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

The 2-[C-14]deoxyglucose (2-DG) quantitative autoradiography technique was used to determine rates of local cerebral glucose utilization (LCGU) in dis crete brain regions in alcohol-chronic (A-C), alcohol-deprived (A-D) and al cohol-naive (A-N) adult, male alcohol-preferring (P) rats. The hypothesis t o be tested is that neuronal alterations occur as a result of chronic alcoh ol drinking and some of these alterations persist for long periods in the a bsence 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 s essions over the next 2 weeks, whereas groups A-C and A-N continued to rece ive ethanol-water and water-water, respectively. On the 14th day of the dep rivation interval, LCGU rates were measured 1 h prior to the scheduled acce ss 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 stru ctures in the mesocorticolimbic and nigrostriatal systems. Following alcoho l deprivation, LCGU values in the A-D group were partially or completely re turned to A-N levels in many, but not all, regions. In several limbic regio ns (e.g., ventral tegmental area, olfactory tubercle, medial prefrontal cor tex, ventral pallidum and lateral septum), no recovery of LCGU rates was ob served after 2 weeks of alcohol deprivation. This study demonstrates that c hronic alcohol consumption produces significant reductions in functional ne uronal 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 a re imbalanced interactions among and within several CNS sites, which do not reflect either the alcohol-naive or chronic alcohol-exposed state. Such ne uronal imbalances may underlie relapse of alcohol drinking following prolon ged abstinence. (C) 2001 Elsevier Science Inc. All rights reserved.