Hypo-response of the hypothalamic-pituitary-adrenocortical axis after an ethanol challenge in prenatally stressed adolescent male rats
European Journal of Neuroscience. 2006-08-01; 24(4): 1193-1200
DOI: 10.1111/j.1460-9568.2006.04973.x
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The period of adolescence and environmental factors, such as stress, are
important in determining ethanol vulnerability in both humans and rats. Ethanol
is a powerful activator of the hypothalamic-pituitary-adrenal (HPA) axis but
attenuated responses of the HPA axis to ethanol have been described in
populations with a high risk of ethanol abuse. In rats, prenatal stress leads to
prolonged stress-induced corticosterone secretion and increases the vulnerability
to drugs of abuse, such as amphetamine and nicotine in adulthood and
3,4-methylenedioxymethamphetamine in adolescent rats. The aim of the present
study was to assess the impact of a prenatal stress on HPA axis responsiveness to
a moderate dose of ethanol (1.5 g/kg i.p.) in adolescent male rats (28 days old).
The parameters evaluated were plasma adrenocorticotropic hormone, plasma
corticosterone and mRNA expression of HPA axis central markers (mineralocorticoid
receptor, glucocorticoid receptor, corticotropin-releasing hormone and
pro-opiomelanocortin). Contrary to prior expectations, our results demonstrate
that prenatal stress blunts the HPA axis responsiveness to a moderate dose of
ethanol in adolescent rats in spite of similar blood ethanol levels. These data
suggest that prenatal stress may have the opposite effect on the response to
stress depending on the attributes of the stressor stimulus. They thus raise
questions about the possible impact of prenatal stress on the further development
of ethanol vulnerability.
DOI: 10.1111/j.1460-9568.2006.04973.x
PMID: 16925589 [Indexed for MEDLINE]