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

Judith E. Grisel, Jeffrey S. Mogil, Nicholas J. Grahame, Marcelo Rubinstein, John K. Belknap, John C. Crabbe, Malcolm J. Low

Research output: Contribution to journalArticlepeer-review

80 Scopus citations


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 β-endorphin deficient mutant mouse line C57BL/6-Pomcl(tm/Low) to investigate the possible role of a specific opioid peptide on EtOH consumption. Homozygous knockout mice (entirely lacking β-endorphin), heterozygous mice (50% β-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 β- endorphin modulates the response to EtOH.

Original languageEnglish (US)
Pages (from-to)62-67
Number of pages6
JournalBrain research
Issue number1
StatePublished - Jul 17 1999
Externally publishedYes


  • C57BL/6 mouse
  • Endogenous opioid
  • Null mutant
  • Oral self-administration
  • β-endorphin

ASJC Scopus subject areas

  • Neuroscience(all)
  • Molecular Biology
  • Clinical Neurology
  • Developmental Biology


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