DOI: 10.1159/000406886
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Neonatal and Long-Term Neuroendocrine Effects of Fetal Alcohol Exposure1

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Cited by 26 publications
(28 citation statements)
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“…Taken together, these findings indicate that a number of physiological measures normally associated with stress are enhanced in pups exposed to alcohol prenatally. The fact that alcohol-treated animals, when adult, were no more sensitive than controls to the cold stressor indicates that alcohol-treated animals do acquire normal thermoregulatory abilities, even though they may be delayed in such development (Taylor, Branch, Kokka, & Poland, 1983). This is in accord with a hypothesis linking the hyperactivity seen in juvenile alcohol-treated offspring with an initial absence of thermoregulatory ability.…”
Section: Discussionsupporting
confidence: 59%
“…Taken together, these findings indicate that a number of physiological measures normally associated with stress are enhanced in pups exposed to alcohol prenatally. The fact that alcohol-treated animals, when adult, were no more sensitive than controls to the cold stressor indicates that alcohol-treated animals do acquire normal thermoregulatory abilities, even though they may be delayed in such development (Taylor, Branch, Kokka, & Poland, 1983). This is in accord with a hypothesis linking the hyperactivity seen in juvenile alcohol-treated offspring with an initial absence of thermoregulatory ability.…”
Section: Discussionsupporting
confidence: 59%
“…Furthermore, reductions in hippocampal cell loss in H animals may influence their performance on tasks associated with spatial learning and memory because performance on such spatial tasks as the Morris water maze has been shown to be disrupted by bilateral lesions to the hippocampus (Morris, Garrud, Rawlings, & O'Keefe, 1982). In contrast to the effects of handling, prenatal ethanol exposure results in prolonged and/or enhanced adrenocort cotropin hormone (ACTH) and CORT responses to a variety of stressors (Taylor, Branch, Kokka, & Poland, 1983;Weinberg, 1992;1993;Angelogianni & Gianoulakis, 1989;Taylor, Branch, Liu, & Kokka, 1982). Therefore, not only may impaired performance on spatial learning and memory tasks in E animals be related to stress-induced performance deficits associated with increased HPA activity but aging E animals also may experience an accelerated rate of impairment in hippocampal-mediated functions.…”
Section: Introductionmentioning
confidence: 99%
“…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).…”
mentioning
confidence: 99%