Behavioral and neuroanatomical consequences of chronic ethanol intake and withdrawal

We have examined if long-term (13 months) alcohol consumption and the same treatment followed by a 6-week withdrawal period cause different neuropatho logical changes in rats. Spatial reference and working memory of alcohol-co nsuming and withdrawn rats were evaluated by comparison of their performanc e with age-matched controls in the Morris water maze. In the reference memo ry task we did not observe significant cognitive deficits in rats continuou sly exposed to ethanol, whereas withdrawn animals showed an obvious impairm ent of their overall performance. The reference memory deficit in withdrawn rats was evident in the spatial probe trial; these animals required signif icantly longer swimming distances to approach the former position of the pl atform when compared with controls and alcohol-consuming animals. In contra st, working memory was not significantly altered in either experimental gro up. Stereological methods were applied to compare the neurodegenerative cha nges produced by alcohol intake and withdrawal in the hippocampal formation . In the alcohol-consuming animals there was a significant cell loss in CA1 (18%) and CA3 (19%) hippocampal regions. Moreover, in withdrawn rats there was a further decay in the total number of pyramidal neurons, which amount ed to 15% relative to nonwithdrawn animals. In the granular layer of the de ntate gyrus there was a trend in the same direction, but it did not reach s ignificance. Thus, our findings indicate that withdrawn rats are cognitivel y impaired relative to animals submitted to continuous alcohol consumption and to age-matched controls, which fits the morphological data showing that withdrawal aggravates ethanol-induced degenerative processes in the hippoc ampal formation. (C) 1999 Elsevier Science Inc.