Organochlorine chemicals such as chlordecone, p,p'-DDT and lindane are widely used in developing countries and to a lesser extent in some industrialized countries. The purpose of this research is to characterize in an animal model the behavioral and neurological toxicity of chlordecone and study the mechanisms by which chlordecone and other organochlorine chemicals produce their neurotoxic effects. Our experiments have shown in rats that chlordecone-induced tremor can be differentiated from that of p,p'-DDT and permethrin by spectral analysis techniques. Lindane is convulsive, but not tremorigenic, while o,p'-DDT and mirex produce little neurotoxicity in rats. Pharmacological and neurochemical studies have indicated that the origin of the tremor is in the brain stem. While chlordecone and p,p'-DDT are similar in that they increase the turnover of serotonin and norepinephrine, they differ in that p,p'-DDT increases dopamine turnover and increases levels of excitatory amino acid transmitters; chlordecone has no effects on these measures. Other studies have shown that dilantin markedly attenuates the tremor produced by p,p'-DDT and permethrin and exacerbates the effects of chlordecone and lindane. These data support the interpretation that p,p'-DDT and permethrin act by holding the sodium channel open and indicate that chlordecone and lindane have different mechanisms of action. Future studies will concern the possible role of calcium in the neurotoxicity produced by these agents and the neuropharmacological basis for other neurobehavioral effects produced by these agents.