Abstract
Synaptic excitation of hippocampal cells during blockade of synaptic inhibition results in an epileptiform "burst" potential followed by a prolonged afterhyperpolarization. This afterhyperpolarization resembles the one that is seen after the epileptic interictal spike and that is considered of critical importance in preventing seizure development. The afterhyperpolarization produced in the presence of y-aminobutyric acid antagonists is associated with a conductance increase and is inhibitory. It can occur in an all-or-none fashion after a burst, is independent of chloride, and is depressed by barium. The afterhyperpolarization has a reversal potential of (-86) millivolts, and the reversal potential is strongly dependent on the extracellular concentration of potassium. The afterhyperpolarization appears to be an intrinsic, inhibitory potassium potential mediated by calcium. This finding has implications for understanding the cellular mechanisms of epilepsy.
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