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

GRISEL JE, MOGIL JS, GRAHAME NJ, RUBINSTEIN M, BELKNAP JK, CRABBE JC, LOW MJ

BRAIN RESEARCH

ELSEVIER SCIENCE BV

Lugar: Amsterdam; Año: 1999 vol. 835 p. 62 - 67

0006-8993

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.