Inhibitory effects of passive ethanol exposure on brain neurogenesis have been extensively documented in animal models. In contrast, a role of brain neurogenesis in ethanol self-administration has not been addressed, as yet.
The aim of the present study was to assess intake of, and preference for, ethanol solutions [2-16% (v/v)] in a mouse model of adult neurogenesis deficiency based on permanent knockout (KO) of cyclin D2. Wild-type (WT) and cyclin D2 KO mice did not differ in 2% and 4% ethanol intake.
The KO group consumed significantly more ethanol in g/kg when offered with 8% or 16% ethanol as compared to the WT controls. The WT and KO mice did not differ in 2% ethanol preference but the KO group showed a significantly higher preference for 4-16% ethanol.
Animal and human studies have suggested that the low level of response to the sedative/hypnotic effects of alcohol is genetically associated with enhanced alcohol consumption.
However, in the present study, there were no between-genotype differences in ethanol-induced loss of righting reflex.
Previous reports have also suggested that high ethanol intake is genetically associated with the avidity for sweets and better acceptance of bitter solutions. However, the KO and WT mice consumed similar amounts of saccharin solutions and the KOs consumed less quinine (i.e. bitter) solutions as compared to the WTs.
In conclusion, the present results may indicate that cyclin D2 and, possibly, brain neurogenesis is involved in central regulation of ethanol intake in mice.
