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Disruption of the NMDA receptor GluN2A subunit abolishes inflammation-induced depression
dc.creator | Francija, Ester | |
dc.creator | Petrović, Zorica | |
dc.creator | Brkić, Željka | |
dc.creator | Mitić, Miloš | |
dc.creator | Radulović, Jelena | |
dc.creator | Adžić, Miroslav | |
dc.date.accessioned | 2020-01-27T09:58:51Z | |
dc.date.available | 2020-01-27T09:58:51Z | |
dc.date.issued | 2019 | |
dc.identifier.issn | 0166-4328 | |
dc.identifier.uri | https://vinar.vin.bg.ac.rs/handle/123456789/8450 | |
dc.description.abstract | Recent reports have demonstrated that lipopolysaccharide (LPS)-induced depressive-like behaviour is mediated via NMDA receptor. In this study, we further investigated the role of GluN2 A subunit of NMDA receptor in synaptic processes in the prefrontal cortex (PFC) and hippocampus of GluN2 A knockout (KO) mice in LPS-induced depressive-like behavior. Our data suggest that LPS-treated mice, lacking GluN2 A subunit, did not exhibit depressive-like behaviour. This was accompanied by unaltered levels of IL-6 and significant changes in neuroplasticity markers and glutamate receptor subunits composition in PFC and hippocampus. In particular, an immune challenge in GluN2 A KO mice resulted in unchanged PSA-NCAM levels and proBDNF increase in both brain structures as well as in increase in BDNF levels in hippocampus. Furthermore, the absence of GluN2 A resulted in increased levels of all NCAM isoforms in PFC upon LPS which was followed with a decrease in GluN1 and GluN2B subunits. The levels of AMPA receptor subunits (GluA1, GluA3, and GluA4) in the hippocampus of GluN2 A mice were unaltered upon the treatment and abundantly present in the PFC of KO mice. These results indicate that the GluN2 A subunit is critical in neuroinflammation-related depression, that its absence abolishes LPS-induced depressive phenotype, sustains PSA-NCAM levels, increases proBDNF signalling in the PFC and hippocampus and potentiates synaptic stabilization through NCAM in the PFC upon an immune challenge. © 2018 Elsevier B.V. | en |
dc.language.iso | en | |
dc.relation | info:eu-repo/grantAgreement/MESTD/Integrated and Interdisciplinary Research (IIR or III)/41029/RS// | |
dc.relation | United States Department of Health & Human Services National Institutes of Health (NIH) - USA [R21MH098793] | |
dc.rights | restrictedAccess | |
dc.source | Behavioural Brain Research | |
dc.subject | GluN2A knockout mice | en |
dc.subject | Lipopolysaccharide | en |
dc.subject | Depressive-like behavior | en |
dc.subject | Synaptosomes | en |
dc.subject | Neuroplasticity | en |
dc.subject | Glutamatergic neurotransmission | en |
dc.title | Disruption of the NMDA receptor GluN2A subunit abolishes inflammation-induced depression | en |
dc.type | article | en |
dc.rights.license | ARR | |
dcterms.abstract | Aджић, Мирослав; Франција, Естер; Бркић, Жељка; Митић, Милош; Радуловић, Јелена; Петровић, Зорица; | |
dc.citation.volume | 359 | |
dc.citation.spage | 550 | |
dc.citation.epage | 559 | |
dc.identifier.wos | 000456222600063 | |
dc.identifier.doi | 10.1016/j.bbr.2018.10.011 | |
dc.citation.rank | M22 | |
dc.identifier.pmid | 30296532 | |
dc.type.version | publishedVersion | |
dc.identifier.scopus | 2-s2.0-85054466831 |
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