential duration and afterhyperpolarization amplitude, but still enhances spike frequency adaptation. We conclude that electrophysiological effects of blocking IK are critically dependent on the levels of other K+ currents found in these cells.