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Neurobehav Toxicol Teratol. 1985 Sep-Oct;7(5):511-7.

A model for later-life effects of perinatal drug exposure: maternal hormone mediation.


In the female rat chronic ethanol intake increased plasma levels of corticosterone; acute stress in the pregnant or lactating rat increased plasma levels of corticosterone in the fetuses or sucklings. In the lactating rat, corticosterone rapidly equilibrated between plasma and milk, so that variations in the mother's adrenocortical secretion could be promptly reflected in the suckling's body. The role of maternal adrenocortical hormone with regard to the development of pituitary-adrenocortical and behavioral activities was indicated by endocrine (plasma corticosterone), neurochemical (hippocampal corticosterone binding) and behavioral (avoidance performance) anomalies in the adult offspring of lactating rats with adrenocortical "hyperfunction" or "insufficiency." Further, the offspring of rats with adrenocortical "insufficiency" showed abnormalities in "in vitro" hypothalamus, pituitary and adrenocortex release of hormones. When searching for later effects in the offspring of drugs given to the mother in perinatal life one must be cognizant that, aside from their expected pharmacological action, drugs can produce variations in the mother pituitary-adrenocortical activity, sensed by the conceptus through the placenta or milk.

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