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Published on: January 7, 2019
Alcohol drinking in MCH receptor-1-deficient mice
Elizabeth A Duncan1, Joyce E Sorrell, Antoine Adamantidis
1Department of Psychiatry, University of Cincinnati, Cincinnati, Ohio, USA.
Alcoholism, Clinical and Experimental Research
|June 7, 2007
Summary
Mice lacking the MCH receptor-1 consumed significantly more alcohol, suggesting endogenous MCH signaling influences alcohol consumption. This finding may offer new insights into alcohol use disorders.
Area of Science:
- Neuroscience
- Endocrinology
- Behavioral Science
Background:
- Melanin-concentrating hormone (MCH) administration increases alcohol intake in rats.
- The physiological role of endogenous MCH in alcohol consumption remains unclear.
Purpose of the Study:
- To investigate the hypothesis that endogenous MCH signaling enhances alcohol consumption.
- To assess the impact of MCH receptor-1 deficiency on alcohol intake.
Main Methods:
- Alcohol consumption was measured in wildtype (WT), heterozygous (HET), and MCH receptor-1-deficient (KO) mice under various access conditions.
- Sucrose/quinine solutions were used to evaluate taste preference.
- Alcohol metabolism was assessed in WT and KO mice.
Main Results:
- Male KO mice consumed significantly more alcohol than WT and HET mice during ad libitum access.
- Alcohol intake did not differ between genotypes during limited access.
- Taste preference and alcohol metabolism were similar between WT and KO mice, suggesting they do not explain the increased alcohol consumption in KO mice.
Conclusions:
- Endogenous MCH signaling, particularly via MCH receptor-1, plays a role in regulating alcohol consumption.
- Male MCH receptor-1 deficient mice exhibit increased alcohol intake, independent of taste preference or metabolism.
- These findings contribute to understanding the neurobiological underpinnings of alcohol use.
