CHARACTERIZATION OF AN EARLY AFTERHYPERPOLARIZATION AFTER A BRIEF TRAIN OF ACTION-POTENTIALS IN RAT HIPPOCAMPAL-NEURONS INVITRO

In rat hippocampal pyramidal cells in vitro, a brief train of action potentials elicited by direct depolarizing current pulses injected through an intracellular recording electrode is followed by a medium-duration afterhyperpolarization (mAHP) and a longer, slow AHP. We studied the mAHP with the use of current-clamp techniques in the presence of dibutyryl cyclic adenosine 3',5'-monophosphate (cAMP) to block the slow AHP and isolate the mAHP. The mAHP evoked at hyperpolarized membrane potentials was complicated by a potential generated by the anomalous rectifier current, I(Q). The mAHP is insensitive to chloride ions (Cl-), whereas it is sensitive to the extracellular potassium concentration ([K+](o)). At slightly depolarized levels, the mAHP is partially Ca2+ dependent, being enhanced by increased [Ca2+](o) and BAY K 8644 and depressed by decreased [Ca2+](o), nifedipine, and Cd2+. The Ca2+-dependent component of the mAHP was also reduced by 100 μM tetraethylammonium (TEA) and charybdotoxin (CTX), suggesting it is mediated by the voltage- and Ca2+-dependent K+ current, I(C). Most the Ca2+-independent mAHP was blocked by carbachol, implying that I(M) plays a major role. In a few cells, a small Ca2+- and carbachol-insensitive mAHP component was detectable, and this component was blocked by 10 mM TEA, suggesting it was mediated by the delayed rectifier current, I(K). The K+ channel antagonist 4-aminopyridine (4-AP, 500 μM) did not reduce the mAHP. We infer that the mAHP is a complex potential due either to I(Q) or to the combined effects of I(M) and I(C). The contributions of each current depend on the recording conditions, with I(C) playing a role when the cells are activated from depolarized potentials and I(M) dominating at the usual resting potential. I(Q) is principally responsible for the mAHP recorded at hyperpolarized membrane potentials.