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 systems 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 lactating dams at birth. Central serotonergic function was determined by the ability of a serotonin releaser, p-chloroamphetamine (PCA), to stimulate 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 contrast, ACTH and corticosterone responses to the 5-HT releaser PCA were significantly attenuated (-28% to 43%) in cocaine progeny, while the renin response to PCA was unaffected. These data suggest that cocaine administration during pregnancy can produce long-term selective alterations in neuroendocrine responses mediated by central serotonergic systems in prepubescent female progeny.