Alcohol-induced stress in painful alcoholic neuropathy

  1. Olayinka A. Dina1,2,
  2. Sachia G. Khasar1,2,
  3. Nicole Alessandri-Haber1,2,
  4. Paul G. Green1,2,
  5. Robert O. Messing3,4,5,
  6. Jon D. Levine1,2,4,6

Article first published online: 17 DEC 2007

DOI: 10.1111/j.1460-9568.2007.05987.x

Issue

European Journal of Neuroscience

European Journal of Neuroscience

Volume 27, Issue 1, pages 83–92, January 2008

Additional Information

How to Cite

Dina, O. A., Khasar, S. G., Alessandri-Haber, N., Green, P. G., Messing, R. O. and Levine, J. D. (2008), Alcohol-induced stress in painful alcoholic neuropathy. European Journal of Neuroscience, 27: 83–92. doi: 10.1111/j.1460-9568.2007.05987.x

Author Information

  1. 1

    Department of Oral & Maxillofacial Surgery, University of California at San Francisco, CA 94143-0440, USA

  2. 2

    UCSF NIH Pain Center, University of California at San Francisco, CA 94143-0440, USA

  3. 3

    Department of Neurology, University of California at San Francisco, CA 94143-0440, USA

  4. 4

    Division of Neuroscience and Biomedical Sciences, University of California at San Francisco, CA 94143-0440, USA

  5. 5

    Ernest Gallo Clinic and Research Center, Emeryville, CA 94608, USA

  6. 6

    Department of Medicine, University of California at San Francisco, CA 94143-0440, USA

*Dr J.D. Levine, as above.2 E-mail: Jon.Levine@ucsf.edu

Publication History

  1. Issue published online: 20 DEC 2007
  2. Article first published online: 17 DEC 2007
  3. Received 2 July 2007, revised 2 November 2007, accepted 9 November 2007

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Keywords:

  • catecholamines;
  • glucocorticoids;
  • hyperalgesia;
  • neuroendocrine;
  • pain

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 β2-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.

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