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      How could stress lead to major depressive disorder?

      review-article
      a , b , c , d , e , *
      IBRO Reports
      Elsevier
      Major depressive disorder, Stress, Memory

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          Abstract

          Stress is associated with major depressive disorder (MDD), but the underlying mechanism remains elusive. However, some experiences, referred to as stress, may actually lead to resilience. It is thus critical first to define what type of stress may lead to MDD. Long-term potentiation (LTP) and long-term depression (LTD) are both sensitive to stress, but particularly to inescapable and not escapable stress. Thus, these are the psychological aspects of stress which contribute to the development of MDD, but by which mechanisms remains still elusive. Interestingly, the same stress may facilitate LTD and impair LTP in the CA1 region. In addition, repeated efforts are often required for learning under neutral conditions but single- or few learning trials are sufficient for forming stress-related memories. If LTP is crucial for normal learning, a combination of limited LTP and facilitated LTD appears to have higher efficiency for storing stress-related memories. Chronic psychological stress may cause a hyper-link among stress-related memories across the spatiotemporal due to shared quality of inescapability, leading to automatically negative appraisal through memory generalization mechanisms in MDD patients when encountering new distinct events which are perceived to share such similarity with previous experiences.

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          Most cited references53

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          Dynamics of a stressful encounter: cognitive appraisal, coping, and encounter outcomes.

          Despite the importance that is attributed to coping as a factor in psychological and somatic health outcomes, little is known about actual coping processes, the variables that influence them, and their relation to the outcomes of the stressful encounters people experience in their day-to-day lives. This study uses an intraindividual analysis of the interrelations among primary appraisal (what was at stake in the encounter), secondary appraisal (coping options), eight forms of problem- and emotion-focused coping, and encounter outcomes in a sample of community-residing adults. Coping was strongly related to cognitive appraisal; the forms of coping that were used varied depending on what was at stake and the options for coping. Coping was also differentially related to satisfactory and unsatisfactory encounter outcomes. The findings clarify the functional relations among appraisal and coping variables and the outcomes of stressful encounters.
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            NMDA Receptor Blockade at Rest Triggers Rapid Behavioural Antidepressant Responses

            Clinical studies consistently demonstrate that a single sub-psychomimetic dose of ketamine, an ionotropic glutamatergic n-methyl-d-aspartate receptor (NMDAR) antagonist, produces fast-acting antidepressant responses in patients suffering from major depressive disorder (MDD), although the underlying mechanism is unclear 1-3 . Depressed patients report alleviation of MDD symptoms within two hours of a single low-dose intravenous infusion of ketamine with effects lasting up to two weeks 1-3 , unlike traditional antidepressants (i.e. serotonin reuptake inhibitors), which take weeks to reach efficacy. This delay is a major drawback to current MDD therapies, leaving a need for faster acting antidepressants particularly for suicide-risk patients 3 . Ketamine's ability to produce rapidly acting, long-lasting antidepressant responses in depressed patients provides a unique opportunity to investigate underlying cellular mechanisms. We show that ketamine and other NMDAR antagonists produce fast-acting behavioural antidepressant-like effects in mouse models that depend on rapid synthesis of brain-derived neurotrophic factor (BDNF). We find that ketamine-mediated NMDAR blockade at rest deactivates eukaryotic elongation factor 2 (eEF2) kinase (also called CaMKIII) resulting in reduced eEF2 phosphorylation and desuppression of BDNF translation. Furthermore, we find inhibitors of eEF2 kinase induce fast-acting behavioural antidepressant-like effects. Our findings suggest that protein synthesis regulation by spontaneous neurotransmission may serve as a viable therapeutic target for fast-acting antidepressant development.
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              Synaptic plasticity and memory: an evaluation of the hypothesis.

              Changing the strength of connections between neurons is widely assumed to be the mechanism by which memory traces are encoded and stored in the central nervous system. In its most general form, the synaptic plasticity and memory hypothesis states that "activity-dependent synaptic plasticity is induced at appropriate synapses during memory formation and is both necessary and sufficient for the information storage underlying the type of memory mediated by the brain area in which that plasticity is observed." We outline a set of criteria by which this hypothesis can be judged and describe a range of experimental strategies used to investigate it. We review both classical and newly discovered properties of synaptic plasticity and stress the importance of the neural architecture and synaptic learning rules of the network in which it is embedded. The greater part of the article focuses on types of memory mediated by the hippocampus, amygdala, and cortex. We conclude that a wealth of data supports the notion that synaptic plasticity is necessary for learning and memory, but that little data currently supports the notion of sufficiency.
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                Author and article information

                Contributors
                Journal
                IBRO Rep
                IBRO Rep
                IBRO Reports
                Elsevier
                2451-8301
                22 April 2018
                June 2018
                22 April 2018
                : 4
                : 38-43
                Affiliations
                [a ]Department of Neurobiology and Ethology, Department of Psychology, University of Haifa, Haifa 3498838, Israel
                [b ]Key Laboratory of Animal Models and Human Disease Mechanisms, Lab of Learning and Memory, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming 650223, China
                [c ]CAS Centre for Excellence in Brain Science and Intelligent Technology, Shanghai 200031, China
                [d ]Mental Health Institute, Second Xiangya Hospital of Central South University, Changsha 410011, China
                [e ]KIZ-SU Joint Laboratory of Animal Model and Drug Development, College of Pharmaceutical Sciences, Soochow University, Suzhou 215123, China
                Author notes
                [* ]Corresponding author at: (LX) Key Laboratory of Animal Models and Human Disease Mechanisms, Lab of Learning and Memory, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming 650223, China, and (GRL) Department of Neurobiology and Ethology, Department of Psychology, University of Haifa, Haifa 3498838, Israel. lxu@ 123456vip.163.com
                Article
                S2451-8301(17)30053-5
                10.1016/j.ibror.2018.04.001
                6111061
                30155523
                1d0bfb09-06d2-4ecf-a308-4e724b68ba7f
                © 2018 The Authors. Published by Elsevier Ltd on behalf of International Brain Research Organization.

                This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).

                History
                : 31 December 2017
                : 17 April 2018
                Categories
                Articles from the Special Issue on Emotion and mood disorders: from molecular mechanisms to neuronal circuits; Edited by Jiang-Ning Zhou

                major depressive disorder,stress,memory
                major depressive disorder, stress, memory

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