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Juvenile mild traumatic brain injury elicits distinct spatiotemporal astrocyte responses

dc.rights.licenseopenen_US
hal.structure.identifierInstitut de Neurosciences cognitives et intégratives d'Aquitaine [INCIA]
dc.contributor.authorCLEMENT, Tifenn
hal.structure.identifierLoma Linda University
dc.contributor.authorLEE, Jeong Bin
hal.structure.identifierInstitut de Neurosciences cognitives et intégratives d'Aquitaine [INCIA]
dc.contributor.authorICHKOVA, Aleksandra
hal.structure.identifierInstitut de Neurosciences cognitives et intégratives d'Aquitaine [INCIA]
dc.contributor.authorRODRIGUEZ-GRANDE, Beatriz
hal.structure.identifierInstitut de Neurosciences cognitives et intégratives d'Aquitaine [INCIA]
dc.contributor.authorFOURNIER, Marie-Line
hal.structure.identifierInstitut de Neurosciences cognitives et intégratives d'Aquitaine [INCIA]
dc.contributor.authorAUSSUDRE, Justine
hal.structure.identifierInstitut de Recherche Biomédicale des Armées [Brétigny-sur-Orge] [IRBA]
dc.contributor.authorOGIER, Michael
dc.contributor.authorHADDAD, Elizabeth
hal.structure.identifierInstitut de Recherche Biomédicale des Armées [Brétigny-sur-Orge] [IRBA]
dc.contributor.authorCANINI, Frederic
hal.structure.identifierNeurocentre Magendie : Physiopathologie de la Plasticité Neuronale [U1215 Inserm - UB]
dc.contributor.authorKOEHL, Muriel
hal.structure.identifierNeurocentre Magendie : Physiopathologie de la Plasticité Neuronale [U1215 Inserm - UB]
dc.contributor.authorABROUS, Nora
hal.structure.identifierLoma Linda University
dc.contributor.authorOBENAUS, Andre
hal.structure.identifierInstitut de Neurosciences cognitives et intégratives d'Aquitaine [INCIA]
dc.contributor.authorBADAUT, Jerome
dc.date.accessioned2023-12-07T15:40:17Z
dc.date.available2023-12-07T15:40:17Z
dc.date.issued2020-03
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/186446
dc.description.abstractEnMild-traumatic brain injury (mTBI) represents ~80% of all emergency room visits and increases the probability of developing long-term cognitive disorders in children. To date, molecular and cellular mechanisms underlying post-mTBI cognitive dysfunction are unknown. Astrogliosis has been shown to significantly alter astrocytes' properties following brain injury, potentially leading to significant brain dysfunction. However, such alterations have never been investigated in the context of juvenile mTBI (jmTBI). A closed-head injury model was used to study jmTBI on postnatal-day 17 mice. Astrogliosis was evaluated using glial fibrillary acidic protein (GFAP), vimentin, and nestin immunolabeling in somatosensory cortex (SSC), dentate gyrus (DG), amygdala (AMY), and infralimbic area (ILA) of prefrontal cortex in both hemispheres from 1 to 30 days postinjury (dpi). In vivo T2-weighted-imaging (T2WI) and diffusion tensor imaging (DTI) were performed at 7 and 30 dpi to examine tissue level structural alterations. Increased GFAP-labeling was observed up to 30 dpi in the ipsilateral SSC, the initial site of the impact. However, vimentin and nestin expression was not perturbed by jmTBI. The morphology of GFAP positive cells was significantly altered in the SSC, DG, AMY, and ILA up to 7 dpi that some correlated with magnetic resonance imaging changes. T2WI and DTI values were significantly altered at 30 dpi within these brain regions most prominently in regions distant from the impact site. Our data show that jmTBI triggers changes in astrocytic phenotype with a distinct spatiotemporal pattern. We speculate that the presence and time course of astrogliosis may contribute to pathophysiological processes and long-term structural alterations following jmTBI. © 2019 Wiley Periodicals, Inc.
dc.description.sponsorshipTranslational Research and Advanced Imaging Laboratoryen_US
dc.description.sponsorshipBordeaux Region Aquitaine Initiative for Neuroscience - ANR-10-LABX-0043en_US
dc.language.isoENen_US
dc.subject.enMRI
dc.subject.enHistology
dc.subject.enNeuroinflammation
dc.subject.enTraumatic brain injury
dc.title.enJuvenile mild traumatic brain injury elicits distinct spatiotemporal astrocyte responses
dc.title.alternativeGliaen_US
dc.typeArticle de revueen_US
dc.identifier.doi10.1002/glia.23736en_US
dc.subject.halSciences du Vivant [q-bio]/Neurosciences [q-bio.NC]en_US
dc.identifier.pubmed31670865en_US
bordeaux.journalGliaen_US
bordeaux.page528-542en_US
bordeaux.volume68en_US
bordeaux.hal.laboratoriesNeurocentre Magendie - U1215en_US
bordeaux.issue3en_US
bordeaux.institutionUniversité de Bordeauxen_US
bordeaux.institutionINSERMen_US
bordeaux.institutionCNRS
bordeaux.teamNeurogénèse et physiopathologieen_US
bordeaux.peerReviewedouien_US
bordeaux.inpressnonen_US
bordeaux.identifier.funderIDDirection Générale de l’Armementen_US
hal.popularnonen_US
hal.audienceInternationaleen_US
hal.exportfalse
dc.rights.ccPas de Licence CCen_US
bordeaux.COinSctx_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.jtitle=Glia&rft.date=2020-03&rft.volume=68&rft.issue=3&rft.spage=528-542&rft.epage=528-542&rft.au=CLEMENT,%20Tifenn&LEE,%20Jeong%20Bin&ICHKOVA,%20Aleksandra&RODRIGUEZ-GRANDE,%20Beatriz&FOURNIER,%20Marie-Line&rft.genre=article


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