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    Neuroscience News

    Established in 1976, Neuroscience is the flagship journal of IBRO and is overseen by the IBRO Publications CommitteeElsevier publishes 28 issues per year. 

    The journal features papers describing the results of original research on any aspect of the scientific study of the nervous system. Any paper, however short, is considered for publication provided that it reports significant, new and carefully confirmed findings with full experimental details.

    READ the current Special Issue of IBRO Neuroscience (vol. 342) on early adversity and brain development, edited by Susanne Brummelte and published on 7 February 2017. Highlighted findings from this issue include:

    Introduction: Early adversity and brain development

    (S. Brummelte)

    Stress has long been known to have a significant effect on brain function in adults, but we are just starting to explore the multifaceted impact that stress and stress-related experiences can have on the developing brain. Exposure to a specific stressor during prenatal, postnatal or adolescent development can each have a very different impact on the structure and function of the brain and neuroendocrine systems. Exploring the relationship between early adversity and risk or resilience for mental health is of utmost importance as not every early adverse event results in devastating consequences, but there is a dearth of knowledge about what could protect the developing brain from potentially harmful insults. This Special Issue is addressing this question, how early adversity impacts brain development and consequent outcomes, from many different angles. The 16 reviews and empirical papers in this issue cover a variety of approaches and different types of ‘adversity’ in animals as well as human subjects.

    Prenatal alcohol exposure and prenatal stress differentially alter glucocorticoid signaling in the placenta and fetal brain

    (N. Lan, M.P.Y. Chiu, L. Ellis, J. Weinberg)

    Adverse intrauterine environments increase vulnerability to chronic diseases across the lifespan. The hypothalamic–pituitary–adrenal (HPA) axis, which integrates multiple neuronal signals and ultimately controls the response to stressors, may provide a final common pathway linking early adversity and adult diseases. Both prenatal alcohol exposure (PAE) and prenatal stress (PS) induce a hyperresponsive HPA phenotype in adulthood. As glucocorticoids are pivotal for the normal development of many fetal tissues including the brain, we used animal models of PAE and PS to investigate possible mechanisms underlying fetal programing of glucocorticoid signaling in the placenta and fetal brain at gestation day (GD) 21. We found that both PAE and PS dams had higher corticosterone (CORT) levels than control dams. However, 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2) enzyme levels were increased in PAE and unchanged in PS placentae, although there were no differences in 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) levels. Moreover, only PAE fetuses showed decreased body weight and increased placental weight, and hence a lower fetal/placental weight ratio, a marker of placenta efficiency, compared to all other prenatal groups. Importantly, PAE and PS differentially altered corticosteroid receptor levels in placentae and brains. In the PS condition, maternal CORT was negatively correlated with both 11β-HSD1 and mineralocorticoid receptor (MR) protein levels in male and female placentae, whereas in the PAE condition, there were trends for a positive correlation between maternal CORT and 11β-HSD1, regardless of sex, and a negative correlation between maternal alcohol intake and MR in male placentae. In fetal brains, sexually dimorphic changes in MR and glucocorticoid receptor (GR) levels, and the MR/GR ratio seen in C fetuses were absent in PAE and PS fetuses. In addition, PS but not PAE female fetuses had higher MR and lower GR expression levels in certain limbic areas compared to C female fetuses. Thus the similar adult HPA hyperresponsive phenotype in PAE and PS animals likely occurs through differential effects on glucocorticoid signaling in the placenta and fetal brain.

    Early deprivation, atypical brain development, and internalizing symptoms in late childhood

    (J. Bick, N. Fox, C. Zeanah, C.A. Nelson)

    Children exposed to extreme early-life neglect such as in institutional rearing are at heightened risk for developing depression and anxiety disorders, and internalizing problems more broadly. These outcomes are believed to be due to alterations in the development of neural circuitry that supports emotion regulation. The specific neurodevelopmental changes that contribute to these difficulties are largely unknown. This study examined whether microstructural alterations in white matter pathways predicted long-term risk for internalizing problems in institutionally reared children. Data from 69 children were drawn from the Bucharest Early Intervention Project, a randomized clinical trial of foster care for institutionally reared children. White matter was assessed using diffusion tensor imaging (DTI) when children were between 8 and 10 years of age. Internalizing symptoms were assessed at the time of the MRI scan, and once children reached 12–14 years of age. Results indicated that neglect-associated alterations in the external capsule and corpus callosum partially explained links between institutional rearing status and internalizing symptoms in middle childhood and early adolescence. Findings shed light on neural mechanisms contributing to increased risk for emotional difficulties among children reared in adverse conditions and have implications for prevention and intervention.

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