Hypo-response of the hypothalamic-pituitary-adrenocortical axis after an ethanol challenge in prenatally stressed adolescent male rats

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...

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Veröffentlicht in:The European journal of neuroscience 2006-08, Vol.24 (4), p.1193-1200
Hauptverfasser: Van Waes, Vincent, Enache, Mihaela, Dutriez, Isabelle, Lesage, Jean, Morley-Fletcher, Sara, Vinner, Elisabeth, Lhermitte, Michel, Vieau, Didier, Maccari, Stefania, Darnaudéry, Muriel
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container_title The European journal of neuroscience
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creator Van Waes, Vincent
Enache, Mihaela
Dutriez, Isabelle
Lesage, Jean
Morley-Fletcher, Sara
Vinner, Elisabeth
Lhermitte, Michel
Vieau, Didier
Maccari, Stefania
Darnaudéry, Muriel
description 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_str_mv 10.1111/j.1460-9568.2006.04973.x
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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). 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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. 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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.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>16925589</pmid><doi>10.1111/j.1460-9568.2006.04973.x</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0003-0209-3880</orcidid></addata></record>
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subjects adrenocorticotropic hormone
Adrenocorticotropic Hormone - blood
alcohol
Animals
Body Weight
corticosterone
Corticosterone - blood
corticotropin-releasing hormone
Corticotropin-Releasing Hormone - genetics
Corticotropin-Releasing Hormone - metabolism
Dentate Gyrus - cytology
Dentate Gyrus - metabolism
Ethanol - pharmacology
Female
Humans
Hypothalamo-Hypophyseal System - drug effects
Hypothalamo-Hypophyseal System - physiology
Life Sciences
Male
maternal stress
Neurons and Cognition
Paraventricular Hypothalamic Nucleus - cytology
Paraventricular Hypothalamic Nucleus - metabolism
Pituitary Gland - cytology
Pituitary Gland - metabolism
Pituitary-Adrenal System - drug effects
Pituitary-Adrenal System - physiology
Pregnancy
Pro-Opiomelanocortin - genetics
Pro-Opiomelanocortin - metabolism
Rats
Rats, Sprague-Dawley
Receptors, Glucocorticoid - genetics
Receptors, Glucocorticoid - metabolism
Receptors, Mineralocorticoid - genetics
Receptors, Mineralocorticoid - metabolism
RNA, Messenger - metabolism
Stress, Psychological
title Hypo-response of the hypothalamic-pituitary-adrenocortical axis after an ethanol challenge in prenatally stressed adolescent male rats
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