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      β-endorphin modulates the effect of stress on novelty-suppressed feeding

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          Abstract

          Although stress is implicated in the pathophysiology of mood and anxiety disorders, not all individuals who suffer stressful life events develop psychopathology. Differential susceptibility to stress may be influenced by genetically mediated differences in hypothalamic-pituitary-adrenal (HPA) axis activity and moderation of the stress response by the opioid peptide β-endorphin (β-E). The present study investigated genetic contributions to coping behavior by examining anxious behavior of transgenic mice with varying capacities to synthesize β-E [B6.129S2- Pomc tm1Low /J; regulated by insertion of a premature stop codon into one or both copies of the proopiomelanocortin ( POMC) gene], both under normal conditions and following 3 min of forced swim (FS). Ten minutes after this stress exposure or a control manipulation, acutely food-deprived female and male transgenic mice were subjected to a novelty-suppressed feeding (NSF) test, during which their interaction with an almond slice located in the center of an open field box was measured. There was an interaction between genotype and stress for latency to approach the almond and whether or not the almond was approached, such that mice with low or absent β-E displayed a stronger aversion to novelty-feeding after stress exposure than did mice with normal levels. These data provide evidence for a moderating effect of β-E on the behavioral response to stress. Genotypic differences in anxious behavior emerged when mice were stressed prior to behavioral assessment, suggesting that β-E plays a role in coping behavior. These findings indicate that genetic variability in sensitivity of the β-E system to stress may contribute, at least in part, to heritable differences in stress reactivity as well as vulnerability to stress-related psychopathology.

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          Most cited references 75

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          Depression: a new animal model sensitive to antidepressant treatments.

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            Genetic epidemiology of major depression: review and meta-analysis.

            The authors conducted a meta-analysis of relevant data from primary studies of the genetic epidemiology of major depression. The authors searched MEDLINE and the reference lists of previous review articles to identify relevant primary studies. On the basis of a review of family, adoption, and twin studies that met specific inclusion criteria, the authors derived quantitative summary statistics. Five family studies met the inclusion criteria. The odds ratios for proband (subjects with major depression or comparison subjects) versus first-degree relative status (affected or unaffected with major depression) were homogeneous across the five studies (Mantel-Haenszel odds ratio=2.84, 95% CI=2.31-3.49). No adoption study met the inclusion criteria, but the results of two of the three reports were consistent with genetic influences on liability to major depression. Five twin studies met the inclusion criteria, and their statistical summation suggested that familial aggregation was due to additive genetic effects (point estimate of heritability of liability=37%, 95% CI=31%-42%), with a minimal contribution of environmental effects common to siblings (point estimate=0%, 95% CI=0%-5%), and substantial individual-specific environmental effects/measurement error (point estimate=63%, 95% CI=58%-67%). The literature suggests that recurrence best predicts the familial aggregation of major depression. Major depression is a familial disorder, and its familiality mostly or entirely results from genetic influences. Environmental influences specific to an individual are also etiologically significant. Major depression is a complex disorder that does not result from either genetic or environmental influences alone but rather from both. These findings are notably consistent across samples and methods and are likely to be generally applicable.
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              Endocrinology of the stress response.

              The stress response is subserved by the stress system, which is located both in the central nervous system and the periphery. The principal effectors of the stress system include corticotropin-releasing hormone (CRH); arginine vasopressin; the proopiomelanocortin-derived peptides alpha-melanocyte-stimulating hormone and beta-endorphin, the glucocorticoids; and the catecholamines norepinephrine and epinephrine. Appropriate responsiveness of the stress system to stressors is a crucial prerequisite for a sense of well-being, adequate performance of tasks, and positive social interactions. By contrast, inappropriate responsiveness of the stress system may impair growth and development and may account for a number of endocrine, metabolic, autoimmune, and psychiatric disorders. The development and severity of these conditions primarily depend on the genetic vulnerability of the individual, the exposure to adverse environmental factors, and the timing of the stressful events, given that prenatal life, infancy, childhood, and adolescence are critical periods characterized by increased vulnerability to stressors.
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                Author and article information

                Journal
                Front Behav Neurosci
                Front Behav Neurosci
                Front. Behav. Neurosci.
                Frontiers in Behavioral Neuroscience
                Frontiers Media S.A.
                1662-5153
                14 March 2013
                2013
                : 7
                Affiliations
                1Department of Neuroscience, Furman University Greenville, SC, USA
                2Neuroscience Graduate Program, University of Southern California Los Angeles, CA, USA
                3Department of Psychology, Bucknell University Lewisburg, PA, USA
                Author notes

                Edited by: Michael V. Baratta, University of Colorado Boulder, USA

                Reviewed by: Osborne F. Almeida, Max Planck Institute of Psychiatry, Germany; Ben N. Greenwood, University of Colorado Boulder, USA; John P. Christianson, University of Colorado Boulder, USA

                *Correspondence: Judith E. Grisel, Department of Psychology, Bucknell University, One Dent Drive, Lewisburg, PA 17837, USA. e-mail: j.grisel@ 123456bucknell.edu
                Article
                10.3389/fnbeh.2013.00019
                3596765
                23503677
                Copyright © 2013 Barfield, Moser, Hand and Grisel.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in other forums, provided the original authors and source are credited and subject to any copyright notices concerning any third-party graphics etc.

                Page count
                Figures: 4, Tables: 0, Equations: 0, References: 88, Pages: 7, Words: 7165
                Categories
                Neuroscience
                Original Research Article

                Neurosciences

                opioids, transgenic, anxiety, depression, mice, hyponeophagia, novelty

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