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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.

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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.