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Reduced alcohol consumption in mice lacking preprodynorphin.

Yuri A Blednov1, Danielle Walker, Marni Martinez

  • 1University of Texas, Waggoner Center for Alcohol and Addiction Research, 1 University Station A4800, Austin, TX 78712-0159, USA. yablednov@mail.utexas.edu

Alcohol (Fayetteville, N.Y.)
|February 20, 2007
PubMed
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Mice lacking the preprodynorphin gene showed reduced alcohol preference, especially females. This suggests dynorphins influence alcohol intake by affecting its rewarding taste and palatability.

Area of Science:

  • Neuroscience
  • Genetics
  • Pharmacology

Background:

  • Endogenous opioid peptides and their receptors regulate ethanol intake.
  • Kappa-opioid receptors and dynorphins are thought to induce dysphoria, promoting alcohol avoidance.

Purpose of the Study:

  • To investigate the role of preprodynorphin (dynorphin precursor) in ethanol intake regulation using knockout mice.
  • To determine if dynorphin deficiency affects alcohol preference, consumption, and related behaviors.

Main Methods:

  • Utilized preprodynorphin null mutant mice and wild-type littermates.
  • Conducted behavioral tests including two-bottle choice (alcohol, saccharin, sucrose) and assessment of ethanol-induced effects (loss of righting reflex, withdrawal, conditioned place preference, taste aversion).

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Main Results:

  • Female null mutant mice exhibited significantly lower alcohol preference and consumption compared to wild-type controls.
  • Both sexes of null mutant mice showed reduced saccharin preference but normal consumption under limited access.
  • Null mutant mice displayed reduced sucrose intake under limited access.
  • No differences were observed in ethanol-induced loss of righting reflex, acute withdrawal, conditioned place preference, or taste aversion.

Conclusions:

  • Deletion of preprodynorphin substantially reduces alcohol intake in female mice.
  • The reduction in alcohol intake is likely due to decreased orosensory reward, specifically the sweet taste and palatability of alcohol.