Article date: June 1982
By: JULIE M. BOWDLER, A. RICHARD GREEN in Volume 76, Issue 2, pages 291-298
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.
No changes were observed in [3H]‐diazepam binding in any other brain region examined 30 min after an ECS.
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.
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.
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.
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.
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.
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.
No changes were observed in [3H]‐diazepam binding in any other brain region examined 30 min after an ECS.
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.
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.
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.
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.
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.
DOI: 10.1111/j.1476-5381.1982.tb09219.x
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