Abstract

The effects of acute and subchronic administration of dimethoate on γ-aminobutyric (GABA) concentration and receptor characteristics in rat cerebral cortices were investigated. After a single (acute exposure) or repeated administration of dimethoate, rat cerebral cortex was found to inhibit acetylcholinesterase (AChE) activity in a dose-dependent manner. No significant alteration in the concentration of GABA or the numbers of GABAA receptor was noted in cortices of rats after acute exposure to dimethoate except the affinities of the receptor was found elevated significantly following the acute administration. But the GABA concentrations were significantly reduced in the 10 and 20 mg/kg groups after the subchronic dimethoate administration. No difference was found statistically in the GABAA receptor binding in cortices after the subchronic administration of dimethoate. But the Kd values were significant decreased reflecting an elevated affinity of receptors in the three dimethoate groups as compared with that of control follow subchronic administration. It is suggested that the GABAergic system is involved in the intoxication of the dimethoate intoxication which is probably to counteract the enhanced cholinergic activity induced by dimethoate.

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