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Autoimmune inflammation triggers aberrant astrocytic calcium signaling to impair synaptic plasticity

dc.rights.licenseopenen_US
dc.contributor.authorBARAIBAR, A.M.
dc.contributor.authorCOLOMER, T.
dc.contributor.authorMORENO-GARCÍA, A.
dc.contributor.authorBERNAL-CHICO, A.
dc.contributor.authorSÁNCHEZ-MARTÍN, E.
dc.contributor.authorUTRILLA, C.
dc.contributor.authorSERRAT, R.
dc.contributor.authorSORIA-GÓMEZ, E.
dc.contributor.authorRODRÍGUEZ-ANTIGÜEDAD, A.
dc.contributor.authorARAQUE, A.
dc.contributor.authorMATUTE, C.
hal.structure.identifierNeurocentre Magendie : Physiopathologie de la Plasticité Neuronale [U1215 Inserm - UB]
dc.contributor.authorMARSICANO, Giovanni
dc.contributor.authorMATO, S.
dc.date.accessioned2025-05-23T13:38:54Z
dc.date.available2025-05-23T13:38:54Z
dc.date.issued2024-10
dc.identifier.issn0889-1591en_US
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/206702
dc.description.abstractEnCortical pathology involving inflammatory and neurodegenerative mechanisms is a hallmark of multiple sclerosis and a correlate of disease progression and cognitive decline. Astrocytes play a pivotal role in multiple sclerosis initiation and progression but astrocyte-neuronal network alterations contributing to gray matter pathology remain undefined. Here we unveil deregulation of astrocytic calcium signaling and astrocyte-to-neuron communication as key pathophysiological mechanisms of cortical dysfunction in the experimental autoimmune encephalomyelitis (EAE) model of multiple sclerosis. Using two-photon imaging ex vivo and fiber photometry in freely behaving mice, we found that acute EAE was associated with the emergence of spontaneously hyperactive cortical astrocytes exhibiting dysfunctional responses to cannabinoid, glutamate and purinoreceptor agonists. Abnormal astrocyte signaling by Gi and Gq protein coupled receptors was observed in the inflamed cortex. This was mirrored by treatments with pro-inflammatory factors both in vitro and ex vivo, suggesting cell-autonomous effects of the cortical neuroinflammatory environment. Finally, deregulated astrocyte calcium activity was associated with an enhancement of glutamatergic gliotransmission and a shift of astrocyte-mediated short-term and long-term plasticity mechanisms towards synaptic potentiation. Overall, our data identify astrocyte-neuronal network dysfunctions as key pathological features of gray matter inflammation in multiple sclerosis and potentially additional neuroimmunological disorders. © 2024 The Author(s)
dc.description.sponsorshipRôle du système endocannabinoïde de l'hippocampe dans le déficits de mémoire associés à l'obésitéen_US
dc.description.sponsorshipInvolvement of the insula in the Autism neurodevelopmental disorderen_US
dc.language.isoENen_US
dc.rightsAttribution-NonCommercial 3.0 United States*
dc.rights.urihttp://creativecommons.org/licenses/by-nc/3.0/us/*
dc.subject.enAstrocyte
dc.subject.enCalcium
dc.subject.enGliotransmission
dc.subject.enMultiple sclerosis
dc.subject.enCortex
dc.title.enAutoimmune inflammation triggers aberrant astrocytic calcium signaling to impair synaptic plasticity
dc.title.alternativeBrain Behav Immunen_US
dc.typeArticle de revueen_US
dc.identifier.doi10.1016/j.bbi.2024.07.010en_US
dc.subject.halSciences du Vivant [q-bio]/Neurosciences [q-bio.NC]en_US
dc.identifier.pubmed39032542en_US
dc.description.sponsorshipEuropeMitochondrial Cannabinoid Receptors in the Brainen_US
bordeaux.journalBrain, Behavior, and Immunityen_US
bordeaux.page192 – 210en_US
bordeaux.volume121en_US
bordeaux.hal.laboratoriesNeurocentre Magendie - U1215en_US
bordeaux.institutionUniversité de Bordeauxen_US
bordeaux.institutionINSERMen_US
bordeaux.teamEndocannabinoïdes et Neuroadaptationen_US
bordeaux.peerReviewedouien_US
bordeaux.inpressnonen_US
bordeaux.identifier.funderIDInstituto de Salud Carlos IIIen_US
bordeaux.identifier.funderIDConseil Régional Aquitaineen_US
bordeaux.identifier.funderIDMinisterio de Ciencia e Innovaciónen_US
hal.identifierhal-05082376
hal.version1
hal.date.transferred2025-05-23T13:38:58Z
hal.popularnonen_US
hal.audienceInternationaleen_US
hal.exporttrue
dc.rights.ccCC BY-NCen_US
bordeaux.COinSctx_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.jtitle=Brain,%20Behavior,%20and%20Immunity&rft.date=2024-10&rft.volume=121&rft.spage=192%20%E2%80%93%20210&rft.epage=192%20%E2%80%93%20210&rft.eissn=0889-1591&rft.issn=0889-1591&rft.au=BARAIBAR,%20A.M.&COLOMER,%20T.&MORENO-GARC%C3%8DA,%20A.&BERNAL-CHICO,%20A.&S%C3%81NCHEZ-MART%C3%8DN,%20E.&rft.genre=article


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