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Mu-opioid receptor knockout mice do not self-administer alcohol

Academic Article
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Overview

authors

  • Roberts, Amanda
  • McDonald, J. S.
  • Heyser, C. J.
  • Kieffer, B. L.
  • Matthes, H. W. D.
  • Koob, George
  • Gold, L. H.

publication date

  • June 2000

journal

  • Journal of Pharmacology and Experimental Therapeutics  Journal

abstract

  • Opioid peptides long have been hypothesized to play a role in ethanol reinforcement. Neuropharmacological studies have shown that opioid receptor antagonists decrease ethanol self-administration in rodents and prevent relapse in humans. However, the exact mechanism for such powerful effects has remained elusive. The availability of mu-opioid receptor knockout mice has made possible the direct examination of the role of the mu-opioid receptor in mediating ethanol self-administration. In the present experiments, both nosepoke and lever operant ethanol self-administration and several tests of two bottle-choice ethanol drinking were studied in these genetically engineered mice. In no case did knockout mice show evidence of ethanol self-administration, and, in fact, these mice showed evidence of an aversion to ethanol under several experimental conditions. These data provide new evidence for a critical role for mu-opioid receptors in ethanol self-administration assessed with a variety of behavioral paradigms and new insights into the neuropharmacological basis for ethanol reinforcement.

subject areas

  • Alcohol Drinking
  • Animals
  • Conditioning, Operant
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Receptors, Opioid, mu
  • Reinforcement (Psychology)
  • Self Administration
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Identity

International Standard Serial Number (ISSN)

  • 0022-3565

PubMed ID

  • 10869404
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Additional Document Info

start page

  • 1002

end page

  • 1008

volume

  • 293

issue

  • 3

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