Inhibitory mechanisms terminating paroxysmal depolarization shifts in hippocampal neurons of rats.

The mechanisms responsible for the termination of paroxysmal depolarization shifts (PDS) were studied with intracellular recordings on CA1 neurons of rat hippocampal slices. Epileptiform activity was induced by application of penicillin, bicuculline or Mg-free artificial cerebrospinal fluid (ACSF). PDS in penicillin-containing and Mg-free ACSF were markedly prolonged when GABAA-dependent IPSPs were blocked by bicuculline. PDS in bicuculline-containing ACSF were furthermore prolonged after block of potential dependent K+ conductances by TEA. TEA also exerted some effect on PDS induced by penicillin containing or Mg-free ACSF. Block of GABAB-dependent IPSPs or Ca(2+)-dependent K+ currents did not affect PDS duration in any of the three models. It is concluded that PDS termination is due to active inhibitory processes which comprise different components. If one of these components is blocked another inhibitory component governs PDS repolarization resulting in PDS with a slightly different duration but otherwise unchanged features.