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      The Role of Neural Plasticity in Depression: From Hippocampus to Prefrontal Cortex

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          Abstract

          Neural plasticity, a fundamental mechanism of neuronal adaptation, is disrupted in depression. The changes in neural plasticity induced by stress and other negative stimuli play a significant role in the onset and development of depression. Antidepressant treatments have also been found to exert their antidepressant effects through regulatory effects on neural plasticity. However, the detailed mechanisms of neural plasticity in depression still remain unclear. Therefore, in this review, we summarize the recent literature to elaborate the possible mechanistic role of neural plasticity in depression. Taken together, these findings may pave the way for future progress in neural plasticity studies.

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          Synaptic plasticity and depression: new insights from stress and rapid-acting antidepressants.

          Ronald S. Duman, George Aghajanian, Gerard Sanacora … (2016)
          Depression is a common, devastating illness. Current pharmacotherapies help many patients, but high rates of a partial response or no response, and the delayed onset of the effects of antidepressant therapies, leave many patients inadequately treated. However, new insights into the neurobiology of stress and human mood disorders have shed light on mechanisms underlying the vulnerability of individuals to depression and have pointed to novel antidepressants. Environmental events and other risk factors contribute to depression through converging molecular and cellular mechanisms that disrupt neuronal function and morphology, resulting in dysfunction of the circuitry that is essential for mood regulation and cognitive function. Although current antidepressants, such as serotonin-reuptake inhibitors, produce subtle changes that take effect in weeks or months, it has recently been shown that treatment with new agents results in an improvement in mood ratings within hours of dosing patients who are resistant to typical antidepressants. Within a similar time scale, these new agents have also been shown to reverse the synaptic deficits caused by stress.
          Article 0 comments Cited 519 times – based on 0 reviews     Review now
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            Synaptic dysfunction in depression: potential therapeutic targets.

            Ronald S. Duman, George Aghajanian (2012)
            Basic and clinical studies demonstrate that depression is associated with reduced size of brain regions that regulate mood and cognition, including the prefrontal cortex and the hippocampus, and decreased neuronal synapses in these areas. Antidepressants can block or reverse these neuronal deficits, although typical antidepressants have limited efficacy and delayed response times of weeks to months. A notable recent discovery shows that ketamine, a N-methyl-D-aspartate receptor antagonist, produces rapid (within hours) antidepressant responses in patients who are resistant to typical antidepressants. Basic studies show that ketamine rapidly induces synaptogenesis and reverses the synaptic deficits caused by chronic stress. These findings highlight the central importance of homeostatic control of mood circuit connections and form the basis of a synaptogenic hypothesis of depression and treatment response.
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              Reciprocal limbic-cortical function and negative mood: converging PET findings in depression and normal sadness.

              H Mayberg, M Liotti, S Brannan … (1999)
              Theories of human behavior from Plato to Freud have repeatedly emphasized links between emotion and reason, a relationship now commonly attributed to pathways connecting phylogenetically "old" and "new" brain regions. Expanding on this theory, this study examined functional interactions between specific limbic and neocortical regions accompanying normal and disease-associated shifts in negative mood state. Regions of concordant functional change accompanying provocation of transient sadness in healthy volunteers and resolution of chronic dysphoric symptoms in depressed patients were examined with two positron emission tomography techniques: [15O]water and [18F]fluorodeoxyglucose, respectively. With sadness, increases in limbic-paralimbic blood flow (subgenual cingulate, anterior insula) and decreases in neocortical regions (right dorsolateral prefrontal, inferior parietal) were identified. With recovery from depression, the reverse pattern, involving the same regions, was seen--limbic metabolic decreases and neocortical increases. A significant inverse correlation between subgenual cingulate and right dorsolateral prefrontal activity was also demonstrated in both conditions. Reciprocal changes involving subgenual cingulate and right prefrontal cortex occur with both transient and chronic changes in negative mood. The presence and maintenance of functional reciprocity between these regions with shifts in mood in either direction suggests that these regional interactions are obligatory and probably mediate the well-recognized relationships between mood and attention seen in both normal and pathological conditions. The bidirectional nature of this limbic-cortical reciprocity provides additional evidence of potential mechanisms mediating cognitive ("top-down"), pharmacological (mixed), and surgical ("bottom-up") treatments of mood disorders such as depression.
              Article 0 comments Cited 302 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): 2017
                Publication date (Electronic): 26 January 2017
                Volume: 2017
                Electronic Location Identifier: 6871089
                Affiliations
                1Jilin Provincial Key Laboratory on Molecular and Chemical Genetic, The Second Hospital of Jilin University, 218 Ziqiang Street, Changchun 130041, China
                2Anesthesiology Department, The Second Hospital of Jilin University, 218 Ziqiang Street, Changchun 130041, China
                3Anesthesiology Department, The Third Hospital of Jilin University, 126 Xiantai Street, Changchun 130033, China
                Author notes

                Academic Editor: Aijun Li

                Author information
                http://orcid.org/0000-0003-0894-4930
                http://orcid.org/0000-0002-4559-213X
                http://orcid.org/0000-0002-4615-0317
                http://orcid.org/0000-0002-8461-6093
                http://orcid.org/0000-0002-3944-4536
                http://orcid.org/0000-0002-1129-3772
                Article
                DOI: 10.1155/2017/6871089
                PMC ID: 5299163
                PubMed ID: 28246558
                SO-VID: cad56866-d3e6-4676-bfc3-9b3f930beb2a
                Copyright © Copyright © 2017 Wei Liu 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 : 3 November 2016
                Date accepted : 4 January 2017
                Funding
                Funded by: National Natural Science Foundation of China
                Award ID: 31471120
                Award ID: 31540076
                Award ID: 31171123
                Funded by: Program for New Century Excellent Talents in University
                Award ID: NCET-13-0715
                Categories
                Subject: Review Article

                ScienceOpen disciplines: Neurosciences
                Data availability:
                ScienceOpen disciplines: Neurosciences

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