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      Decreased Plasma BDNF Levels of Patients with Somatization Disorder

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          Abstract

          Objective

          Brain-derived neurotrophic factor (BDNF), one of the most abundant and important neurotrophins, is known to be involved in the development, survival, maintenance, and plasticity of neurons in the nervous system. Some studies have suggested that BDNF may play a role in the pathophysiology of several psychiatric illnesses such as depression and schizophrenia. Similarly, it is likely that the alteration of BDNF may be associated with the neuro-modulation that contributes to the development of somatization disorder.

          Methods

          The purpose of this study was to determine whether there is an abnormality of plasma BDNF levels in patients with somatization disorder, and to analyze the nature of the alteration after pharmacotherapy using an enzyme-linked immunosorbent assay (ELISA).

          Results

          The plasma BDNF levels of the patients with a somatization disorder were significantly lower compared with those of the control volunteers (83.61±89.97 pg/mL vs. 771.36±562.14 pg/mL); moreover, the plasma BDNF levels of those patients who received an antidepressant were significantly increased after the treatment (118.13±91.45 pg/mL vs. 72.92±88.21 pg/mL).

          Conclusion

          These results suggest that BDNF may play a role in the pathophysiology of somatization disorder.

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          Most cited references 59

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          Diagnostic and statistical manual of mental disorders.

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            Chronic antidepressant treatment increases neurogenesis in adult rat hippocampus.

            Recent studies suggest that stress-induced atrophy and loss of hippocampal neurons may contribute to the pathophysiology of depression. The aim of this study was to investigate the effect of antidepressants on hippocampal neurogenesis in the adult rat, using the thymidine analog bromodeoxyuridine (BrdU) as a marker for dividing cells. Our studies demonstrate that chronic antidepressant treatment significantly increases the number of BrdU-labeled cells in the dentate gyrus and hilus of the hippocampus. Administration of several different classes of antidepressant, but not non-antidepressant, agents was found to increase BrdU-labeled cell number, indicating that this is a common and selective action of antidepressants. In addition, upregulation of the number of BrdU-labeled cells is observed after chronic, but not acute, treatment, consistent with the time course for the therapeutic action of antidepressants. Additional studies demonstrated that antidepressant treatment increases the proliferation of hippocampal cells and that these new cells mature and become neurons, as determined by triple labeling for BrdU and neuronal- or glial-specific markers. These findings raise the possibility that increased cell proliferation and increased neuronal number may be a mechanism by which antidepressant treatment overcomes the stress-induced atrophy and loss of hippocampal neurons and may contribute to the therapeutic actions of antidepressant treatment.
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              Transport of brain-derived neurotrophic factor across the blood–brain barrier

              Brain-derived neurotrophic factor (BDNF) is a potential therapeutic agent for degenerative disorders of the central nervous system. In this report, we investigated the ability of BDNF to cross the blood-brain barrier (BBB). BDNF was stable in blood up to 60 min after i.v. injection, with evidence for aggregation, and had an early, rapid influx into brain. By 10 min, most of the BDNF sequestered by the cerebral cortex was associated with the parenchyma rather than with the endothelial cells, demonstrating complete passage across the BBB. A small dose of unlabeled BDNF enhanced the entry of 125I-BDNF from blood to brain after an i.v. bolus injection, whereas larger doses had no effect. In contrast, a large dose of unlabeled BDNF inhibited the influx of 125I-BDNF during in situ brain perfusion. After intracerebroventricular injection, the efflux of BDNF from brain to blood occurred at a rate similar to that for reabsorption of cerebrospinal fluid, and no evidence for self-inhibition was found. Therefore, we conclude that intact BDNF in the peripheral circulation crosses the BBB by a high-capacity, saturable transport system.
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                Author and article information

                Journal
                Psychiatry Investig
                Psychiatry Investig
                PI
                Psychiatry Investigation
                Korean Neuropsychiatric Association
                1738-3684
                1976-3026
                September 2016
                30 September 2016
                : 13
                : 5
                : 526-530
                Affiliations
                [1 ]Department of Psychiatry, Maeumsarang Hospital, Wanju, Republic of Korea.
                [2 ]Department of Psychiatry, Chonbuk National University Medical School, Jeonju, Republic of Korea.
                [3 ]Research Institute of Clinical Medicine of Chonbuk National University-Biomedical Research Institute of Chonbuk National University Hospital, Jeonju, Republic of Korea.
                [4 ]Department of Psychiatry, Korea University Ansan Hospital, Korea University College of Medicine, Ansan, Republic of Korea.
                Author notes
                Correspondence: Jong-Chul Yang, MD, PhD Department of Psychiatry, Chonbuk National University Medical School, 20 Geonji-ro, Deokjin-gu, Jeonju 54907, Republic of Korea Tel: +82-63-250-2580, Fax: +82-63-275-3157, yangjc@ 123456jbnu.ac.kr
                Correspondence: Yong-Ku Kim, MD, PhD. Department of Psychiatry, Korea University Ansan Hospital, Korea University College of Medicine, 122 Jeokgeum-ro, Danwon-gu, Ansan 15355, Republic of Korea. Tel: +82-31-412-5140, Fax: +82-31-412-5144, yongku@ 123456korea.ac.kr
                Article
                10.4306/pi.2016.13.5.526
                5067347
                Copyright © 2016 Korean Neuropsychiatric Association

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                Funding
                Funded by: Chonbuk National University Hospital, CrossRef http://dx.doi.org/10.13039/501100002864;
                Categories
                Original Article

                Clinical Psychology & Psychiatry

                neurotrophin, bdnf, somatization disorder

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