Interactions between the organism and its environment, during pregnancy as well as during the postnatal period, can lead to important neurobehavioral changes. We briefly review the literature, and successively present the main results from our laboratory concerning the behavioral effects of prenatal stress, differential rearing conditions, and postnatal handling. We show that submitting primiparous DA/HAN rats to an acute emotional stress (exposure to a cat) at gestational day10, 14, or 19 leads to greatly increased mortality of pups and to decreased body weight of surviving animals. The effects of such a stressor on emotional reactivity are less obvious. Cognitive processes are impaired depending on the learning task. Enriched environments restore abnormal behaviors (emotional reactivity, motor skills, motor and spatial learning) due to brain trauma or genetic deficiencies. In any case, environmental enrichment does prevent or slow down aging effects. The effects of postnatal handling noted when using classical tests of emotional reactivity also are clear when defensive reaction paradigms are used. Furthermore, pregnant females that are early handled are less anxious than nonhandled females. We hypothesize that, when subjected to a stressor, the offspring of early-handled females would be protected from the deleterious effects of this stress compared to pups of nonhandled females.

Prenatal alcohol exposure affects cortical angiogenesis both in mice and in pFAS/FAS patients, suggesting that vascular defects contribute to alcohol-induced brain abnormalities.

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Selenoprotein T (SelT) is a newly discovered thioredoxin-like protein, which is abundantly but transiently expressed in the neural lineage during brain ontogenesis. Because its physiological function in the brain remains unknown, we developed a conditional knockout mouse line (Nes-Cre/SelT) in which SelT gene is specifically disrupted in nerve cells. At postnatal day 7 (P7), these mice exhibited reduced volume of different brain structures, including hippocampus, cerebellum, and cerebral cortex. This phenotype, which is observed early during the first postnatal week, culminated at P7 and was associated with increased loss of immature neurons but not glial cells, through apoptotic cell death. This phenomenon was accompanied by elevated levels of intracellular reactive oxygen species, which may explain the increased neuron demise and reduced brain structure volumes. At the second postnatal week, an increase in neurogenesis was observed in the cerebellum of Nes-Cre/SelT mice, suggesting the occurrence of developmental compensatory mechanisms in the brain. In fact, the brain volume alterations observed at P7 were attenuated in adult mice. Nevertheless, SelT mutant mice exhibited a hyperactive behavior, suggesting that despite an apparent morphological compensation, SelT deficiency leads to cerebral malfunction in adulthood. Altogether, these results demonstrate that SelT exerts a neuroprotective role which is essential during brain development, and that its loss impairs mice behavior.

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