Ethanol oral self-administration is increased in mutant mice with decreased beta-endorphin expression.
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.
Grisel
J E
JE
Department of Psychology, Furman University, Greenville, SC 29613, USA.judy.grisel@furman.edu
Mogil
J S
JS
Grahame
N J
NJ
Rubinstein
M
M
Belknap
J K
JK
Crabbe
J C
JC
Low
M J
MJ
D000428:Alcohol Drinking / Q000235:genetics*; D000483:Alleles; D000818:Animals; D005260:Female; D005838:Genotype; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009154:Mutation / Q000502:physiology*; D011333:Pro-Opiomelanocortin / Q000096:biosynthesis / Q000235:genetics; D001615:beta-Endorphin / Q000096:biosynthesis / Q000172:deficiency* / Q000235:genetics
D001615:beta-Endorphin; D011333:Pro-Opiomelanocortin