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      Chronic Stress and Glucocorticoids: From Neuronal Plasticity to Neurodegeneration

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          Abstract

          Stress and stress hormones, glucocorticoids (GCs), exert widespread actions in central nervous system, ranging from the regulation of gene transcription, cellular signaling, modulation of synaptic structure, and transmission and glial function to behavior. Their actions are mediated by glucocorticoid and mineralocorticoid receptors which are nuclear receptors/transcription factors. While GCs primarily act to maintain homeostasis by inducing physiological and behavioral adaptation, prolonged exposure to stress and elevated GC levels may result in neuro- and psychopathology. There is now ample evidence for cause-effect relationships between prolonged stress, elevated GC levels, and cognitive and mood disorders while the evidence for a link between chronic stress/GC and neurodegenerative disorders such as Alzheimer's (AD) and Parkinson's (PD) diseases is growing. This brief review considers some of the cellular mechanisms through which stress and GC may contribute to the pathogenesis of AD and PD.

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          Epigenetic programming by maternal behavior.

          Ian Weaver, Nadia Cervoni, Frances Champagne … (2004)
          Here we report that increased pup licking and grooming (LG) and arched-back nursing (ABN) by rat mothers altered the offspring epigenome at a glucocorticoid receptor (GR) gene promoter in the hippocampus. Offspring of mothers that showed high levels of LG and ABN were found to have differences in DNA methylation, as compared to offspring of 'low-LG-ABN' mothers. These differences emerged over the first week of life, were reversed with cross-fostering, persisted into adulthood and were associated with altered histone acetylation and transcription factor (NGFI-A) binding to the GR promoter. Central infusion of a histone deacetylase inhibitor removed the group differences in histone acetylation, DNA methylation, NGFI-A binding, GR expression and hypothalamic-pituitary-adrenal (HPA) responses to stress, suggesting a causal relation among epigenomic state, GR expression and the maternal effect on stress responses in the offspring. Thus we show that an epigenomic state of a gene can be established through behavioral programming, and it is potentially reversible.
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            Adult hippocampal neurogenesis buffers stress responses and depressive behavior

            Jason Snyder, Amélie Soumier, Michelle Brewer … (2011)
            Summary Glucocorticoids are released in response to stressful experiences and serve many beneficial homeostatic functions. However, dysregulation of glucocorticoids is associated with cognitive impairments and depressive illness 1, 2 . In the hippocampus, a brain region densely populated with receptors for stress hormones, stress and glucocorticoids strongly inhibit adult neurogenesis 3 . Decreased neurogenesis has been implicated in the pathogenesis of anxiety and depression, but direct evidence for this role is lacking 4, 5 . Here we show that adult-born hippocampal neurons are required for normal expression of the endocrine and behavioral components of the stress response. Using transgenic and radiation methods to specifically inhibit adult neurogenesis, we find that glucocorticoid levels are slower to recover after moderate stress and are less suppressed by dexamethasone in neurogenesis-deficient mice compared with intact mice, consistent with a role for the hippocampus in regulation of the hypothalamic-pituitary-adrenal (HPA) axis 6, 7 . Relative to controls, neurogenesis-deficient mice showed increased food avoidance in a novel environment after acute stress, increased behavioral despair in the forced swim test, and decreased sucrose preference, a measure of anhedonia. These findings identify a small subset of neurons within the dentate gyrus that are critical for hippocampal negative control of the HPA axis and support a direct role for adult neurogenesis in depressive illness.
            Article 0 comments Cited 490 times – based on 0 reviews     Review now
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              Neuronal loss correlates with but exceeds neurofibrillary tangles in Alzheimer's disease.

              T Gomez-Isla, R M HOLLISTER, H West … (1997)
              To assess the relationship between dementia, neuronal loss, and neuropathological findings in Alzheimer's disease (AD), we counted the number of neurons, senile plaques, and neurofibrillary tangles in a high-order association cortex. We studied the superior temporal sulcus of 34 individuals with AD and 17 nondemented control subjects, using statistically unbiased, stereological counting techniques. The number of superior temporal sulcus neurons in nondemented control subjects was stable across the sixth to ninth decades. In AD, more than 50% of the neurons were lost. Both neuronal loss and neurofibrillary tangles increased in parallel with the duration and severity of illness, but the amount of neuronal loss exceeded by manyfold the amount of neurofibrillary tangles accumulated. In contrast to the correlation between neurofibrillary tangles and neuronal loss, the number of senile plaques and the percentage of the superior temporal sulcus that was covered by Abeta (amyloid burden) were not related to neuronal loss, number of neurofibrillary tangles, or duration of disease. Neither the amount nor the rate of neuronal loss in the superior temporal sulcus in AD correlated with apolipoprotein E genotype. These data suggest that neuronal loss in association areas such as the superior temporal sulcus contributes directly to cognitive impairment in AD.
              Article 0 comments Cited 377 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Neural Plast
                Journal ID (iso-abbrev): Neural Plast
                Journal ID (publisher-id): NP
                Title: Neural Plasticity
                Publisher: Hindawi Publishing Corporation
                ISSN (Print): 2090-5904
                ISSN (Electronic): 1687-5443
                Publication date (Print): 2016
                Publication date (Electronic): 10 March 2016
                Volume: 2016
                Electronic Location Identifier: 6391686
                Affiliations
                1Laboratory of Gene Regulation and Adaptive Behaviors, Department of Neuroscience Paris Seine, INSERM U1130, CNRS UMR 8246, Université Pierre et Marie Curie, Paris Cedex 05, France
                2Life and Health Sciences Research Institute (ICVS), School of Health Sciences, University of Minho, Campus de Gualtar, 4710-057 Braga, Portugal
                3ICVS/3B's-PT Government Associate Laboratory, Guimarães, Braga, Portugal
                4Max Planck Institute of Psychiatry, Kraepelinstrasse 2-10, 80804 Munich, Germany
                Author notes
                *Sheela Vyas: sheela.vyas@ 123456upmc.fr and
                *Ioannis Sotiropoulos: ioannis@ 123456ecsaude.uminho.pt

                Academic Editor: Inmaculada C. Ibañez

                Article
                DOI: 10.1155/2016/6391686
                PMC ID: 4806285
                PubMed ID: 27034847
                SO-VID: a1bc846f-27c9-4d6d-a6a0-8deee3771c37
                Copyright © Copyright © 2016 Sheela Vyas et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 6 November 2015
                Date accepted : 31 January 2016
                Categories
                Subject: Review Article

                ScienceOpen disciplines: Neurosciences
                Data availability:
                ScienceOpen disciplines: Neurosciences

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