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      Acute stress enhances the expression of neuroprotection- and neurogenesis-associated genes in the hippocampus of a mouse restraint model

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          Abstract

          Stress arises from an external demand placed on an organism that triggers physiological, cognitive and behavioural responses in order to cope with that request. It is thus an adaptive response useful for the survival of an organism. The objective of this study was to identify and characterize global changes in gene expression in the hippocampus in response to acute stress stimuli, by employing a mouse model of short-term restraint stress. In our experimental design mice were subjected to a one time exposure of restraint stress and the regulation of gene expression in the hippocampus was examined 3, 12 and 24 hours thereafter. Microarray analysis revealed that mice which had undergone acute restraint stress differed from non-stressed controls in global hippocampal transcriptional responses. An up-regulation of transcripts contributing directly or indirectly to neurogenesis and neuronal protection including, Ttr, Rab6, Gh, Prl, Ndufb9 and Ndufa6, was observed. Systems level analyses revealed a significant enrichment for neurogenesis, neuron morphogenesis- and cognitive functions-related biological process terms and pathways. This work further supports the hypothesis that acute stress mediates a positive action on the hippocampus favouring the formation and the preservation of neurons, which will be discussed in the context of current data from the literature.

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          Chronic psychological stress and the regulation of pro-inflammatory cytokines: a glucocorticoid-resistance model.

          This study examined whether chronic stress impairs the immune system's capacity to respond to hormonal signals that terminate inflammation. Fifty healthy adults were studied; half were parents of cancer patients, and half were parents of healthy children. Parents of cancer patients reported more psychological distress than parents of healthy children. They also had flatter diurnal slopes of cortisol secretion, primarily because of reduced output during the morning hours. There was also evidence that chronic stress impaired the immune system's response to anti-inflammatory signals: The capacity of a synthetic glucocorticoid hormone to suppress in vitro production of the pro-inflammatory cytokine interleukin-6 was diminished among parents of cancer patients. Findings suggest a novel pathway by which chronic stress might alter the course of inflammatory disease.
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            Neuroimaging and neuropathological studies of depression: implications for the cognitive-emotional features of mood disorders.

            Neuroimaging technology has provided unprecedented opportunities for elucidating the anatomical correlates of major depression. The knowledge gained from imaging research and from the postmortem studies that have been guided by imaging data is catalyzing a paradigm shift in which primary mood disorders are conceptualized as illnesses that involve abnormalities of brain structure, as well as of brain function. These data suggest specific hypotheses regarding the neural mechanisms underlying pathological emotional processing in mood disorders. They particularly support a role for dysfunction within the prefrontal cortical and striatal systems that normally modulate limbic and brainstem structures involved in mediating emotional behavior in the pathogenesis of depressive symptoms.
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              Pregnancy-stimulated neurogenesis in the adult female forebrain mediated by prolactin.

              Neurogenesis occurs in the olfactory system of the adult brain throughout life, in both invertebrates and vertebrates, but its physiological regulation is not understood. We show that the production of neuronal progenitors is stimulated in the forebrain subventricular zone of female mice during pregnancy and that this effect is mediated by the hormone prolactin. The progenitors then migrate to produce new olfactory interneurons, a process likely to be important for maternal behavior, because olfactory discrimination is critical for recognition and rearing of offspring. Neurogenesis occurs even in females that mate with sterile males. These findings imply that forebrain olfactory neurogenesis may contribute to adaptive behaviors in mating and pregnancy.
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                Author and article information

                Journal
                Oncotarget
                Oncotarget
                Oncotarget
                ImpactJ
                Oncotarget
                Impact Journals LLC
                1949-2553
                23 February 2016
                6 February 2016
                : 7
                : 8
                : 8455-8465
                Affiliations
                1 Department of Medicine, School of Medicine, University of California, La Jolla, California, USA
                2 Facoltà di Scienze, Università Politecnica delle Marche, Ancona, Italy
                3 Laboratory for Pediatric Sarcoma Biology, Institute of Pathology of the LMU Munich, Munich, Germany
                4 Department of Urology, Medical University of Innsbruck, Innsbruck, Austria
                5 Centre de Recherches en Cancérologie de Toulouse – CRCT, Toulouse, France
                6 School of Pharmacy, Pharmacology Unit, University of Camerino, Camerino, Italy
                7 Medical Research Council – Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, King's College London, London, United Kingdom
                8 Institute of Pathology of the LMU Munich, Munich, Germany
                9 Departments of Medicine, Public Health and Center for Genomics Medicine, Medical University of South Carolina, Charleston, South Carolina, USA
                Author notes
                Correspondence to: Gary Hardiman, hardiman@ 123456musc.edu
                [*]

                These authors are joint first authors

                Article
                7225
                10.18632/oncotarget.7225
                4890979
                26863456
                29089bc9-5f87-45eb-8871-382005416332
                Copyright: © 2016 Sannino et al.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

                History
                : 19 December 2015
                : 26 January 2016
                Categories
                Research Perspective: Neuroscience

                Oncology & Radiotherapy
                acute,restraint stress,hippocampus,neurogenesis,neuroprotection
                Oncology & Radiotherapy
                acute, restraint stress, hippocampus, neurogenesis, neuroprotection

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