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Open AccessJournal ArticleDOI

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

Wei Liu, +6 more
- 26 Jan 2017 - 
- Vol. 2017, Iss: 2017, pp 6871089-6871089
TLDR
The recent literature is summarized to elaborate the possible mechanistic role of neural plasticity in depression and find findings that may pave the way for future progress in neural Plasticity studies.
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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Citations
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Antidepressant-like Effects of BDNF and NGF Individual Loop Dipeptide Mimetics Depend on the Signal Transmission Patterns Associated with Trk

TL;DR: Comparative research of the antidepressant-like activity of the dimeric dipeptide mimetics of brain-derived neurotrophic factor and BDNF at acute and subchronic administration in the forced swim test in mice demonstrates that the low-molecular weight BDNF mimetic GSB-106 that activates all three main post-receptor TrkB signaling pathways is the most promising for the development as an antidepressant.
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Phencynonate hydrochloride exerts antidepressant effects by regulating the dendritic spine density and altering glutamate receptor expression.

TL;DR: Phencynonate hydrochloride (PCH) is a drug that crosses the blood-brain barrier as mentioned in this paper and has been shown to alleviate depression-like behaviors induced by chronic unpredictable mild stress (CUMS).
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Relationships of Physical Activity, Depression, and Sleep with Cognitive Function in Community-Dwelling Older Adults

TL;DR: In this article , a cross-sectional, observational study aimed to integrate the analyses of relationships of physical activity, depression, and sleep with cognitive function in community-dwelling older adults using a single model.
Book ChapterDOI

Impaired mitochondrial bioenergetics in psychiatric disorders

TL;DR: In this paper, the authors focus on the links between mitochondrial energy production, calcium homeostasis, apoptosis and synaptic plasticity, and the above disorders; discussing evidence for the involvement of mitochondrial and mitochondria-related nuclear genes, presenting a critical view about causal inference based on the accumulated evidence.
References
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Journal ArticleDOI

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TL;DR: It is proposed that cognitive control stems from the active maintenance of patterns of activity in the prefrontal cortex that represent goals and the means to achieve them, which provide bias signals to other brain structures whose net effect is to guide the flow of activity along neural pathways that establish the proper mappings between inputs, internal states, and outputs needed to perform a given task.
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LTP and LTD: an embarrassment of riches.

TL;DR: This work reviews those forms of LTP and LTD for which mechanisms have been most firmly established and examples are provided that show how these mechanisms can contribute to experience-dependent modifications of brain function.
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Deep brain stimulation for treatment-resistant depression.

TL;DR: It is suggested that disrupting focal pathological activity in limbic-cortical circuits using electrical stimulation of the subgenual cingulate white matter can effectively reverse symptoms in otherwise treatment-resistant depression.
Journal ArticleDOI

Reciprocal limbic-cortical function and negative mood: converging PET findings in depression and normal sadness

TL;DR: Reciprocal changes involving subgenual cingulate and right prefrontal cortex occur with both transient and chronic changes in negative mood, suggesting that these regional interactions are obligatory and probably mediate the well-recognized relationships between mood and attention seen in both normal and pathological conditions.
Journal ArticleDOI

Resting-State Functional Connectivity in Major Depression: Abnormally Increased Contributions from Subgenual Cingulate Cortex and Thalamus

TL;DR: The findings provide cross-modality confirmation of PET studies demonstrating increased thalamic and subgenual cingulate activity in major depression and suggest that a quantitative, resting-state fMRI measure could be used to guide therapy in individual subjects.
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Taken together, these findings may pave the way for future progress in neural plasticity studies.