Benzodiazepine receptor declines in hippocampal formation following limbic seizures.
Electrolytic lesions of entorhinal cortex have previously been shown to consistently produce limbic seizures. We report a bilateral and symmetrical decline in benzodiazepine receptor number in dentate gyrus of the hippocampal formation in unilateral entorhinal cortex-lesioned animals. We think this decline is caused by seizures since phenobarbital pretreatment prevented the appearance of limbic seizures and blocked the receptor decline. We postulate that these receptor declines may contribute to decreased endogenous recurrent inhibition (a presumed GABAergic synapse) of dentate granule cells which could lead to their repetitive firing. Thus these benzodiazepine receptor declines may be a consequence of limbic seizures yet increase the likelihood of subsequent seizures.
D000344:Afferent Pathways / Q000378:metabolism; D000818:Animals; D003975:Diazepam / Q000378:metabolism; D004292:Dominance, Cerebral / Q000502:physiology; D005445:Flunitrazepam / Q000378:metabolism; D006624:Hippocampus / Q000187:drug effects / Q000378:metabolism*; D008032:Limbic System / Q000187:drug effects / Q000378:metabolism*; D008297:Male; D010634:Phenobarbital / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D011956:Receptors, Cell Surface / Q000187:drug effects / Q000378:metabolism*; D011963:Receptors, GABA-A; D012640:Seizures / Q000378:metabolism*
D011956:Receptors, Cell Surface; D011963:Receptors, GABA-A; D005445:Flunitrazepam; D003975:Diazepam; D010634:Phenobarbital