Ethanol oral self-administration is increased in mutant mice with decreased beta-endorphin expression

Brain Res. 1999 Jul 17;835(1):62-7. doi: 10.1016/s0006-8993(99)01384-0.


The relationship between ethanol (EtOH) administration and the endogenous opioid system has been studied for many years and a considerable body of evidence supports the contention that EtOH modulates the production and/or release of endogenous opioid peptides. However, substantially less is known about the converse influence: the effect that opioids have on EtOH sensitivity. In this study, we used the beta-endorphin deficient mutant mouse line C57BL/6-Pomc1(tm1Low) to investigate the possible role of a specific opioid peptide on EtOH consumption. Homozygous knockout mice (entirely lacking beta-endorphin), heterozygous mice (50% beta-endorphin expression) and sibling wildtype mice from the same strain were evaluated in a two-bottle free choice paradigm for oral self-administration of EtOH. Across varying EtOH concentrations only the heterozygous mice were found to consistently drink more than wildtype mice. These data support the hypothesis that beta-endorphin modulates the response to EtOH.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Alcohol Drinking / genetics*
  • Alleles
  • Animals
  • Female
  • Genotype
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mutation / physiology*
  • Pro-Opiomelanocortin / biosynthesis
  • Pro-Opiomelanocortin / genetics
  • beta-Endorphin / biosynthesis
  • beta-Endorphin / deficiency*
  • beta-Endorphin / genetics


  • beta-Endorphin
  • Pro-Opiomelanocortin