Interactions of etifoxine with the chloride channel coupled to the GABAAreceptor complex

THIS study examined the nature of the interactions of etifoxine, an anxiolytic and anticonvulsant compound, with the GABAAreceptor/chloride channel complex. In membrane preparations of Sprague–Dawley rat cerebral cortex, etifoxine competitively inhibited the binding of [35S]t-butylbicyclophosphoro-thionate (TBPS), a specific ligand of the GABAAreceptor chloride channel site. In vivostudies demonstrated an anticonvulsant effect of etifoxine (50 and 75 mg/kg, i.p.) against the clonic convulsions induced by TBPS in CD1mice. Flumazenil (10 and 40 mg/kg, i.p.), an antagonist of benzodiazepine sites at GABAAreceptors, had no effect on the action of etifoxine. These findings suggest that etifoxine exerts its effect by interacting with the Cl−channel of GABAAreceptors and probably by facilitating GABAergic inhibition.