Premium
Alcohol‐induced stress in painful alcoholic neuropathy
Author(s) -
Dina Olayinka A.,
Khasar Sachia G.,
AlessandriHaber Nicole,
Green Paul G.,
Messing Robert O.,
Levine Jon D.
Publication year - 2008
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.2007.05987.x
Subject(s) - corticosterone , endocrinology , medicine , glucocorticoid , peripheral neuropathy , mifepristone , ethanol , antagonist , epinephrine , sympathoadrenal system , alcohol , nociception , glucocorticoid receptor , hormone , receptor , chemistry , pregnancy , biology , biochemistry , organic chemistry , genetics , diabetes mellitus
Abstract Chronic alcohol consumption induces a painful small‐fiber peripheral neuropathy, the severity of which increases during alcohol withdrawal. Chronic alcohol consumption also produces a sustained increase in stress hormones, epinephrine and corticosterone, that is exacerbated during alcohol withdrawal. We report that adrenal medullectomy and administration of a glucocorticoid receptor antagonist, mifepristone (RU 38486), both prevented and reversed a model of painful peripheral neuropathy in alcohol binge‐drinking rats. Chronic administration of stress levels of epinephrine to rats that had undergone adrenal medullectomy and were being fed the alcohol diet reconstituted this phenotype. Intrathecal administration of oligodeoxynucleotides antisense to the β 2 ‐adrenergic‐ or glucocorticoid‐receptor also prevented and reversed the pro‐nociceptive effects of ethanol. Our results suggest a convergence of the effects of mediators of the hypothalamic‐pituitary‐ and sympathoadrenal‐stress axes on sensory neurons in the induction and maintenance of alcohol‐induced painful peripheral neuropathy.