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dc.rights.licenseopenen_US
hal.structure.identifierNeurocentre Magendie : Physiopathologie de la Plasticité Neuronale [U1215 Inserm - UB]
dc.contributor.authorMOREAU, Maite M.
hal.structure.identifierInstitut de Neurosciences cognitives et intégratives d'Aquitaine [INCIA]
dc.contributor.authorPIETROPAOLO, Susanna
hal.structure.identifierNeurocentre Magendie : Physiopathologie de la Plasticité Neuronale [U1215 Inserm - UB]
dc.contributor.authorEZAN, Jerome
hal.structure.identifierNeurocentre Magendie : Physiopathologie de la Plasticité Neuronale [U1215 Inserm - UB]
dc.contributor.authorROBERT, Benjamin J. A.
hal.structure.identifierCentre de résonance magnétique des systèmes biologiques [CRMSB]
dc.contributor.authorMIRAUX, Sylvain
IDREF: 150967047
hal.structure.identifierNeurocentre Magendie : Physiopathologie de la Plasticité Neuronale [U1215 Inserm - UB]
dc.contributor.authorMAITRE, Marlene
hal.structure.identifierInstitut de Neurosciences cognitives et intégratives d'Aquitaine [INCIA]
dc.contributor.authorCHO, Yoon
hal.structure.identifierInstitut de Neurosciences cognitives et intégratives d'Aquitaine [INCIA]
dc.contributor.authorCRUSIO, Wim E.
hal.structure.identifierNeurocentre Magendie : Physiopathologie de la Plasticité Neuronale [U1215 Inserm - UB]
dc.contributor.authorMONTCOUQUIOL, Mireille
hal.structure.identifierNeurocentre Magendie : Physiopathologie de la Plasticité Neuronale [U1215 Inserm - UB]
dc.contributor.authorSANS, Nathalie
dc.date.accessioned2022-06-30T09:26:11Z
dc.date.available2022-06-30T09:26:11Z
dc.date.issued2022-05-10
dc.identifier.issn2073-4409en_US
dc.identifier.urioai:crossref.org:10.3390/cells11101601
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/140342
dc.description.abstractEnSocial behavior is a basic domain affected by several neurodevelopmental disorders, including ASD and a heterogeneous set of neuropsychiatric disorders. The SCRIB gene that codes for the polarity protein SCRIBBLE has been identified as a risk gene for spina bifida, the most common type of neural tube defect, found at high frequencies in autistic patients, as well as other congenital anomalies. The deletions and mutations of the 8q24.3 region encompassing SCRIB are also associated with multisyndromic and rare disorders. Nonetheless, the potential link between SCRIB and relevant social phenotypes has not been fully investigated. Hence, we show that Scribcrc/+ mice, carrying a mutated version of Scrib, displayed reduced social motivation behavior and social habituation, while other behavioral domains were unaltered. Social deficits were associated with the upregulation of ERK phosphorylation, together with increased c-Fos activity. Importantly, the social alterations were rescued by both direct and indirect pERK inhibition. These results support a link between polarity genes, social behaviors and hippocampal functionality and suggest a role for SCRIB in the etiopathology of neurodevelopmental disorders. Furthermore, our data demonstrate the crucial role of the MAPK/ERK signaling pathway in underlying social motivation behavior, thus supporting its relevance as a therapeutic target.
dc.description.sponsorshipCodage de l'information sociale dans l'hippocampe et la synchronie des réseaux neuronaux dans l'autisme - ANR-13-SAMA-0012en_US
dc.description.sponsorshipDéveloppment d'une infrastructure française distribuée coordonnéeen_US
dc.description.sponsorshipBordeaux Region Aquitaine Initiative for Neuroscience - ANR-10-LABX-0043en_US
dc.language.isoENen_US
dc.rightsAttribution 3.0 United States*
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/us/*
dc.sourcecrossref
dc.subjectHumans
dc.subject.enAnimals
dc.subject.enIntracellular Signaling Peptides and Proteins
dc.subject.enGenetics
dc.subject.enMAP Kinase Signaling System
dc.subject.enMice
dc.subject.enMotivation
dc.subject.enMutation
dc.subject.enProtein Serine-Threonine Kinases
dc.subject.enMetabolism
dc.subject.enSignal Transduction
dc.subject.enSocial Behavior
dc.title.enScribble Controls Social Motivation Behavior through the Regulation of the ERK/Mnk1 Pathway
dc.typeArticle de revueen_US
dc.identifier.doi10.3390/cells11101601en_US
dc.subject.halSciences du Vivant [q-bio]/Neurosciences [q-bio.NC]en_US
dc.identifier.pubmed35626639en_US
bordeaux.journalCellsen_US
bordeaux.page1601en_US
bordeaux.volume11en_US
bordeaux.hal.laboratoriesNeurocentre Magendie - UMR-S 1215en_US
bordeaux.issue10en_US
bordeaux.institutionUniversité de Bordeauxen_US
bordeaux.institutionCNRSen_US
bordeaux.institutionINSERMen_US
bordeaux.peerReviewedouien_US
bordeaux.inpressnonen_US
bordeaux.identifier.funderIDAgence Nationale de la Rechercheen_US
bordeaux.import.sourcedissemin
hal.identifierhal-03709848
hal.version1
hal.date.transferred2022-06-30T09:26:22Z
hal.exporttrue
workflow.import.sourcedissemin
dc.rights.ccCC BYen_US
bordeaux.COinSctx_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.jtitle=Cells&rft.date=2022-05-10&rft.volume=11&rft.issue=10&rft.spage=1601&rft.epage=1601&rft.eissn=2073-4409&rft.issn=2073-4409&rft.au=MOREAU,%20Maite%20M.&PIETROPAOLO,%20Susanna&EZAN,%20Jerome&ROBERT,%20Benjamin%20J.%20A.&MIRAUX,%20Sylvain&rft.genre=article


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