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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.

Human epidemiological and animal-model studies suggest that separate exposure to stress or serotonin-selective reuptake inhibitor (SSRI) antidepressants during pregnancy increases risks for neurodevelopmental disorders in offspring. Yet, little is known about the combined effects of maternal stress and SSRIs with regard to brain development in utero. We found that the placenta is *

Children with cerebral palsy have feeding difficulties that can contribute to undernutrition. The aim of this study was to investigate the effect of early undernutrition on locomotor activity and the expression of the myofibrillar protein MuRF-1 in an experimental model of cerebral palsy (CP). In order to achieve this aim, pregnant rats were divided into two groups according to the diet provided: Normal Protein (NP, n=9) and Low Protein (LP, n=12) groups. After birth, the pups were divided into four groups: Normal Protein Sham (NPS, n=16), Normal Protein Cerebral Palsy (NPCP, n=21), Low Protein Sham (LPS, n=20) and Low Protein Cerebral Palsy (LPCP, n=18) groups. The experimental cerebral palsy protocol consisted of two episodes of anoxia at birth and during the first days of life. Each day, nitrogen flow was used (9l/min during 12min). After nitrogen exposure, sensorimotor restriction was performed 16h per day, from the 2nd to the 28th postnatal day (PND). Locomotor activity was evaluated at 8th, 14th, 17th, 21th and 28th PND. At PND 29, soleus muscles were collected to analyse myofibrillar protein MuRF-1. Our results show that CP animals decreased body weight (p<0.001), which were associated with alterations of various parameters of locomotor activity (p<0.05), compared to their control. Undernourished animals also showed a decrease (p<0.05) in body weight and locomotor activity parameters. Moreover, CP decreased MuRF-1 levels in nourished rats (p=0.015) but not in undernourished rats. In summary, perinatal undernutrition exacerbated the negative effects of cerebral palsy on locomotor activity and muscle atrophy, but it appears not be mediated by changes in MuRF-1 levels.

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