Methanol extract of G. elata inhibited the binding of [³H]Ro15-1788, a selective benzodiazepine receptor antagonist, to benzodiazepine receptor of rat cortices. Saturation experiments followed by Scatchard analysis of the results showed that the inhibition of [³H]Ro15-1788 binding by G. elata. appeared to be competitive. These competitive inhibiton of the butanol fraction was observed to be higher than the methanol extract. Methanol extract of G. elata inhibited a [³H]flunitrazepam, a selective benzodiazepine receptor agonist, binding to benzodiazepine receptor. GABA significantly enhanced the inhibition of [³H]flunitrazepam binding by G. elata, and these "positive GABA shift" supported the strong possibility of agonistic activity to benzodiazepine receptor. Butanol fraction was observed to be higher than crude extract by methanol in an agonistic activity to benzodiazepine receptor, furthermore enhanced the binding of [³H]SR95531 to GABA_A, receptor. Butanol fraction of G. elata significantly diminished the pentylenetetrazole-induced lethality of mice. From these results, it can be concluded that substance or substances with neurochemical properties characteristic of a benzodiazepine receptor agonist may be important components, and contribute to the anticonvulsant property of G. elata.