Widespread neuroanatomical damage and learning deficits following chronic alcohol consumption or vitamin-B1 (thiamine) deficiency in rats.

Consequences of long-term consumption of alcohol (20 months) and of pyrithiamine-induced blockade of vitamin-B1-uptake on the shape of individual brain structures and on the acquisition of two learning tasks have been investigated in 3 groups of rats (alcohol group, AL; thiamine-deficient group, TH; control group, CG). Groups AL and TH wee allowed an 8, or 3 week recovery period, respectively, with normal food and water available ad libitum before behavioral testing started. This consisted of training an active two-way avoidance task and a spatial reversal task. Rats of both experimental groups were, compared to rats of the control group, significantly impaired in acquiring the avoidance task and in acquiring the original discrimination of the spatial reversal task. No differences were found among the two experimental groups. Histological and microscopical examinations of the brains of the rats with a history of thiamine-deficiency or of chronic alcohol consumption revealed a variety of severely affected brain areas. In both groups hippocampal and cerebellar damage was prominent. Furthermore, the mamillary nuclei, certain brainstem regions situated around the ventricles and a few cortical areas contained loss or damage of neurons. It is concluded that the anatomical changes, especially, can be related to those seen in chronic alcoholics and that consequently animal models can be established to investigate in detail the multiple interactions of alcohol consumption, thiamine deficiency, brain damage and behavioral deterioration.