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      Plasma Corticosterone Activates SGK1 and Induces Morphological Changes in Oligodendrocytes in Corpus Callosum

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          Abstract

          Repeated stressful events are known to be associated with onset of depression. Further, stress activates the hypothalamic–pituitary–adrenocortical (HPA) system by elevating plasma cortisol levels. However, little is known about the related downstream molecular pathway. In this study, by using repeated water-immersion and restraint stress (WIRS) as a stressor for mice, we attempted to elucidate the molecular pathway induced by elevated plasma corticosterone levels. We observed the following effects both, in vivo and in vitro: (1) repeated exposure to WIRS activates the 3-phosphoinositide-dependent protein kinase (PDK1)–serum glucocorticoid regulated kinase (SGK1)– N-myc downstream-regulated gene 1 (NDRG1)–adhesion molecule (i.e., N-cadherin, α-catenin, and β-catenin) stabilization pathway via an increase in plasma corticosterone levels; (2) the activation of this signaling pathway induces morphological changes in oligodendrocytes; and (3) after recovery from chronic stress, the abnormal arborization of oligodendrocytes and depression-like symptoms return to the control levels. Our data strongly suggest that these abnornalities of oligodendrocytes are possibly related to depression-like symptoms.

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          Causal relationship between stressful life events and the onset of major depression.

          L M Karkowski, De Prescott, K Kendler (1999)
          Stressful life events are associated with the onset of episodes of major depression. However, exposure to stressful life events is influenced by genetic factors, and these factors are correlated with those that predispose to major depression. The aim of this study was to clarify the degree to which stressful life events cause major depression. The authors assessed the occurrence of 15 classes of stressful life events and the onset of DSM-III-R major depression over a 1-year period in female twins ascertained from a population-based registry. The sample contained 24,648 person-months and 316 onsets of major depression. Stressful life events were individually rated on contextual threat and dependence (the degree to which the stressful life event could have resulted from the respondent's behavior). The nature of the relationship between stressful life events and major depression was tested by 1) discrete-time survival analysis examining the relationship between dependence and the depressogenic effect of stressful life events and 2) a co-twin control analysis. While independent stressful life events were significantly associated with onsets of depression, when level of threat was controlled, the association was significantly stronger for dependent events. The odds ratio for onset of major depression in the month of a stressful life event was 5.64 in all subjects, 4.52 within dizygotic pairs, and 3.58 within monozygotic pairs. Stressful life events have a substantial causal relationship with the onset of episodes of major depression. However, about one-third of the association between stressful life events and onsets of depression is noncausal, since individuals predisposed to major depression select themselves into high-risk environments.
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            Elevated concentrations of CSF corticotropin-releasing factor-like immunoreactivity in depressed patients.

            I Karlsson, H Walléus, G Bissette … (1984)
            The possibility that hypersecretion of corticotropin-releasing factor (CRF) contributes to the hyperactivity of the hypothalamo-pituitary-adrenal axis observed in patients with major depression was investigated by measuring the concentration of this peptide in cerebrospinal fluid of normal healthy volunteers and in drug-free patients with DSM-III diagnoses of major depression, schizophrenia, or dementia. When compared to the controls and the other diagnostic groups, the patients with major depression showed significantly increased cerebrospinal fluid concentrations of CRF-like immunoreactivity; in 11 of the 23 depressed patients this immunoreactivity was greater than the highest value in the normal controls. These findings are concordant with the hypothesis that CRF hypersecretion is, at least in part, responsible for the hyperactivity of the hypothalamo-pituitary-adrenal axis characteristic of major depression.
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              Transcriptional profiling reveals evidence for signaling and oligodendroglial abnormalities in the temporal cortex from patients with major depressive disorder.

              C Aston, Vladimir B Sokolov, L Jiang (2005)
              Major depressive disorder is one of the most common and devastating psychiatric disorders. To identify candidate mechanisms for major depressive disorder, we compared gene expression in the temporal cortex from 12 patients with major depressive disorder and 14 matched controls using Affymetrix HgU95A microarrays. Significant expression changes were revealed in families of genes involved in neurodevelopment, signal transduction and cell communication. Among these, the expression of 17 genes related to oligodendrocyte function was significantly (P 1.4) decreased in patients with major depressive disorder. Eight of these 17 genes encode structural components of myelin (CNP, MAG, MAL, MOG, MOBP, PMP22, PLLP, PLP1). Five other genes encode enzymes involved in the synthesis of myelin constituents (ASPA, UGT8), or are essential in regulation of myelin formation (ENPP2, EDG2, TF, KLK6). One gene, that is, SOX10, encodes a transcription factor regulating other myelination-related genes. OLIG2 is a transcription factor present exclusively in oligodendrocytes and oligodendrocyte precursors. Another gene, ERBB3, is involved in oligodendrocyte differentiation. In addition to myelination-related genes, there were significant changes in multiple genes involved in axonal growth/synaptic function. These findings suggest that major depressive disorder may be associated with changes in cell communication and signal transduction mechanisms that contribute to abnormalities in oligodendroglia and synaptic function. Taken together with other studies, these findings indicate that major depressive disorder may share common oligodendroglial abnormalities with schizophrenia and bipolar disorder.
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                Author and article information

                Contributors
                : Role: Editor
                Journal
                Journal ID (nlm-ta): PLoS One
                Journal ID (publisher-id): plos
                Journal ID (pmc): plosone
                Title: PLoS ONE
                Publisher: Public Library of Science (San Francisco, USA )
                ISSN (Electronic): 1932-6203
                Publication date Collection: 2011
                Publication date (Electronic): 31 May 2011
                Volume: 6
                Issue: 5
                Electronic Location Identifier: e19859
                Affiliations
                [1 ]Department of Anatomy and Neuroscience, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan
                [2 ]Department of Clinical Disorder Research, The Osaka-Hamamatsu Joint Research Center For Child Mental Development, Suita, Osaka, Japan
                [3 ]Center for Behavioral Neuroscience, Yerkes National Primate Research Center, Emory University, Atlanta, Georgia, United States of America
                [4 ]Department of Neuroanatomy, Graduate School of Medical Science, Kanazawa University, Kanazawa, Ishikawa, Japan
                [5 ]Department of Child Development and Molecular Brain Science, United Graduate School of Child Development, Osaka University, Kanazawa University and Hamamatsu University School of Medicine, Suita, Osaka, Japan
                Rikagaku Kenkyūsho Brain Science Institute, Japan
                Author notes

                Conceived and designed the experiments: SM M. Tohyama. Performed the experiments: SM YK KT KY TI M. Taniguchi KI MA. Analyzed the data: SM YK KI TK M. Tohyama. Contributed reagents/materials/analysis tools: OH KI TK. Wrote the paper: SM M. Tohyama.

                Article
                Publisher ID: PONE-D-11-01825
                DOI: 10.1371/journal.pone.0019859
                PMC ID: 3104997
                PubMed ID: 21655274
                SO-VID: 15ef9d25-d600-4c62-adb1-a5977a96d019
                Copyright © Miyata 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
                Date received : 23 January 2011
                Date accepted : 5 April 2011
                Page count
                Pages: 16
                Categories
                Subject: Research Article
                Subject: Biology
                Subject: Molecular Cell Biology
                Subject: Cell Adhesion
                Subject: Cadherins
                Subject: Signal Transduction
                Subject: Signaling Cascades
                Subject: Polyphosphoinositide Signaling Cascade
                Subject: Stress Signaling Cascade
                Subject: Signaling Pathways
                Subject: Phosphoinositide Signal Transduction
                Subject: Neuroscience
                Subject: Molecular Neuroscience
                Subject: Signaling Pathways
                Subject: Neurobiology of Disease and Regeneration
                Subject: Neuropsychology
                Subject: Medicine
                Subject: Mental Health
                Subject: Psychiatry
                Subject: Mood Disorders

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                ScienceOpen disciplines: Uncategorized

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