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      Acupuncture modulates stress response by the mTOR signaling pathway in a rat post-traumatic stress disorder model

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          Abstract

          Post-traumatic stress disorder (PTSD) is a psychiatric disease that can form following exposure to a traumatic event. Acupuncture has been proposed as a beneficial treatment for PTSD, but the underlying mechanisms remain unclear. The present study investigated whether acupuncture improves depression- and anxiety-like behaviors induced using a single prolonged stress (SPS) as a PTSD rat model. In addition, we investigated whether the effects were mediated by increased mTOR activity and its downstream signaling components, which contribute to protein synthesis required for synaptic plasticity in the hippocampus. We found that acupuncture at HT8 significantly alleviated both depression- and anxiety-like behaviors induced by SPS in rats, as assessed by the forced swimming, elevated plus maze, and open field tests; this alleviation was blocked by rapamycin. The effects of acupuncture were equivalent to those exerted by fluoxetine. Acupuncture regulated protein translation in the mTOR signaling pathway and enhanced the activation of synaptic proteins, PSD95, Syn1, and GluR1 in the hippocampus. These results suggest that acupuncture exerts antidepressant and anxiolytic effects on PTSD-related symptoms by increasing protein synthesis required for synaptic plasticity via the mTOR pathway in the hippocampus. Acupuncture may be a promising treatment for patients with PTSD and play a role as an alternative PTSD treatment.

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          Glutamate N-methyl-D-aspartate receptor antagonists rapidly reverse behavioral and synaptic deficits caused by chronic stress exposure.

          Despite widely reported clinical and preclinical studies of rapid antidepressant actions of glutamate N-methyl-D-aspartate (NMDA) receptor antagonists, there has been very little work examining the effects of these drugs in stress models of depression that require chronic administration of antidepressants or the molecular mechanisms that could account for the rapid responses. We used a rat 21-day chronic unpredictable stress (CUS) model to test the rapid actions of NMDA receptor antagonists on depressant-like behavior, neurochemistry, and spine density and synaptic function of prefrontal cortex neurons. The results demonstrate that acute treatment with the noncompetitive NMDA channel blocker ketamine or the selective NMDA receptor 2B antagonist Ro 25-6981 rapidly ameliorates CUS-induced anhedonic and anxiogenic behaviors. We also found that CUS exposure decreases the expression levels of synaptic proteins and spine number and the frequency/amplitude of synaptic currents (excitatory postsynaptic currents) in layer V pyramidal neurons in the prefrontal cortex and that these deficits are rapidly reversed by ketamine. Blockade of the mammalian target of rapamycin protein synthesis cascade abolishes both the behavioral and biochemical effects of ketamine. The results indicate that the structural and functional deficits resulting from long-term stress exposure, which could contribute to the pathophysiology of depression, are rapidly reversed by NMDA receptor antagonists in a mammalian target of rapamycin dependent manner. Copyright © 2011 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.
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            Diagnostic and Statistical Manual of Mental Disorders (DSM).

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              Linking molecules to mood: new insight into the biology of depression.

              Major depressive disorder is a heritable psychiatric syndrome that appears to be associated with subtle cellular and molecular alterations in a complex neural network. The affected brain regions display dynamic neuroplastic adaptations to endocrine and immunologic stimuli arising from within and outside the CNS. Depression's clinical and etiological heterogeneity adds a third level of complexity, implicating different pathophysiological mechanisms in different patients with the same DSM diagnosis. Current pharmacological antidepressant treatments improve depressive symptoms through complex mechanisms that are themselves incompletely understood. This review summarizes the current knowledge of the neurobiology of depression by combining insights from human clinical studies and molecular explanations from animal models. The authors provide recommendations for future research, with a focus on translating today's discoveries into improved diagnostic tests and treatments.
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                Author and article information

                Contributors
                acufind@khu.ac.kr
                Journal
                Sci Rep
                Sci Rep
                Scientific Reports
                Nature Publishing Group UK (London )
                2045-2322
                8 August 2018
                8 August 2018
                2018
                : 8
                : 11864
                Affiliations
                [1 ]ISNI 0000 0001 2171 7818, GRID grid.289247.2, Acupuncture and Meridian Science Research Center, , Kyung Hee University, ; 26 Kyungheedae-ro, Dongdaemun-gu, Seoul, 02447 Republic of Korea
                [2 ]ISNI 0000 0001 2171 7818, GRID grid.289247.2, Department of Korean Medical Science, Graduate School of Korean Medicine, , Kyung Hee University, ; 26 Kyungheedae-ro, Dongdaemoon-gu, Seoul, 02447 Republic of Korea
                [3 ]ISNI 0000 0001 2171 7818, GRID grid.289247.2, BK21 PLUS Korean Medicine Science Center, College of Korean Medicine, , Kyung Hee University, ; 26 Kyungheedae-ro, Dongdaemoon-gu, Seoul, 02447 Republic of Korea
                [4 ]ISNI 0000 0001 0671 5021, GRID grid.255168.d, College of Korean Medicine, , Dongguk University, ; 32, Dongguk-ro, Ilsandong-gu, Goyang-si, Gyeonggi-do 10326 Republic of Korea
                [5 ]Korean Institute of Oriental Medicine, 1672 Yuseong-daero, Yuseong-gu, Daejeon, 34054 Republic of Korea
                Article
                30337
                10.1038/s41598-018-30337-5
                6082850
                30089868
                4ddfd266-6f45-4926-ae2f-42c714040bf1
                © The Author(s) 2018

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

                History
                : 14 November 2017
                : 25 July 2018
                Funding
                Funded by: FundRef https://doi.org/10.13039/501100003725, National Research Foundation of Korea (NRF);
                Award ID: NRF-2015M3A9E3052338
                Award ID: NRF-2015M3A9E3052338
                Award ID: NRF-2015M3A9E3052338
                Award Recipient :
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