Role of glutamate receptors and glial cells in the pathophysiology of treatment-resistant depression
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Kim, Yong-Ku | - |
dc.contributor.author | Na, Kyoung-Sae | - |
dc.date.available | 2020-02-28T00:42:09Z | - |
dc.date.created | 2020-02-07 | - |
dc.date.issued | 2016-10-03 | - |
dc.identifier.issn | 0278-5846 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/7779 | - |
dc.description.abstract | Treatment-resistant depression (TRD) causes substantial socioeconomic burden. Although a consensus on the definition of TRD has not yet been reached, it is certain that classic monoaminergic antidepressants are ineffective for TRD. One decade ago, many researchers found ketamine, an N-methyl-D-aspartate receptor (NMDAR) antagonist, to be an alternative to classic monoaminergic antidepressants. The major mechanisms of action of ketamine rapidly induce synaptogenesis in the brain-derived neurotrophic factor (BDNF) pathway. Although excessive glutamatergic neurotransmission and consequent excitotoxicity were considered a major cause of TRD, recent evidence suggests that the extrasynaptic glutamatergic receptor signal pathway mainly contributes to the detrimental effects of TRD. Glial cells such as microglia and astrocytes, early life adversity, and glucocorticoid receptor dysfunction participate in complex cross-talk. An appropriate reuptake of glutamate at the astrocyte is crucial for preventing 'spillover' of synaptic glutamate and binding to the extrasynaptic NMDA receptor. Excessive microglial activation and the inflammatory process cause astrocyte glutamatergic dysfunction, which in turn activates microglial function. Early life adversity and glucocorticoid receptor dysfunction result in vulnerability to stress in adulthood. A maladaptive response to stress leads to increased glutamatergic release and pro-inflammatory cytokines, which then activate microglia. However, since the role of inflammatory mediators such as pro-inflammatory cytokines is not specific for depression, more disease-specific mechanisms should be identified. Last, although much research has focused on ketamine as an alternative antidepressant for TRD, its long-lasting effectiveness and adverse events have not been rigorously demonstrated. Additionally, evidence suggests that substantial brain abnormalities develop in ketamine abusers. Thus, more investigations for ketamine and other novel glutamatergic agents are needed. (C) 2016 Elsevier Inc. All rights reserved. | - |
dc.language | 영어 | - |
dc.language.iso | en | - |
dc.publisher | PERGAMON-ELSEVIER SCIENCE LTD | - |
dc.relation.isPartOf | PROGRESS IN NEURO-PSYCHOPHARMACOLOGY & BIOLOGICAL PSYCHIATRY | - |
dc.subject | EXTRASYNAPTIC NMDA RECEPTORS | - |
dc.subject | RANDOMIZED CONTROLLED-TRIAL | - |
dc.subject | ANTIDEPRESSANT TREATMENT RESPONSE | - |
dc.subject | TREATMENT-REFRACTORY DEPRESSION | - |
dc.subject | STATE FUNCTIONAL CONNECTIVITY | - |
dc.subject | FIBRILLARY ACIDIC PROTEIN | - |
dc.subject | D-ASPARTATE RECEPTOR | - |
dc.subject | EARLY-LIFE ADVERSITY | - |
dc.subject | MAJOR DEPRESSION | - |
dc.subject | ACTIVATED MICROGLIA | - |
dc.title | Role of glutamate receptors and glial cells in the pathophysiology of treatment-resistant depression | - |
dc.type | Article | - |
dc.type.rims | ART | - |
dc.description.journalClass | 1 | - |
dc.identifier.wosid | 000378854200015 | - |
dc.identifier.doi | 10.1016/j.pnpbp.2016.03.009 | - |
dc.identifier.bibliographicCitation | PROGRESS IN NEURO-PSYCHOPHARMACOLOGY & BIOLOGICAL PSYCHIATRY, v.70, pp.117 - 126 | - |
dc.identifier.scopusid | 2-s2.0-84963656264 | - |
dc.citation.endPage | 126 | - |
dc.citation.startPage | 117 | - |
dc.citation.title | PROGRESS IN NEURO-PSYCHOPHARMACOLOGY & BIOLOGICAL PSYCHIATRY | - |
dc.citation.volume | 70 | - |
dc.contributor.affiliatedAuthor | Na, Kyoung-Sae | - |
dc.type.docType | Article | - |
dc.subject.keywordAuthor | Treatment-resistant depression | - |
dc.subject.keywordAuthor | Ketamine | - |
dc.subject.keywordAuthor | Glutamate receptors | - |
dc.subject.keywordAuthor | Neuroinflammation | - |
dc.subject.keywordAuthor | Glia | - |
dc.subject.keywordPlus | EXTRASYNAPTIC NMDA RECEPTORS | - |
dc.subject.keywordPlus | RANDOMIZED CONTROLLED-TRIAL | - |
dc.subject.keywordPlus | ANTIDEPRESSANT TREATMENT RESPONSE | - |
dc.subject.keywordPlus | TREATMENT-REFRACTORY DEPRESSION | - |
dc.subject.keywordPlus | STATE FUNCTIONAL CONNECTIVITY | - |
dc.subject.keywordPlus | FIBRILLARY ACIDIC PROTEIN | - |
dc.subject.keywordPlus | D-ASPARTATE RECEPTOR | - |
dc.subject.keywordPlus | EARLY-LIFE ADVERSITY | - |
dc.subject.keywordPlus | MAJOR DEPRESSION | - |
dc.subject.keywordPlus | ACTIVATED MICROGLIA | - |
dc.relation.journalResearchArea | Neurosciences & Neurology | - |
dc.relation.journalResearchArea | Pharmacology & Pharmacy | - |
dc.relation.journalResearchArea | Psychiatry | - |
dc.relation.journalWebOfScienceCategory | Clinical Neurology | - |
dc.relation.journalWebOfScienceCategory | Neurosciences | - |
dc.relation.journalWebOfScienceCategory | Pharmacology & Pharmacy | - |
dc.relation.journalWebOfScienceCategory | Psychiatry | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.
1342, Seongnam-daero, Sujeong-gu, Seongnam-si, Gyeonggi-do, Republic of Korea(13120)031-750-5114
COPYRIGHT 2020 Gachon University All Rights Reserved.
Certain data included herein are derived from the © Web of Science of Clarivate Analytics. All rights reserved.
You may not copy or re-distribute this material in whole or in part without the prior written consent of Clarivate Analytics.