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Increased ethanol intake and preference in cyclin D2 knockout mice
P Jaholkowski1, P Mierzejewski, P Zatorski
1Laboratory of Molecular Neurobiology, Nencki Institute, Warsaw, Poland.
Genes, Brain, and Behavior
|March 25, 2011
Summary
Cyclin D2 (Ccnd2) knockout mice, deficient in brain neurogenesis, showed increased ethanol intake and preference at higher concentrations. This suggests Ccnd2 and neurogenesis play a role in regulating alcohol consumption.
Area of Science:
- Neuroscience
- Genetics
- Pharmacology
Background:
- Passive ethanol exposure impacts brain neurogenesis.
- The role of neurogenesis in ethanol self-administration remains unclear.
Purpose of the Study:
- To investigate the role of adult neurogenesis in ethanol intake and preference.
- To utilize a cyclin D2 (Ccnd2) knockout mouse model with deficient neurogenesis.
Main Methods:
- Compared ethanol intake and preference (2-16% solutions) in wild-type (WT) and Ccnd2 knockout (KO) mice.
- Assessed ethanol-induced loss of righting reflex.
- Evaluated responses to saccharin and quinine solutions.
Main Results:
- Ccnd2 KO mice consumed more ethanol (8-16%) and showed higher preference (4-16%) than WT mice.
- No significant differences in ethanol intake (2-4%), preference (2%), or sedative effects were observed.
- KO mice consumed similar saccharin amounts but less quinine than WT mice.
Conclusions:
- Results suggest Ccnd2 and brain neurogenesis are involved in the central regulation of ethanol intake.
- This provides insight into the neurobiological mechanisms underlying alcohol consumption.
