Abstract
The kinetic characteristics of binding of [ 3H]-GABA and the pattern of isoniazid-induced convulsions were studied in rats treated with repeated intraventricular injections of ethyl-β-carboline-3-carboxylate (β-CCE) (10 μg/rat, twice daily for 8 days). Thirty-six hours after the last injection, the total number of binding sites for [ 3H]-GABA was decreased (25%) in the cerebral cortex and hippocampus. On the other hand, there was no significant difference in the dissociation constant ( K d ) between β-CCE and solvent-treated rats. The decrease in binding sites for [ 3H]-GABA was paralleled by a strong potentiation of the convulsant pattern elicited by isoniazid. The results suggest that the proconvulsant effect elicited by β-CCE is mediated by the decrease in the total number of binding sites for GABA, secondary to the interaction between β-CCE and the benzodiazepine receptor coupled to the GABA receptor.
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