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Brain Res. 1999 Jul 17;835(1):62-7.

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

Author information

1
Department of Psychology, Furman University, Greenville, SC 29613, USA.judy.grisel@furman.edu

Abstract

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.

PMID:
10448196
DOI:
10.1016/s0006-8993(99)01384-0
[Indexed for MEDLINE]

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