title: Glucocorticoid fast feedback is not altered in rats prenatally exposed to ethanol.
abstract: Animals exposed in utero to ethanol exhibit hormonal hyperresponsiveness to stressors in adulthood. One possible mechanism for this hyperresponsiveness is a deficit in negative feedback regulation of the hypothalamic-pituitary-adrenal axis. The present study tested the hypothesis that a deficit in the fast feedback time domain may play a role in the hormonal hyperresponsiveness in ethanol-exposed rats. Sprague-Dawley offspring from prenatal ethanol (E), pair-fed (PF), and ad lib-fed control (C) groups were tested in two experiments. Experiment 1 used a swim stress paradigm and tested animals at the trough of the corticosterone (CORT) circadian rhythm. Experiment 2 used ether stress and tested animals at the peak of the circadian rhythm. Animals were injected subcutaneously with CORT or saline and were immediately subjected to either a 5-min swim stress or a 1-min ether stress. Half the animals were terminated immediately after stress (5-min postinjection), and the rest were terminated 25 min later. Plasma levels of CORT and ACTH were assayed to determine whether E animals differed from control animals in showing a CORT-induced blunting of the ACTH response to the stressor, indicating alterations in fast feedback regulation. Injection of CORT significantly blunted the ACTH response to swim stress (experiment 1) in E, PF, and C females and males, compared with their saline-injected counterparts. There were no significant differences among groups. Similarly, CORT-injected males in E, PF, and C groups all exhibited a significantly blunted ACTH response to ether stress (experiment 2). CORT-injected C females also exhibited a significantly blunted ACTH response to ether stress, whereas E females showed an obvious CORT decrease that approached significance. However, PF females showed a clear deficit in fast feedback regulation. Together, these data suggest that: (1) CORT injection can serve as a fast feedback signal that can blunt the ACTH response to a stressor; and (2) prenatal ethanol exposure does not produce a deficit in hypothalamic-pituitary-adrenal feedback regulation in the fast feedback time domain.
authors.affiliation: Department of Psychology, Faculty of Medicine, University of British Columbia, Vancouver, Canada.
authors.forename: C
authors.initials: C
authors.lastname: Hofmann
authors.forename: M
authors.initials: M
authors.lastname: Glavas
authors.forename: W
authors.initials: W
authors.lastname: Yu
authors.forename: J
authors.initials: J
authors.lastname: Weinberg
mesh_terms: D000305:Adrenal Cortex Hormones / Q000097:blood*; D000324:Adrenocorticotropic Hormone / Q000097:blood; D000818:Animals; D003345:Corticosterone / Q000097:blood; D000431:Ethanol / Q000009:adverse effects* / Q000494:pharmacology; D005246:Feedback / Q000502:physiology*; D005260:Female; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D000305:Adrenal Cortex Hormones; D000431:Ethanol; D000324:Adrenocorticotropic Hormone; D003345:Corticosterone