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dc.contributor.authorHan, Young-Min-
dc.contributor.authorKim, Min Sun-
dc.contributor.authorJo, Juyeong-
dc.contributor.authorShin, Daiha-
dc.contributor.authorKwon, Seung-Hae-
dc.contributor.authorSeo, Jong Bok-
dc.contributor.authorKang, Dongmin-
dc.contributor.authorLee, Byoung Dae-
dc.contributor.authorRyu, Hoon-
dc.contributor.authorHwang, Eun Mi-
dc.contributor.authorKim, Jae-Min-
dc.contributor.authorPatel, Paresh D.-
dc.contributor.authorLyons, David M.-
dc.contributor.authorSchatzberg, Alan F.-
dc.contributor.authorHer, Song-
dc.date.accessioned2024-01-19T14:01:10Z-
dc.date.available2024-01-19T14:01:10Z-
dc.date.created2022-01-10-
dc.date.issued2021-09-
dc.identifier.issn1359-4184-
dc.identifier.urihttps://pubs.kist.re.kr/handle/201004/116513-
dc.description.abstractThe fine-tuning of neuroinflammation is crucial for brain homeostasis as well as its immune response. The transcription factor, nuclear factor-kappa-B (NF kappa B) is a key inflammatory player that is antagonized via anti-inflammatory actions exerted by the glucocorticoid receptor (GR). However, technical limitations have restricted our understanding of how GR is involved in the dynamics of NF kappa B in vivo. In this study, we used an improved lentiviral-based reporter to elucidate the time course of NF kappa B and GR activities during behavioral changes from sickness to depression induced by a systemic lipopolysaccharide challenge. The trajectory of NF kappa B activity established a behavioral basis for the NF kappa B signal transition involved in three phases, sickness-early-phase, normal-middle-phase, and depressive-like-late-phase. The temporal shift in brain GR activity was differentially involved in the transition of NF kappa B signals during the normal and depressive-like phases. The middle-phase GR effectively inhibited NF kappa B in a glucocorticoid-dependent manner, but the late-phase GR had no inhibitory action. Furthermore, we revealed the cryptic role of basal GR activity in the early NF kappa B signal transition, as evidenced by the fact that blocking GR activity with RU486 led to early depressive-like episodes through the emergence of the brain NF kappa B activity. These results highlight the inhibitory action of GR on NF kappa B by the basal and activated hypothalamic-pituitary-adrenal (HPA)-axis during body-to-brain inflammatory spread, providing clues about molecular mechanisms underlying systemic inflammation caused by such as COVID-19 infection, leading to depression.-
dc.languageEnglish-
dc.publisherSPRINGERNATURE-
dc.titleDecoding the temporal nature of brain GR activity in the NF kappa B signal transition leading to depressive-like behavior-
dc.typeArticle-
dc.identifier.doi10.1038/s41380-021-01016-1-
dc.description.journalClass1-
dc.identifier.bibliographicCitationMOLECULAR PSYCHIATRY, v.26, no.9, pp.5087 - 5096-
dc.citation.titleMOLECULAR PSYCHIATRY-
dc.citation.volume26-
dc.citation.number9-
dc.citation.startPage5087-
dc.citation.endPage5096-
dc.description.isOpenAccessY-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.identifier.wosid000610020200006-
dc.identifier.scopusid2-s2.0-85099857293-
dc.relation.journalWebOfScienceCategoryBiochemistry & Molecular Biology-
dc.relation.journalWebOfScienceCategoryNeurosciences-
dc.relation.journalWebOfScienceCategoryPsychiatry-
dc.relation.journalResearchAreaBiochemistry & Molecular Biology-
dc.relation.journalResearchAreaNeurosciences & Neurology-
dc.relation.journalResearchAreaPsychiatry-
dc.type.docTypeArticle; Early Access-
dc.subject.keywordPlusPITUITARY-ADRENAL AXIS-
dc.subject.keywordPlusINNATE IMMUNE-SYSTEM-
dc.subject.keywordPlusGLUCOCORTICOID-RECEPTOR-
dc.subject.keywordPlusGENE-EXPRESSION-
dc.subject.keywordPlusRATS-
dc.subject.keywordPlusHPA-
dc.subject.keywordPlusPATHOPHYSIOLOGY-
dc.subject.keywordPlusINFLAMMATION-
dc.subject.keywordPlusACTIVATION-
dc.subject.keywordPlusCOMPLEXITY-
dc.subject.keywordAuthorNFkB signal-
dc.subject.keywordAuthorglucocorticoid-
dc.subject.keywordAuthordepressive-like behavior-
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KIST Article > 2021
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