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

Neurones of the bullfrog sympathetic ganglion exhibit at least 5 distinct K⁺ currents. Two calcium-dependent K⁺ currents I_C and I_AHP, the delayed rectifier I_K, the muscarinic-sensitive I_M and the transient outward current I_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 block I_K and I_A. Concentrations as high as 2 mM have no effect on I_C, I_AHP or I_M. Since I_A is mostly inactivated at resting potentials in these cells, DAP can be used to explore the electrophysiological function of I_K. Under normal conditions DAP has no effect on action potential duration or on patterns of repetitive activity. This indicates that I_K is normally not involved in modulating these parameters. When I_C and I_AHP are blocked by removing extracellular calcium, however, inhibition of I_K prolongs action potential duration, reduces a fast afterhypolarization and enhances spike frequency adaptation. When I_M and I_AHP are reduced by barium (1 mM), inhibition of I_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 blocking I_K are critically dependent on the levels of other K⁺ currents found in these cells.