Chronic stress-induced dendritic reorganization and abundance of synaptosomal PKA-dependent CP-AMPA receptor in the basolateral amygdala in a mouse model of depression
DC Field | Value | Language |
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dc.contributor.author | Yi, Eun-Surk | - |
dc.contributor.author | Oh, Seikwan | - |
dc.contributor.author | Lee, Jang-kyu | - |
dc.contributor.author | Leem, Yea-Hyun | - |
dc.date.available | 2020-02-27T18:43:12Z | - |
dc.date.created | 2020-02-06 | - |
dc.date.issued | 2017-05-06 | - |
dc.identifier.issn | 0006-291X | - |
dc.identifier.uri | https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/6109 | - |
dc.description.abstract | Chronic stress is a precipitating factor for disorders including depression. The basolateral amygdala (BLA) is a critical substrate that interconnects with stress-modulated neural networks to generate emotion and mood-related behaviors. The current study shows that 3 h per day of restraint stress for 14 days caused mice to exhibit long-term depressive behaviors, manifested by disrupted sociality and despair levels, which were rescued by fluoxetine. These behavioral changes corresponded with morphological and molecular changes in BLA neurons, including chronic stress-elicited increases in arborization, dendritic length, and spine density of BLA principal neurons. At the molecular level, calcium-permeable alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (CP-AMPARs) within the synaptosome exhibited an increased GluR1:GluR2 subunit ratio. We also observed increased GluR1 phosphorylation at Ser 845 and enhanced cyclic AMP-dependent protein kinase (PICA) activity in the BLA. These molecular changes reverted to the basal state post-treatment with fluoxetine. The expression of synaptophysin (SYP) and postsynaptic density protein 95 (PSD-95) at BLA neuronal synapses was also enhanced by chronic stress, which was reversed post-treatment. Finally, chronic stress-provoked depressive behavior was overcome by local blockage of CP-AMPARs in the BLA via stereotaxic injection (IEM-1460). Chronic stress-elicited depressive behavior may be due to hypertrophy of BLA neuronal dendrites and increased of PICA-dependent CP-AMPAR levels in BLA neurons. Furthermore, fluoxetine can reverse chronic stress triggered cytoarchitectural and functional changes of BLA neurons. These findings provide insights into depression-linked structural and functional changes in BLA neurons. (C) 2017 Elsevier Inc. All rights reserved. | - |
dc.language | 영어 | - |
dc.language.iso | en | - |
dc.publisher | ACADEMIC PRESS INC ELSEVIER SCIENCE | - |
dc.relation.isPartOf | BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | - |
dc.subject | SYNAPTIC CHANGES | - |
dc.subject | PHOSPHORYLATION | - |
dc.subject | SITES | - |
dc.title | Chronic stress-induced dendritic reorganization and abundance of synaptosomal PKA-dependent CP-AMPA receptor in the basolateral amygdala in a mouse model of depression | - |
dc.type | Article | - |
dc.type.rims | ART | - |
dc.description.journalClass | 1 | - |
dc.identifier.wosid | 000399966700012 | - |
dc.identifier.doi | 10.1016/j.bbrc.2017.03.093 | - |
dc.identifier.bibliographicCitation | BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.486, no.3, pp.671 - 678 | - |
dc.identifier.scopusid | 2-s2.0-85016482478 | - |
dc.citation.endPage | 678 | - |
dc.citation.startPage | 671 | - |
dc.citation.title | BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | - |
dc.citation.volume | 486 | - |
dc.citation.number | 3 | - |
dc.contributor.affiliatedAuthor | Yi, Eun-Surk | - |
dc.type.docType | Article | - |
dc.subject.keywordAuthor | Chronic restraint stress | - |
dc.subject.keywordAuthor | Depression | - |
dc.subject.keywordAuthor | BLA | - |
dc.subject.keywordAuthor | CP-AMPAR | - |
dc.subject.keywordAuthor | PKA | - |
dc.subject.keywordAuthor | Dendritic remodeling | - |
dc.subject.keywordPlus | SYNAPTIC CHANGES | - |
dc.subject.keywordPlus | PHOSPHORYLATION | - |
dc.subject.keywordPlus | SITES | - |
dc.relation.journalResearchArea | Biochemistry & Molecular Biology | - |
dc.relation.journalResearchArea | Biophysics | - |
dc.relation.journalWebOfScienceCategory | Biochemistry & Molecular Biology | - |
dc.relation.journalWebOfScienceCategory | Biophysics | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
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