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

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Abstract
Neurones of the bullfrog sympathetic ganglion exhibit at least 5 distinct K+ currents. Two calcium-dependent K+ currentsI C andI AHP, the delayed rectifierI K, the muscarinic-sensitiveI M and the transient outward currentI A. 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) (>0.1 mM) will selectively blockI K andI A. Concentrations as high as 2 mM have no effect onI C,I AHP orI M. SinceI A is mostly inactivated at resting potentials in these cells, DAP can be used to explore the electrophysiological function ofI K. Under normal conditions DAP has no effect on action potential duration or on patterns of repetitive activity. This indicates thatI K is normally not involved in modulating these parameters. WhenI C andI AHP are blocked by removing extracellular calcium, however, inhibition ofI K prolongs action potential duration, reduces a fast afterhypolarization and enhances spike frequency adaptation. WhenI M andI AHP are reduced by barium (1 mM), inhibition ofI K by DAP has smaller effects on action potential duration and atterhyperpolarization amplitude, but still enhances spike frequency adaptation. We conclude that electrophysiological effects of blockingI K are critically dependent on the levels of other K+ currents found in these cells.