Silent cells during interictal discharges and seizures in hippocampal penicillin foci. Evidence for the role of extracellular K + in the transition from the interictal state to seizures

Abstract

Intracellular recordings were obtained from silent cells during penicillin-induced interictal discharges and seizures in the cat hippocampus. Silent cell membrane potential changes were used as an index of changes in local extracellular K + concentrations. During interictal discharges silent cells depolarize more slowly than neurons, reaching a peak at the end of the neuronal PDS (150–200 msec), and then repolarize over 3–5 sec. When seizures develop by evoking interictal discharges at rates slightly above spontaneous rates, the silent cells are not able to repolarize to baseline before the onset of each subsequent interictal discharge. During the seizure the silent cells depolarize further. It is suggested that K + accumulation in the extracellular space occurs as a result of the action potential and synaptic activity during interictal discharges and is independent of the mechanism of action of the epileptogenic agent. On the other hand, some evidence suggests a possible causative role of extracellular K + accumulation in the transition from interictal discharges to seizures.