Spontaneous EEG spikes in the normal hippocampus. V. Effects of ether, urethane, pentobarbital, atropine, diazepam and bicuculline.

Spontaneous EEG spikes (SPKs) were recorded from the CA1 region of the dorsal hippocampus in normal rats during behavioral states not accompanied by rhythmical slow activity (RSA) such as awake immobility and slow wave sleep. In the present study we examined the effects of various systemically administered drugs on hippocampal SPK activity. Three general anesthetics (ether, urethane and pentobarbital) all reduced SPK activity. At anesthetic doses both ether and pentobarbital completely abolished SPKs. This SPK abolition during anesthesia seemed qualitatively different from RSA-related SPK suppression in undrugged animals in that unlike the latter case RSA generation was not the cause of SPK abolition in the former case. Atropine (50-100 mg/kg, i.p.) did not change greatly SPK activity or its behavioral correlation. Diazepam (5-10 mg/kg, i.p.) increased amplitude and decreased frequency of hippocampal fast EEG activity, and reduced SPK activity. These effects may be based on the known action of diazepam to enhance GABA-mediated postsynaptic inhibition. At subepileptic doses (1-6 mg/kg, i.p.) the GABA antagonist bicuculline enhanced dramatically SPK-related activities. Particularly, SPK-concurrent population burst discharges in the pyramidal cell layer were greatly increased in amplitude and complexity after bicuculline. These results suggest that the SPK generation mechanism in the hippocampus is sensitive to the level of GABA-mediated inhibition.