Abstracts

Cooling terminates extracellularly recorded spontaneous epileptiform discharges induced by chemoconvulsants in the hippocampal slice (G.K. Motamedi et al., [italic]Epilepsy Res.[/italic], in press). Small temperature drops are effective when cooling is applied rapidly. Here we investigated the cellular mechanisms underlying the effects of rapid cooling on epileptiform activity in different regions of the hippocampus., Whole-cell patch clamp recordings were carried out from neurons in mouse hippocampal slices perfused with 50 mM 4-aminopyridine at an initial temperature of 32 [deg]C. Rapid cooling was induced at a rate of 2[ndash]3 [deg]C/s by switching to cold aCSF., In CA1 and CA2 neurons, rapid cooling typically induced a 10[ndash]20 mV membrane depolarization associated with a large inward current, which was eliminated by 1 mM tetrodotoxin (TTX). In contrast, most CA3 neurons responded to cooling with TTX- and bicuculline (25 mM)-insensitive hyperpolarizations that were associated with a steady outward current and decreased conductance., Termination of epileptiform discharges in CA1 and CA2 neurons by rapid cooling may occur by synaptically-driven depolarization block. In CA3 neurons, cooling seems to inhibit a persistent depolarizing conductance, raising the possibility that closure of temperature sensitive TRP channels could mediate the suppression of discharges., (Supported by Grant # R01 NS047700 to S.V.)