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Glucocorticoid receptor antagonism decreases alcohol seeking in alcohol-dependent individuals

Academic Article
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Overview

authors

  • Vendruscolo, L. F.
  • Estey, D.
  • Goodell, V.
  • Macshane, L. G.
  • Logrip, M. L.
  • Schlosburg, J. E.
  • McGinn, M. A.
  • Zamora-Martinez, E. R.
  • Belanoff, J. K.
  • Hunt, H. J.
  • Sanna, Pietro
  • George, Olivier
  • Koob, George
  • Edwards, S.
  • Mason, Barbara

publication date

  • August 2015

journal

  • Journal of Clinical Investigation  Journal

abstract

  • Alcoholism, or alcohol use disorder, is a major public health concern that is a considerable risk factor for morbidity and disability; therefore, effective treatments are urgently needed. Here, we demonstrated that the glucocorticoid receptor (GR) antagonist mifepristone reduces alcohol intake in alcohol-dependent rats but not in nondependent animals. Both systemic delivery and direct administration into the central nucleus of the amygdala, a critical stress-related brain region, were sufficient to reduce alcohol consumption in dependent animals. We also tested the use of mifepristone in 56 alcohol-dependent human subjects as part of a double-blind clinical and laboratory-based study. Relative to placebo, individuals who received mifepristone (600 mg daily taken orally for 1 week) exhibited a substantial reduction in alcohol-cued craving in the laboratory, and naturalistic measures revealed reduced alcohol consumption during the 1-week treatment phase and 1-week post-treatment phase in mifepristone-treated individuals. Mifepristone was well tolerated and improved liver-function markers. Together, these results support further exploration of GR antagonism via mifepristone as a therapeutic strategy for alcoholism.

subject areas

  • Administration, Oral
  • Adult
  • Alcohol Drinking
  • Alcoholism
  • Animals
  • Female
  • Hormone Antagonists
  • Humans
  • Male
  • Mifepristone
  • Rats
  • Receptors, Glucocorticoid
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Identity

International Standard Serial Number (ISSN)

  • 0021-9738

Digital Object Identifier (DOI)

  • 10.1172/jci79828

PubMed ID

  • 26121746
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Additional Document Info

start page

  • 3193

end page

  • 3197

volume

  • 125

issue

  • 8

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