Antagonism of caffeine-induced convulsions by ethanol and dizocilpine (MK-801) in mice.

Ethanol (1 and 2 g/kg, i.p.) and MK-801 (1 mg/kg, i.p.), N-methyl-D-aspartate (NMDA) receptor antagonist, offered protection against caffeine-induced convulsions in mice. Subeffective doses of ethanol (0.5-g/kg, i.p.) and MK-801 (0.5 mg/kg, i.p.) when administered concurrently, did not provide a facilitatory anticonvulsant action against caffeine-induced convulsions. Ethanol (0.5 g/kg, i.p.) when administered concurrently with adenosine (100 mg/kg, i.p.) or dipyridamole (5 mg/kg, i.p.) elicited a facilitatory anticonvulsant action. However, concurrent administration of subeffective doses of MK-801 (0.5 mg/kg i.p.) with adenosine (100 mg/kg, i.p.) did not offer a facilitatory anticonvulsant action against caffeine-induced convulsions. The protective effect of ethanol (1 g/kg, i.p.) against caffeine-induced convulsions was reversed by an imidazobenzodiazepine, Ro 15-4513 (4 mg/kg, i.p.). Ro 15-4513 did not produce any proconvulsant effect with caffeine. It is suggested that ethanol and MK-801 elicit their anticonvulsant actions against caffeine-induced convulsions through different receptor mechanisms and that the anticonvulsant action of ethanol may be partly attributed to its ability to act via central adenosinergic mechanisms.