REGIONAL RAT BRAIN BENZODIAZEPINE RECEPTOR NUMBER AND γ‐AMINOBUTYRIC ACID CONCENTRATION FOLLOWING A CONVULSION

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Abstract
1 Following administration to rats of an electroconvulsive shock (ECS) which resulted in a major tonic-clonic seizure, no changes in [3H]-diazepam binding characteristics were observed in cortex or hippocampus with either a well washed membrane preparation or a crude synaptosomal preparation. 2 No changes were observed in [3H]-diazepam binding in any other brain region examined 30 min after an ECS. 3 Thirty min following an ECS, regional brain γ-aminobutyric acid (GABA) concentrations increased in hippocampus, cortex and hypothalamus. Only in the hippocampus did the increase occur within 5 min of the seizure. 4 Similar increases in GAB A concentration were seen after a bicuculline-induced seizure but not after a seizure induced by flurothyl; both treatments produced a tonic-clonic seizure. 5 Pretreatment of the rats with (+)-propranolol 5 min before the ECS abolished the tonic extension and prevented the brain GAB A concentration changes that occur 30 min after the seizure. 6 No increase in GABA concentration was seen in hippocampus, cortex or hypothalamus 30 min after the final ECS of a course of 10 ECS given once daily for 10 days. In contrast a marked increase in striatal GABA concentration was observed. 7 These changes in GABA biochemistry following a seizure are discussed in relation to the post-ictal rise in seizure threshold that is occurring at the same time.
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