PharmacyNeuroscienceToxicologyDevelopmental NeuroscienceDevelopmental ToxicologyNeurotoxicologyDevelopmental NeurotoxicityDevelopmental NeurotoxicologyNeonatal DevelopmentPerinatal ToxicologyPrenatal DevelopmentPrenatal ToxicityDevelopmental Neurotoxicity In AnimalsEarly-life Neurotoxic ExposureFetal NeurotoxicityNeurobehavioral DevelopmentPerinatal Drug ExposurePerinatal Exposure EffectsPrenatal Neurotoxicity
Fischer-344 rats were exposed throughout gestation and the first 12 days of lactation to 1 or 6 ppm chlordecone via the maternal diet. Exposure to chlordecone had no effect on maternal weight gains after gestation nor did it affect birth weights, litter sizes, or sex ratio of the litters. Offspring tested at 30 and 100 days of age for behavioral performance showed no significant changes in fore- and hindlimb grip strength, spontaneous motor activity, startle responsiveness, or tail flick latencies to thermal stimulation. Negative geotaxis latencies were not affected at 30 days of age, but were increased in males at 100 days of age. Male rats exposed to chlordecone were found to be hypersensitive to the motility increasing effects of 1 mg/kg of apomorphine, which is a dopamine receptor agonist. In another pharmacological challenge with 2 mg/kg of d-amphetamine, a presynaptic releaser or dopamine and norepinephrine, the motility response was not significantly exaggerated in chlordecone exposed rats. These results suggest that fetal and neonatal exposure to chlordecone produces subtle alterations in the neurogenic function of rats.