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Isoniazid, administered to rats one hour before killing produced a dose-dependent enhancement of [35S]t-butylbiciclophosphorothionate ([35S]TBPS, 2 nM) measured ex vivo in unwashed membrane preparation of the cerebral cortex. Saturation experiments revealed that the effect of isoniazid was due to an increase (+36%) in the total number of [35S]TBPS binding sites. Diazepam (3 mg/kg i.p.) administered 15 min after isoniazid antagonized the enhancement of [35S]TBPS binding elicited by isoniazid. Moreover, diazepam itself induced a significant decrease (-30%) in the total number of [35S]TBPS binding sites. These results provide the first direct evidence that 'in vivo' alterations in the function of the GABA-dependent chloride channel can be detected in vitro by studying the binding of [35S]TBPS to its recognition sites in the GABAA receptor complex. Our finding suggests a new model suitable to study biochemically the function of GABAergic synapses under various physiological and pharmacological conditions.
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