Mifepristone Pretreatment Reduces Ethanol Withdrawal Severity In Vivo

Background Prolonged ethanol (EtOH) intake may perturb function of the hypothalamic–pituitary–adrenal axis in a manner that promotes dependence and influences EtOH withdrawal severity. Prior in vivo and in vitro studies suggest that corticosteroids, in particular, may be elevated during EtOH intoxic...

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Published in:Alcoholism, clinical and experimental research clinical and experimental research, 2013-08, Vol.37 (8), p.1417-1423
Main Authors: Sharrett-Field, Lynda, Butler, Tracy R., Berry, Jennifer N., Reynolds, Anna R., Prendergast, Mark A.
Format: Article
Language:English
Subjects:
Alcoholism
Alcoholism - prevention & control
Animals
Body Weight - drug effects
Corticosterone - blood
Dependence
Drug Evaluation, Preclinical
Eating - drug effects
Ethanol - administration & dosage
Ethanol - blood
Hormone
Hormone Antagonists - pharmacology
Hormone Antagonists - therapeutic use
Hypothalamic-Pituitary-Adrenal Axis
Male
Mifepristone - pharmacology
Mifepristone - therapeutic use
Rats
Rats, Sprague-Dawley
Receptors, Glucocorticoid - antagonists & inhibitors
Severity of Illness Index
Stress
Substance Withdrawal Syndrome - prevention & control
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Summary:Background Prolonged ethanol (EtOH) intake may perturb function of the hypothalamic–pituitary–adrenal axis in a manner that promotes dependence and influences EtOH withdrawal severity. Prior in vivo and in vitro studies suggest that corticosteroids, in particular, may be elevated during EtOH intoxication and withdrawal, suggesting that intracellular glucocorticoid receptors (GRs) may promote the development of EtOH dependence. Methods Adult male Sprague‐Dawley rats were subjected to a 4‐day binge‐like EtOH administration regimen (3 to 5 g/kg/i.g. every 8 hours designed to produce peak blood EtOH levels (BELs) of
ISSN:0145-6008
1530-0277
DOI:10.1111/acer.12093