Influence of a GABA transaminase inhibitor on central nervous system oxygen toxicity.
A decrease in brain GABA concentration has been implied as the cause of convulsions induced by hyperbaric oxygen (HOP). We therefore examined the influence of sodium valproate, an anticonvulsant and GABA transaminase inhibitor on HOP-induced convulsions in rats. The mean latency of occurrence of the first electrical discharge in the ECoG and the appearance of the first clinical seizure in awake chronically implanted rats was unchanged by administration of sodium valproate prior to HOP exposure. We conclude that either the sodium valproate inhibition of GABA removal is insufficient to compensate for HOP inhibition of its production, or else that GABA concentration changes are not causally related to HOP-induced seizures.
D000612:4-Aminobutyrate Transaminase / Q000037:antagonists & inhibitors*; D000818:Animals; D004569:Electroencephalography; D006931:Hyperbaric Oxygenation / Q000009:adverse effects*; D008297:Male; D051381:Rats; D012640:Seizures / Q000188:drug therapy* / Q000209:etiology / Q000503:physiopathology; D000637:Transaminases / Q000037:antagonists & inhibitors*; D014631:Valerates / Q000627:therapeutic use*; D014635:Valproic Acid / Q000494:pharmacology / Q000627:therapeutic use*
D014631:Valerates; D014635:Valproic Acid; D000637:Transaminases; D000612:4-Aminobutyrate Transaminase