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Ethanol Sensitivity in High Drinking in the Dark Selectively Bred Mice

Authors

  • John C. Crabbe,

    Corresponding author
    • Portland Alcohol Research Center, Department of Behavioral Neuroscience, Oregon Health & Science University, and VA Medical Center, Portland, Oregon
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  • Lauren C. Kruse,

    1. Portland Alcohol Research Center, Department of Behavioral Neuroscience, Oregon Health & Science University, and VA Medical Center, Portland, Oregon
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  • Alexandre M. Colville,

    1. Portland Alcohol Research Center, Department of Behavioral Neuroscience, Oregon Health & Science University, and VA Medical Center, Portland, Oregon
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  • Andy J. Cameron,

    1. Portland Alcohol Research Center, Department of Behavioral Neuroscience, Oregon Health & Science University, and VA Medical Center, Portland, Oregon
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  • Stephanie E. Spence,

    1. Portland Alcohol Research Center, Department of Behavioral Neuroscience, Oregon Health & Science University, and VA Medical Center, Portland, Oregon
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  • Jason P. Schlumbohm,

    1. Portland Alcohol Research Center, Department of Behavioral Neuroscience, Oregon Health & Science University, and VA Medical Center, Portland, Oregon
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  • Lawrence C. Huang,

    1. Portland Alcohol Research Center, Department of Behavioral Neuroscience, Oregon Health & Science University, and VA Medical Center, Portland, Oregon
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  • Pamela Metten

    1. Portland Alcohol Research Center, Department of Behavioral Neuroscience, Oregon Health & Science University, and VA Medical Center, Portland, Oregon
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Reprint requests: John C. Crabbe, PhD, VA Medical Center (R&D 12), Portland, OR 97239; Tel.: 503-273-5298; Fax: 503-721-1029; E-mail: crabbe@ohsu.edu

Abstract

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.

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