Mechanisms underlying activation of the slow AHP in rat hippocampal neurons

The firing of a train of action potentials in hippocampal pyramidal neurons is terminated by an afterhyperpolarization (AHP) that displays two main components; the medium AHP (I-mAHP), lasting a few hundred milliseconds and the slow AHP (I-sAHP), that has a duration of several seconds. it is unclear how much Of I-mAHP is dependent on the entry of calcium ions (Ca. 21), whereas it is accepted that IsAHP is caused by activation of Ca2+-activated potassium channels. There has been controversy regarding the subcellular localization and mechanism of activation of these channels. Whole-cell recordings from CAI neurons in the hippocampal slice preparation showed that inhibition of L-type, but not N-, P/Q-, T- and R-type Ca2+ channels, reduced both I-mAHp and I-sAHP. Inhibition of both AHP components by L-type Ca 21 channel antagonists was not complete, with I-sAHp being significantly more sensitive than I-mAHP. Somatic extracellular ionophoresis of BAPTA during I-sAHP caused a transient inhibition, but had no effect on I-mAHP. Cell-attached patch recordings from the soma of CAI neurons within a slice displayed channels that produced an ensemble waveform reminiscent Of I-sAHP when the patch was subjected to a train of action potential waveforms. The channels were Ca2+-activated, exhibited a limiting slope conductance of 19 pS and were not observed in dendritic membrane patches. These data demonstrate that the IsAHP is somatic in origin and arises from continued Ca2+ entry through functionally co-localized L-type channels.