Abstract
Hyperbaric oxygen (HBO2) inhibits the GABAergic function in the brain, which leads to the development of convulsive reactions in the form of paroxysmal discharges on the EEG and movement disorders, similar to a generalized epileptic seizure. We hypothesize that the deficiency of GABAergic neurotransmission in HBO2, which occurs due to suppression of GABA synthesis, can be overcome by blocking the clearance of GABA from the synaptic cleft and slowing down its enzymatic degradation. The present study is aimed at studying the development of seizure reactions in rats under oxygen pressure of 5 ATA after blockade of GABA transporters with tiagabine and inhibition of GABA-transaminase with vigabatrin. New data obtained in this study are: (1) inhibition of GABA transaminase by vigabatrin or GABA transporters by tiagabine prevented the development of seizures in rats under oxygen pressure of 5 ATA; (2) oxygen convulsions in HBO2 appeared with a decrease in the brain GABA by 30-40% from the initial level; (3) inhibition of GABA transaminase by vigabatrin prevented a decrease in GABA in the striatum of rats under 5 ATA pressure. Consequently, a slowdown in synaptic clearance of GABA or a weakening of the enzymatic destruction of a mediator can compensate reduced GABA synthesis in HBO2 and increase its concentration to a level sufficient for the restoration of GABAergic function preventing the development of convulsive syndrome.
Published Version
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