Long-term effects of alcohol drinking on cerebral glucose utilization in alcohol-preferring rats

The 2-[14C]deoxyglucose (2-DG) quantitative autoradiography technique was used to determine rates of local cerebral glucose utilization (LCGU) in discrete brain regions in alcohol-chronic (A-C), alcohol-deprived (A-D) and alcohol-naïve (A-N) adult, male alcohol-preferring (P) rats. The hypothesis to be tested is that neuronal alterations occur as a result of chronic alcohol drinking and some of these alterations persist for long periods in the absence of alcohol. Following 6 weeks of daily 4-h scheduled access sessions to 15% (v/v) ethanol and water, group A-D received only water during the sessions over the next 2 weeks, whereas groups A-C and A-N continued to receive ethanol-water and water-water, respectively. On the 14th day of the deprivation interval, LCGU rates were measured 1 h prior to the scheduled access period. Mean ethanol intake for the A-D and A-C groups was 1.5+/-0.1 g ethanol/kg body weight per 4 h. LCGU rates were significantly decreased in 49 of 57 regions or subregions examined in the A-C group compared to the A-N group, including subregions of the cerebral cortex, hippocampus and structures in the mesocorticolimbic and nigrostriatal systems. Following alcohol deprivation, LCGU values in the A-D group were partially or completely returned to A-N levels in many, but not all, regions. In several limbic regions (e.g., ventral tegmental area, olfactory tubercle, medial prefrontal cortex, ventral pallidum and lateral septum), no recovery of LCGU rates was observed after 2 weeks of alcohol deprivation. This study demonstrates that chronic alcohol consumption produces significant reductions in functional neuronal activity in P rats, some of which persist in the absence of ethanol. The extent to which LCGU rates returned to normal levels following 2 weeks of alcohol deprivation varied among brain regions, suggesting that there are imbalanced interactions among and within several CNS sites, which do not reflect either the alcohol-naïve or chronic alcohol-exposed state. Such neuronal imbalances may underlie relapse of alcohol drinking following prolonged abstinence.