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Fluoxetine treatment of rat neonates significantly reduces oxidative stress in the hippocampus and in behavioral indicators of anxiety later in postnatal life

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The brain, more than any other organ in the body, is vulnerable to oxidative stress damage, owing to its requirement for high levels of oxygenation. This is needed to fulfill its metabolic needs in the face of relatively low levels of protective antioxidants. Recent studies have suggested that oxidative stress is directly involved in the etiology of both eating and anxiety behavior. The aim of this study was to evaluate the effect of fluoxetine-inhibited serotonin reuptake in nursing rat neonates on behavior and on oxidative stress in the hypothalamus and the hippocampus; brain areas responsible for behavior related to food and anxiety, respectively. The results show that increased serotonin levels during a critical period of development do not induce significant differences in food-related behavior (intake and satiety), but do result in a in a significant decrease in anxiety. Measurements of oxidative stress showed a significant reduction of lipid peroxidation in the hippocampus (57%). In the hypothalamus, antioxidant enzymes were unchanged, but in the hippocampus, the activity of catalase and glutathione-S-transferase was increased (80% and 85% respectively). This suggests that protecting neural cells from oxidative stress during brain development contributes to the anxiolytic effects of serotonin.
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Keywords: anxiety; anxiété; fluoxetine; fluoxétine; oxidative stress; serotonin; stress oxydant; sérotonine

Document Type: Research Article

Affiliations: 1: Nutrition Graduate Program and Department of Nutrition, Federal University of Pernambuco Recife, Brazil. 2: Department of Anatomy and Morphology, Federal University of Pernambuco Recife, Brazil. 3: Laboratory of Biochemistry and Exercise Biochemistry, Centro Academico de Vitoria-Federal University of Pernambuco, Alto do Reservatorio s/n, Vitoria de Santo Antao 55608-680, Brazil.

Publication date: January 1, 2014

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