Chlordecone became widely recognized as a neurotoxicant when, in 1975, several individuals received high level acute exposure in a factory in Hopewell, Virginia. Symptoms of exposure include tremors, hyperreactivity, and reproductive malfunction. Since tremor and hyperreactivity are indicative of functional changes in the CNS, we are investigating the effects of chlordecone poisoning on neurotransmitter receptor binding site density, levels, and turnover; and levels of neuroactive peptides are being examined. Pituitary gonadotrophins and steroid hormone levels are being measured to assess the contribution of neuroendocrine changes to the neurotoxicity of chlordecone. In addition, the interaction of chlordecone with the estrogen receptor is being measured and the effect of estrogen on symptoms of chlordecone neurotoxicity are being examined.