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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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Illness Progression, Recent Stress, and Morphometry of Hippocampal Subfields and Medial Prefrontal Cortex in Major Depression

TL;DR: In this paper, structural magnetic resonance imaging was performed to examine relationships between number of prior depressive episodes, current stress, hippocampal subfield volume and cortical thickness, and they found evidence for morphometric changes that are consistent with stress-sensitization models of recurrence in MDD.
Journal ArticleDOI

The Role of BDNF on Neural Plasticity in Depression.

TL;DR: The studies reviewed here may suggest new possible targets for antidepressant drugs such as neurotrophins, their receptors, and relevant signaling pathways, and agents facilitating the activation of gene expression and increasing the transcription of neurotrophic factors in the brain.
Journal ArticleDOI

Chronic Pain: Structural and Functional Changes in Brain Structures and Associated Negative Affective States.

TL;DR: The results of previous studies are summarized, focusing on the mechanisms underlying chronic pain development and the identification of neural areas related to chronic pain, to provide guidance for the development of future therapeutic approaches that could be used in the management of chronic pain.
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Antidepressants affect gut microbiota and Ruminococcus flavefaciens is able to abolish their effects on depressive-like behavior

TL;DR: It is demonstrated that various types of antidepressants alter gut microbiota composition, and further implicate a role for R. flavefaciens in alleviating depressive-like behavior, and a mechanism for microbial regulation of antidepressant treatment efficiency is suggested.
Journal ArticleDOI

Circulating microRNAs as potential biomarkers for psychiatric and neurodegenerative disorders.

TL;DR: This review aims to provide a comprehensive assessment on the current progress regarding the potential value of cimiRNAs as central nervous system (CNS) biomarkers and shows that the type of bodily fluid used for measuring cimi RNAs is important as inconsistencies in cimiRNAAs expression directions are found when comparing CSF, blood cell-free andBlood cell-bound samples.
References
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Journal ArticleDOI

Dysfunctional Glutamatergic and γ-Aminobutyric Acidergic Activities in Prefrontal Cortex of Mice in Social Defeat Model of Depression

TL;DR: Molecular mechanisms in the prefrontal cortex of mice showing depression-like phenotype induced by chronic defeat stress indicate that the activities of glutamatergic and GABAergic neurons are reduced in mice showing a depression- like phenotype, supported by molecular data for the expression of genes involved in glutamate and GABA pathways.
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The effects of low-dose ketamine on the prefrontal cortex and amygdala in treatment-resistant depression: A randomized controlled study.

TL;DR: Low‐dose ketamine has been found to have robust and rapid antidepressant effects, but it is unclear whether the rapid antidepressant mechanisms of ketamine on TRD involve changes in glutamatergic neurotransmission in the PFC and the amygdala.
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Grey matter volume increase following electroconvulsive therapy in patients with late life depression: a longitudinal MRI study.

TL;DR: Electroconvulsive therapy in patients with severe late life depression is associated with significant grey matter volume increase, which is most pronounced ipsilateral to the stimulation side.
Journal ArticleDOI

Increased neurogenesis in a rat ketamine model of schizophrenia.

TL;DR: In the animal model of schizophrenia, ketamine may evoke its stimulating effect on neurogenesis via a block of the N-methyl-D-aspartate receptor directly by reducing the c-Fos/c-Jun expression, resulting in a depression of the AP1 transcription factor complex and/or by a reduced nitric oxide production or an enhanced serotonergic activity.
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Transcutaneous vagus nerve stimulation modulates amygdala functional connectivity in patients with depression.

TL;DR: TVNS can significantly modulate the amygdala-lateral prefrontal rsFC ofMDD patients; the results provide insights into the brain mechanism of tVNS treatment for MDD patients.
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Taken together, these findings may pave the way for future progress in neural plasticity studies.