Photolytic manipulation of [Ca2+](i) reveals slow kinetics of potassium channels underlying the afterhyperpolarization in hipppocampal pyramidal neurons

The identity of the potassium channel underlying the slow, apamin-insensiti ve component of the afterhyperpolarization current (sl(AHP)) remains unknow n. We studied sl(AHP) in CA1 pyramidal neurons using simultaneous whole-cel l recording, calcium fluorescence imaging, and flash photolysis of caged co mpounds. Intracellular calcium concentration ([Ca2+](i)) peaked earlier and decayed more rapidly than sl(AHP). Loading cells with low concentrations o f the calcium chelator EGTA slowed the activation and decay of sl(AHP). In the presence of EGTA, intracellular calcium decayed with two time constants . When [Ca2+](i) was increased rapidly after photolysis of DM-Nitrophen, bo th apamin-sensitive and apamin-insensitive outward currents were activated. The apamin-sensitive current activated rapidly (<20 msec), whereas the apa min-insensitive current activated more slowly (180 msec). The apamin-insens itive current was reduced by application of serotonin and carbachol, confir ming that it was caused by sl(AHP) channels. When [Ca2+](i) was decreased r apidly via photolysis of diazo-2, the decay of sl(AHP) was similar to contr ol (1.7 sec). All results could be reproduced by a model potassium channel gated by calcium, suggesting that the channels underlying sl(AHP) have intr insically slow kinetics because of their high affinity for calcium.