Document Detail


Chronic prenatal ethanol exposure alters glucocorticoid signalling in the hippocampus of the postnatal Guinea pig.
MedLine Citation:
PMID:  16101899     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The present study tested the hypothesis that chronic prenatal ethanol exposure causes long-lasting changes in glucocorticoid signalling in postnatal offspring. Pregnant guinea pigs were treated with ethanol (4 g/kg maternal body weight/day), isocaloric-sucrose/pair-feeding or water throughout gestation, and maternal saliva cortisol concentration was determined 2 h after treatment at different stages of gestation. Electrically-stimulated release of glutamate and GABA, in the presence or absence of dexamethasone, as well as glucocorticoid and mineralocorticoid receptor mRNA expression, was determined in the hippocampus and prefrontal cortex of adult offspring of treated pregnant guinea pigs. Maternal saliva cortisol concentration increased throughout pregnancy, which was associated with increased foetal plasma and amniotic fluid cortisol concentration. Ethanol administration to pregnant guinea pigs increased maternal saliva cortisol concentration during early and mid-gestation. In late gestation, ethanol administration did not increase saliva cortisol concentration above that induced by pregnancy. Chronic prenatal ethanol exposure had no effect on stimulated glutamate or GABA release, but selectively prevented dexamethasone-mediated suppression of stimulated glutamate release, and decreased expression of mineralocorticoid, but not glucocorticoid, receptor mRNA in the hippocampus of adult offspring. These data indicate that maternal ethanol administration leads to excessively increased maternal cortisol concentration that can impact negatively the developing foetal brain, leading to persistent postnatal deficits in glucocorticoid regulation of glutamate signalling in the adult hippocampus.
Authors:
U Iqbal; J F Brien; S Banjanin; M H Andrews; S G Matthews; J N Reynolds
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of neuroendocrinology     Volume:  17     ISSN:  0953-8194     ISO Abbreviation:  J. Neuroendocrinol.     Publication Date:  2005 Sep 
Date Detail:
Created Date:  2005-08-16     Completed Date:  2005-10-04     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  8913461     Medline TA:  J Neuroendocrinol     Country:  England    
Other Details:
Languages:  eng     Pagination:  600-8     Citation Subset:  IM    
Affiliation:
Department of Pharmacology and Toxicology, Queen's University, Kingston, Ontario, Canada.
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MeSH Terms
Descriptor/Qualifier:
Amniotic Fluid / metabolism
Animals
Animals, Newborn
Central Nervous System Depressants / toxicity*
Circadian Rhythm / physiology
Ethanol / toxicity*
Female
Glucocorticoids / physiology*
Glutamic Acid / metabolism
Guinea Pigs
Hippocampus / drug effects,  physiology*
Hydrocortisone / metabolism
In Situ Hybridization
Maternal-Fetal Exchange
Paraventricular Hypothalamic Nucleus / drug effects,  metabolism
Pregnancy
Prenatal Exposure Delayed Effects
RNA, Messenger / biosynthesis,  genetics
Receptors, Mineralocorticoid / drug effects
Saliva / metabolism
Signal Transduction / physiology*
gamma-Aminobutyric Acid / metabolism
Chemical
Reg. No./Substance:
0/Central Nervous System Depressants; 0/Glucocorticoids; 0/RNA, Messenger; 0/Receptors, Mineralocorticoid; 50-23-7/Hydrocortisone; 56-12-2/gamma-Aminobutyric Acid; 56-86-0/Glutamic Acid; 64-17-5/Ethanol

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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