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dc.rights.licenseopenen_US
dc.contributor.authorFREITAS, Andiara E.
dc.contributor.authorFENG, Bo
dc.contributor.authorWOO, Timothy
dc.contributor.authorGALLI, Shae
dc.contributor.authorBAKER, Clayton
dc.contributor.authorBAN, Yue
dc.contributor.authorTRUONG, Jonathan
hal.structure.identifierNeurocentre Magendie : Physiopathologie de la Plasticité Neuronale [U1215 Inserm - UB]
dc.contributor.authorBEYELER, Anna
ORCID: 0000-0003-2371-5706
IDREF: 141902892
dc.contributor.authorZOU, Yimin
dc.date.accessioned2025-05-30T12:44:41Z
dc.date.available2025-05-30T12:44:41Z
dc.date.issued2024-06-10
dc.identifier.issn2041-1723en_US
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/206792
dc.description.abstractEnSingle administration of low-dose ketamine has both acute and sustained anti-depressant effects. Sustained effect is associated with restoration of glutamatergic synapses in medial prefrontal cortic (mFPC) neurons. Ketamine induced profound changes in a number of molecular pathways in a mouse model for chronic stress. Cell-cell communication analyses predicted that planar-cell-polarity (PCP) signaling was decreased after chronic administration of corticosterone but increased following ketamine administration in most of the excitatory neurons. Similar decrease of PCP signaling in excitatory neurons was predicted in dorsolateral prefrontal cortical (dl-PFC) neurons of patients with major depressive disorder (MDD). We showed that the basolateral amygdala (BLA)-projecting infralimbic prefrontal cortex (IL PFC) neurons regulate immobility time in the tail suspension test and food consumption. Conditionally knocking out Celsr2 and Celsr3 or Prickle2 in the BLA-projecting IL PFC neurons abolished ketamine-induced synapse restoration and behavioral remission. Therefore, PCP proteins in IL PFC-BLA neurons mediate synapse restoration induced by of low-dose ketamine. © The Author(s) 2024.
dc.language.isoENen_US
dc.rightsAttribution 3.0 United States*
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/us/*
dc.subject.enAnimals
dc.subject.enAntidepressive Agents
dc.subject.enBasolateral Nuclear Complex
dc.subject.enCell Polarity
dc.subject.enCorticosterone
dc.subject.enDepressive Disorder Major
dc.subject.enDisease Models
dc.subject.enGlutamic Acid
dc.subject.enHumans
dc.subject.enKetamine
dc.subject.enLIM Domain Proteins
dc.subject.enMale
dc.subject.enMice
dc.subject.enInbred C57BL
dc.subject.enKnockout
dc.subject.enNeurons
dc.subject.enPrefrontal Cortex
dc.subject.enStress Psychological
dc.subject.enSynapses
dc.title.enPlanar cell polarity proteins mediate ketamine-induced restoration of glutamatergic synapses in prefrontal cortical neurons in a mouse model for chronic stress
dc.title.alternativeNat Communen_US
dc.typeArticle de revueen_US
dc.identifier.doi10.1038/s41467-024-48257-6en_US
dc.subject.halSciences du Vivant [q-bio]/Neurosciences [q-bio.NC]en_US
dc.identifier.pubmed38858386en_US
bordeaux.journalNature Communicationsen_US
bordeaux.volume15en_US
bordeaux.hal.laboratoriesNeurocentre Magendie - U1215en_US
bordeaux.issue1en_US
bordeaux.institutionUniversité de Bordeauxen_US
bordeaux.institutionINSERMen_US
bordeaux.teamCircuits Neuronaux de l'Anxiétéen_US
bordeaux.peerReviewedouien_US
bordeaux.inpressnonen_US
hal.identifierhal-05090776
hal.version1
hal.date.transferred2025-05-30T12:44:48Z
hal.popularnonen_US
hal.audienceInternationaleen_US
hal.exporttrue
dc.rights.ccCC BYen_US
bordeaux.COinSctx_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.jtitle=Nature%20Communications&rft.date=2024-06-10&rft.volume=15&rft.issue=1&rft.eissn=2041-1723&rft.issn=2041-1723&rft.au=FREITAS,%20Andiara%20E.&FENG,%20Bo&WOO,%20Timothy&GALLI,%20Shae&BAKER,%20Clayton&rft.genre=article


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