The functional outcome of the dynamic interplay between the greater susceptibility to disruption and the greater capacity for reorganization and recovery (or sparing) of function of the immature central nervous system was examined with respect to maturation of the hypothalamic-pituitary-adrenal axis and the hippocampus. Various toxicants were used to perturb these systems. Neonatal exposure to chlordecone, an organochlorine insecticide, produced functional imbalances in circulating and adrenal steroids as well as extremely rapid and apparently permanent changes in adrenal morphology. These changes were mirrored in behavioral dysfunction indicative of alterations in the sexual differentiation of hypothalamic nuclei and were not attributable to the long-term presence of chlordecone in neural tissue. Neonatal exposure to triethyl lead (TEL), the active metabolite of leaded gasoline, produced a preferential and permanent destruction of hippocampal pyramidal cell fields as indicated by quantitative neuromorphometry. Distributional and pharmacokinetic studies indicate this permanent brain damage was highly related to the early accumulation of lead in specific limbic regions of the central nervous system, but not to its persistence through adulthood. Prenatal exposure to carbon monoxide, with carboxyhemoglobin levels within the range experienced by cigarette smokers, was used to induce mild tissue hypoxia. The disruption of hippocampal function previously suggested by impairment in acquisition and retention of a two-way avoidance task in juvenile-aged offspring was substantially attenuated upon maturation to adulthood. However, a marked exacerbation of learning and memory dysfunction was noted with continued aging.
