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dc.relation.isnodoublecc41509b-60ca-4086-bab3-cbcf9a2ccb03*
dc.relation.isnodouble6678be63-f982-490c-904a-a9685ecdfb9d*
hal.structure.identifierUniversité de Bordeaux [UB]
hal.structure.identifierPhysiopathologie du système nerveux central - Institut François Magendie
dc.contributor.authorPLANCHE, Vincent
hal.structure.identifierPhysiopathologie du système nerveux central - Institut François Magendie
dc.contributor.authorPANATIER, Aude
hal.structure.identifierInstitut de Neurosciences cognitives et intégratives d'Aquitaine [INCIA]
dc.contributor.authorHIBA, Bassem
dc.contributor.authorDUCOURNEAU, Eva-Gunnel
hal.structure.identifierCentre de résonance magnétique des systèmes biologiques [CRMSB]
dc.contributor.authorRAFFARD, Gérard
hal.structure.identifierPhysiopathologie du système nerveux central - Institut François Magendie
dc.contributor.authorDUBOURDIEU, Nadège
hal.structure.identifierPhysiopathologie du système nerveux central - Institut François Magendie
dc.contributor.authorMAITRE, Marlène
hal.structure.identifierPhysiopathologie du système nerveux central - Institut François Magendie
dc.contributor.authorLESTE-LASSERRE, Thierry
hal.structure.identifierService de neurologie [Bordeaux]
dc.contributor.authorBROCHET, Bruno
hal.structure.identifierService de neurologie [Bordeaux]
dc.contributor.authorDOUSSET, Vincent
hal.structure.identifierPhysiopathologie du système nerveux central - Institut François Magendie
dc.contributor.authorDESMEDT, Aline
hal.structure.identifierPhysiopathologie du système nerveux central - Institut François Magendie
dc.contributor.authorOLIET, Stéphane
hal.structure.identifierService de neurologie [Bordeaux]
dc.contributor.authorTOURDIAS, Thomas
dc.date.accessioned2021-10-07T16:29:22Z
dc.date.available2021-10-07T16:29:22Z
dc.date.issued2017-02
dc.identifier.issn0889-1591
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/112648
dc.description.abstractEnMemory impairment is an early and disabling manifestation of multiple sclerosis whose anatomical and biological substrates are still poorly understood. We thus investigated whether memory impairment encountered at the early stage of the disease could be explained by a differential vulnerability of particular hippocampal subfields. By using experimental autoimmune encephalomyelitis (EAE), a mouse model of multiple sclerosis, we identified that early memory impairment was associated with selective alteration of the dentate gyrus as pinpointed in vivo with diffusion-tensor-imaging (DTI). Neuromorphometric analyses and electrophysiological recordings confirmed dendritic degeneration, alteration in glutamatergic synaptic transmission and impaired long-term synaptic potentiation selectively in the dentate gyrus, but not in CA1, together with a more severe pattern of microglial activation in this subfield. Systemic injections of the microglial inhibitor minocycline prevented DTI, morphological, electrophysiological and behavioral impairments in EAE-mice. Furthermore, daily infusions of minocy-cline specifically within the dentate gyrus were sufficient to prevent memory impairment in EAE-mice while infusions of minocycline within CA1 were inefficient. We conclude that early memory impairment in EAE is due to a selective disruption of the dentate gyrus associated with microglia activation. These results open new pathophysiological, imaging, and therapeutic perspectives for memory impairment in multiple sclerosis.
dc.language.isoen
dc.publisherElsevier
dc.title.enSelective dentate gyrus disruption causes memory impairment at the early stage of experimental multiple sclerosis
dc.typeArticle de revue
dc.identifier.doi10.1016/j.bbi.2016.11.010
dc.subject.halSciences du Vivant [q-bio]
bordeaux.journalBrain, Behavior, and Immunity
bordeaux.page240-254
bordeaux.volume60
bordeaux.hal.laboratoriesCentre de Résonance Magnétique des Systèmes Biologiques (CRMSB) - UMR 5536*
bordeaux.institutionUniversité de Bordeaux
bordeaux.institutionCNRS
bordeaux.peerReviewedoui
hal.identifierhal-02404774
hal.version1
hal.origin.linkhttps://hal.archives-ouvertes.fr//hal-02404774v1
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