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Human and Animal Genetics
Ethanol Sensitivity in High Drinking in the Dark Selectively Bred Mice
Article first published online: 8 FEB 2012
DOI: 10.1111/j.1530-0277.2012.01735.x
Copyright © 2012 by the Research Society on Alcoholism
Additional Information
How to Cite
Crabbe, J. C., Kruse, L. C., Colville, A. M., Cameron, A. J., Spence, S. E., Schlumbohm, J. P., Huang, L. C. and Metten, P. (2012), Ethanol Sensitivity in High Drinking in the Dark Selectively Bred Mice. Alcoholism: Clinical and Experimental Research, 36: 1162–1170. doi: 10.1111/j.1530-0277.2012.01735.x
Publication History
- Issue published online: 10 JUL 2012
- Article first published online: 8 FEB 2012
- Manuscript Accepted: 2 DEC 2011
- Manuscript Received: 26 JUL 2011
Funded by
- NIAAA
- US Department of Veterans Affairs
- Abstract
- Article
- References
- Cited By
Keywords:
- Selected Mouse Lines;
- High Drinking in the Dark Mice;
- Activity;
- Hypothermia;
- Loss of Righting Reflex;
- Ataxia;
- Genetic Correlation
Background
Mouse lines are being selectively bred in replicate for high blood ethanol concentrations (BECs) achieved after a short period of ethanol (EtOH) drinking early in the circadian dark phase. High Drinking in the Dark-1 (HDID-1) mice were in selected generation S18, and the replicate HDID-2 line in generation S11.
Methods
To determine other traits genetically correlated with high DID, we compared naïve animals from both lines with the unselected, segregating progenitor stock, HS/Npt. Differences between HDID-1 and HS would imply commonality of genetic influences on DID and these traits.
Results
HDID-1 mice showed less basal activity, greater EtOH stimulated activity, and greater sensitivity to EtOH-induced foot slips than HS. They showed lesser sensitivity to acute EtOH hypothermia and longer duration loss of righting reflex than HS. HDID-1 and control HS lines did not differ in sensitivity on 2 measures of intoxication, the balance beam and the accelerating rotarod. None of the acute response results could be explained by differences in EtOH metabolism. HDID-2 differed from HS on some, but not all, of the above responses.
Conclusions
These results show that some EtOH responses share common genetic control with reaching high BECs after DID, a finding consistent with other data regarding genetic contributions to EtOH responses.