TRANSIENT IMPAIRMENT OF THE GABAERGIC FUNCTION DURING INITIATION OF SOMAN-INDUCED SEIZURES

The changes in extracellular gamma-aminobutyric acid (GABA) levels, th e modifications in binding capacities of GABA-receptor subtypes A and B and of the Cl- ionophore sites localized in the ionic-channel associ ated to the GABA, receptors were;studied in hippocampus of rats subjec ted to a convulsive dose of the acetylcholinesterase inhibitor soman. Whereas extracellular GABA levels, just as binding on GABAA and GABA, receptors, were not modified under soman, a significant transient decr ease in the binding capacities of the Cl- ionophore site of the GABA, receptor complex occurred within the first 10 min of seizures in CA1, CA3 areas, and in the dentate gyrus with return to basal values after 30 min. Accordingly, a transient decrease of the brain muscimol-gated Cl- influx was observed after 10 min of seizures. An increased ability of diazepam to potentiate the GABA, gated Cl- influx occurred at the same time. Altogether, these data demonstrated that an impairment of t he GABA(A) receptor function occurs at the beginning of seizures. This suggests that a temporary decrease of GABA(A)ergic function may contr ibute to the onset of seizures.