COCAINE-INDUCED DEFICITS IN ACTH AND CORTICOSTERONE RESPONSES IN FEMALE RAT PROGENY

The objective of this study was to determine whether prenatal exposure to cocaine could produce functional changes in central serotonergic s ystems mediating neuroendocrine responses in female progeny. Pregnant rats were administered either saline or (-) cocaine (15 mg/kg, SC, b.i .d.) from gestational day 13-20. Progeny were fostered to nontreated l actating dams at birth. Central serotonergic function was determined b y the ability of a serotonin releaser, p-chloroamphetamine (PCA), to s timulate plasma adrenocorticotropin (ACTH), corticosterone, and renin secretion in female progeny at postnatal day (PD) 30. Prenatal cocaine did not alter basal levels of ACTH, corticosterone, or renin. In cont rast, ACTH and corticosterone responses to the 5-HT releaser PCA were significantly attenuated (-28 to 43%) in cocaine progeny, while the re nin response to PCA was unaffected. These data suggest that cocaine ad ministration during pregnancy can produce long-term selective alterati ons in neuroendocrine responses mediated by central serotonergic syste ms in prepubescent female progeny.