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Background. Chronic alcohol exposure is associated to neurotoxic and neurodegenerative mechanisms that lead to several cognitive and memory dysfunctions. Alcohol-induced damage depends on ethanol consumption patterns. Prolonged alcohol exposure induces damage in distinct brain regions (prefrontal, perirhinal, entorhinal and parahippocampal cortices, thalamus, hypothalamus, hippocampus and cerebellum) in both alcoholic patients and animal models of alcoholism. However, brain areas of the drug reinforcement and reward circuit have not been investigated. Objective. To investigate if chronic alcohol exposure induces neurodegenerative damage in the rat brain, particularly in the mesocorticolimbic system and the amygdala. Method. Male Wistar rats were exposed to ethanol (10% v/v) or water by oral consumption during 30 days. In another set of experiments, animals similarly treated with ethanol were withdrawn from the drug for 24 and 48 h. At the end of the treatments, animals were sacrificed, whole blood samples were obtained and the brains were removed. A fluorescence marker (Fluoro-Jade B) was used to assess neurodegenerative damage in the brain. Blood alcohol concentration was evaluated by spectrophotometry. Results. We observed a low number of Fluoro-Jade B positive cells in different brain regions, including the piriform cortex, frontal cortex of association, caudate-putamen and dorsal thalamus. No differences were found between chronic alcohol or ethanol withdrawn groups versus control animals. Discussion and conclusion. Our results suggest that chronic alcohol exposure does not induce neurodegeneration under the present experimental conditions. Alcohol blood concentrations attained during treatment may not be sufficient to induce cell death.

Ontogeny is a critical period in terms of developing affinity to ethanol. Additionally, early manipulations are critical factors to mediate sensitivity to ethanol's effects. Associations between alcohol intake in infant rats and stressful events during late gestation were assessed. This work sought to characterize changes in opioid gene expression …

The endogenous opioid system is involved in ethanol reinforcement. Ethanol-induced changes in opioidergic transmission have not been extensively studied during infancy (postnatal days –PDs- 14 and 15). We investigated the effect of prenatal ethanol exposure on alcohol intake in rat pups. After behavioral tests, Methionine-enkephalin …