REDUCTION OF REGIONAL BRAIN GLUCOSE-METABOLISM FOLLOWING DIFFERENT DURATIONS OF CHRONIC ETHANOL-CONSUMPTION IN MICE - A SELECTIVE EFFECT ONDIENCEPHALIC STRUCTURES

The effects of chronic alcohol consumption on regional brain glucose m etabolism were examined in Balb/c mice using the [C-14]2-deoxyglucose autoradiographic technique. Animals were given a solution of 12% v/v e thanol as their only source of fluid for either 6, 12 or 18 months and compared to control groups receiving either an isocaloric solution of saccharose or tap water. Alterations of cerebral brain glucose metabo lism were assessed in mice who were returned to a non-alcoholic diet a nd allowed to freely explore a T-maze. The results showed that chronic ethanol consumption induced reductions of regional metabolic activity which were functions both of the duration of alcohol treatment and of the structure studied. Whereas a six month period of alcoholization d id not induce any significant effects on metabolic activity, 12 months of treatment were necessary to induce the first observable and signif icant reductions in [C-14]2-deoxyglucose labelling. These effects were mainly limited to diencephalic structures such as the lateral mammill ary nuclei and the anterodorsal thalamic nuclei. The cerebellum was al so affected, but to a lesser degree. After 18 months of alcoholization , a generalized spread of the metabolic reduction to the entire mammil lary complex (lateral, medial and posterior nuclei) and to the thalami c nuclei was observed. This same duration of treatment was necessary t o induce the first detectable decrease of metabolic activity in the hi ppocampus. In agreement with data from human neuropathology, these fin dings confirm the particular vulnerability of diencephalic structures to ethanol and suggest that damage limited to diencephalic regions rat her than to hippocampal or cortical areas could be primarily responsib le for the memory disorders observed in Korsakoff's syndrome.