Prolonged epileptiform bursting induced by 0-Mg2+ in rat hippocampal slices depends on gap junctional coupling

The transition from brief interictal to prolonged seizure, or 'ictal', acti vity is a crucial event in epilepsy. In vitro slice models can mimic many p henomena observed in the electroencephalogram of patients, including transi tion from interictal to ictaform or seizure-like activity. In field potenti al recordings, three discharge types can be distinguished: (1) primary disc harges making up the typical interictal burst, (2) secondary bursts, lastin g several hundred milliseconds, and (3) tertiary discharges lasting for sec onds, constituting the ictal series of bursts. The roles of chemical synaps es in these classes of burst have been explored in detail. Here we test the hypothesis that gap junctions are necessary for the generation of secondar y bursts. In rat hippocampal slices, epileptiform activity was induced by exposure to 0-Mg2+. Epileptiform discharges started in the CA3 subfield, and generally consisted of primary discharges followed by 4-13 secondary bursts. Three d rugs that block gap junctions, halothane (5-10 mM), carbenoxolone (100 muM) and octanol (0.2-1.0 mM), abolished the secondary discharges, but left the primary bursts intact. The gap junction opener trimethylamine (10 mM) reve rsibly induced secondary and tertiary discharges. None of these agents alte red intrinsic or synaptic properties of CA3 pyramidal cells at the doses us ed. Surgically isolating the CA3 subfield made secondary discharges disappe ar, and trimethylamine under these conditions was able to restore them. We conclude that gap junctions can contribute to the prolongation of epilep tiform discharges. (C) 2001 IBRO. Published by Elsevier Science Ltd. All ri ghts reserved.