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      Effects of stress throughout the lifespan on the brain, behaviour and cognition.

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          Chronic exposure to stress hormones, whether it occurs during the prenatal period, infancy, childhood, adolescence, adulthood or aging, has an impact on brain structures involved in cognition and mental health. However, the specific effects on the brain, behaviour and cognition emerge as a function of the timing and the duration of the exposure, and some also depend on the interaction between gene effects and previous exposure to environmental adversity. Advances in animal and human studies have made it possible to synthesize these findings, and in this Review a model is developed to explain why different disorders emerge in individuals exposed to stress at different times in their lives.

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          Social Deprivation of Neonatal, Adolescent, and Adult Rats Has Distinct Neurochemical and Behavioral Consequences

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            Effects of chronic glucocorticoid administration on insulin-degrading enzyme and amyloid-beta peptide in the aged macaque.

            Insulin-degrading enzyme (IDE) has been identified as a candidate protease in the clearance of amyloid-delta (Abeta) peptides from the brain. IDE activity and binding to insulin are known to be inhibited by glucocorticoids in vitro. In Alzheimer disease (AD), both a decrease in IDE levels and an increase in peripheral glucocorticoid levels have been documented. Our study investigated the effects of glucocorticoid treatment on IDE expression in vivo in 12 nonhuman primates (Macaca nemestrina). Year-long, high-dose exposure to the glucocorticoid cortisol (hydrocortisone acetate) was associated with reduced IDE protein levels in the inferior frontal cortex and reduced IDE mRNA levels in the dentate gyrus of the hippocampus. We assessed Abeta40 and Abeta42 levels by ELISA in the brain and in plasma, total plaque burden by immunohistochemistry, and relative Abeta1-40 and Abeta1-42 levels in the brain by mass spectrometry. Glucocorticoid treatment increased Abeta42 relative to Abeta40 levels without a change in overall plaque burden within the brain, while Abeta42 levels were decreased in plasma. These findings support the notion that glucocorticoids regulate IDE and provide a mechanism whereby increased glucocorticoid levels may contribute to AD pathology.
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              Corticosterone alters N-methyl-D-aspartate receptor subunit mRNA expression before puberty.

              Stress and stress hormones alter the expression of mRNA for the NR1, NR2A and NR2B subunits of the N-methyl-D-aspartate (NMDA) receptor in brain regions associated with the stress response. Early life stress contributes to the risk and pathophysiology of mental illness. Examining how stress hormones modulate NMDA receptor subunit gene expression before and after pubertal onset will further contribute to the understanding of how stress during adolescence relates to adult mental illness. Using in situ hybridization histochemistry, we measured NR1, NR2A and NR2B mRNA expression in the hippocampus and in the hypothalamic paraventricular nucleus (PVN) of rats that had undergone adrenalectomy (ADX) or sham surgery before or after puberty. Some ADX rats received corticosterone pellets that released either normal or stress levels of corticosterone for 14 days prior to sacrifice. There was a significant increase in NR1 subunit mRNA expression throughout the subfields of the hippocampus and in the PVN of ADX prepubertal rats. However, similar changes in hippocampal NR1 expression were not observed in postpubertal ADX rats. Pre- and postpubertal ADX rats implanted with a high-dose corticosterone pellet had decreased expression of PVN NR1 mRNA. Only prepubertal rats had an increase in dentate gyrus NR2A mRNA and CA3 region NR2B mRNA following high-dose replacement. These results provide evidence that glucocorticoids have differential effects on the regional expression of mRNA NMDA receptor subunits and elucidate a window during adolescence in which the NR1, NR2A and NR2B genes are responsive to glucocorticoids.

                Author and article information

                Nat. Rev. Neurosci.
                Nature reviews. Neuroscience
                Jun 2009
                : 10
                : 6
                [1 ] Université de Montréal, Mental Health Research Centre, Fernand Seguin Hôpital Louis-H Lafontaine, Quebec, Canada. sonia.lupien@umontreal.ca


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