“…Of particular relevance to the present study, prenatal ethanol exposure is known to alter the responsivity and regulation of the hypothalamic-pituitary-adrenal (HPA) axis. Under nonstressed conditions, rats prenatally exposed to ethanol (E) typically exhibit normal levels of the stress hormones adrenocorticotropin (ACTH) and corticosterone (CORT) (Kim et al, 1999b;Osborn et al, 1996;Taylor et al, 1983;Weinberg, 1992;Weinberg and Gallo, 1982), released from the anterior pituitary and adrenal glands, respectively. However, in response to stressors including intermittent foot shock (Nelson et al, 1986), novel environment (Weinberg, 1988), restraint (Gabriel et al, 2001;Weinberg, 1988Weinberg, , 1992, ether (Angelogianni and Gianoulakis, 1989;Weinberg and Gallo, 1982), and cold (Angelogianni and Gianoulakis, 1989;Kim et al, 1999a), as well as to drugs such as ethanol and morphine (Nelson et al, 1986;Taylor et al, 1981) and to immune challenges (Lee and Rivier, 1996;Lee et al, 2000), E animals show increased and/or prolonged ACTH and/or CORT elevations compared with controls (C).…”