Abstract
Benzodiazepine GABA-ionophore receptor complex ligands showed persistent modulation of the chloride ionophore, labeled by [(35)S]TBPS, even after receptor complex extensive purification. GABA caused inhibition of [(35)S]TBPS binding, while benzodiazepine agonists increased and benzodiazepine inverse agonists decreased the specific [(35)S]TBPS binding to the purified receptor. When GABA binding sites were occupied by the neurotransmitter benzodiazepine receptor agonists and antagonists reversed their effects clonazepam in fact inhibited and ?-carboline ethyl ester increased [(35)S]TBPS binding in the presence of GABA. The antagonist flumazenil showed no effect both in the presence or absence of GABA.
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