Role of GABA receptor complex in low dose lindane (HCH) induced neurotoxicity: neurobehavioural, neurochemical and electrophysiological studies.

摘要

Lindane is widely used as an insecticide and scabicide in mammals. High doses in chronic exposures caused hyperexcitability and convulsions and impaired motor activity involving GABA-ergic mechanism. To investigate the role of GABA/Benzodiazepine mechanism in the neurotoxicity of low doses of lindane, rats were administered 2, 3, or 5 mg/kg orally for 90 days and behavioural, electrophysiological, and neurochemical studies were conducted. The animals exposed to lindane exhibited increased geotaxis and decreased spontaneous drug-induced locomotor activity (which further potentiated by phenobarbitone and increased after leptazol). The EEG of the treated rats showed high voltage slow-wave activity (HVSA) patterns with occasional spindles (9-10 HZ-amplitude of 100 uv). A significant increase (p < 0.01) in GABA levels in cerebellum and significant increase in benzodiazepine receptors in cerebellar membrane measured by (3H)flunitrazepam binding were observed in the animals exposed to 3 and 5 mg lindane. The study suggests that low dose chronic exposure of lindane causes neurobehavioral, neurochemical, and electrophysiological effects involving GABA-ergic mechanism(s).