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The aim of this study was to investigate differences in shock-prod induced defensive burying and vulnerability to stress gastric ulcerations in two lines of rats selectively bred for alcohol-preference (AA) and alcohol-avoidance (ANA). Alcohol-naïve animals from the AA and ANA lines were tested in the shock-prod defensive burying test and (after an interval of approximately 2 months) in a 75 min water-immersion stress ulceratjon-inducing procedure. The AA rats showed longer latencies (327.5 s) for burying after shock-prod compared with the ANA animals (128.0 s). Furthermore, the ANA rats developed more stomach ulcerations (12.35 mm) compared with the AA rats (1.30 mm). Animals also differed based on whether they had been tested for defensive burying or not, with the tested animals showing less ulceration development than the control group. We hypothesize that the difference between AA and ANA rats is controlled by some common biochemical mechanism. One likely candidate is the dopaminergic system, which is involved in both the motivational effects of alcohol, as well as anxiety and stomach ulceration. In addition, the alcohol-preferring strain seems to be less fearful and generally may be less sensitive to aversive stimuli, be it shock prod, the aversive properties of alcohol, or water immersion stress. [ABSTRACT FROM AUTHOR]

Aging and chronic alcohol consumption can cause degenerative changes in the cerebellar cortex. In this study, the effects of aging and lifelong alcohol consumption on cerebellar cortical layer volumes (molecular and granular) and also white matter layer volumes were studied in alcohol-preferring (AA) and nonpreferring (ANA) rats of both sexes. The ethanol-consuming animals (EtOH) had 12% (w/v) ethanol as the only available fluid from 4 to 22 months of age, whereas the young (3 month) and old controls (24 months) had only water to drink. The volumes of molecular, granular, and white matter layers of the cerebellar vermis in folia II, IV, VII, and X were measured by using systematic sampling and a point-counting method. The volumes of the granular and white matter layers showed consistent increase between 3 and 24 months of age, whereas the volume of the molecular layer remained unchanged with increasing age. Individual ethanol intake was measured over a 1-week period at the beginning and at the end of chronic ethanol exposure. Significant (ANOVA, P= 0.000) sex difference was found in the drinking behavior in both lines, with females consuming more alcohol than males (daily ethanol consumption at 22 months of age 3.2 ± 0.3 vs. 7.1 ± 0.3 g/kg for AA males and females; 3.2 ± 0.3 vs. 5.4 ± 0.4 g/kg for ANA males and females, respectively). The only ethanol-induced effect on the cerebellum was observed in ANA-EtOH females with a 15% reduction in the volumes of the molecular and granular layer in folium II compared with age-matched controls and a significant ( P < 0.05, analysis of covariance with ethanol intake as a covariate) line difference in folium II (molecular and granular layers) was observed between ANA-EtOH females and AA-EtOH females. Furthermore, the volume of the molecular layer in folium II was significantly ( P < 0.05, analysis of covariance with ethanol intake and body weights as covariates) reduced for ANA-EtOH females, compared with ANA-EtOH males indicating a sex difference in the cerebellar degeneration due to chronic alcohol consumption. Of the three layers studied, the white matter layer was the most resistant layer to the effects caused by chronic alcohol consumption. In view of the fact that AA and ANA rats of both sexes differ regarding the drinking behavior and ethanol metabolism, they provide an important model for further research on ethanol-induced pathological changes in the central nervous system. [ABSTRACT FROM AUTHOR]