Afficher la notice abrégée

dc.rights.licenseopenen_US
hal.structure.identifierNeurocentre Magendie : Physiopathologie de la Plasticité Neuronale [U1215 Inserm - UB]
dc.contributor.authorSHERWOOD, Mark W.
hal.structure.identifierNeurocentre Magendie : Physiopathologie de la Plasticité Neuronale [U1215 Inserm - UB]
dc.contributor.authorOLIET, Stéphane
hal.structure.identifierNeurocentre Magendie : Physiopathologie de la Plasticité Neuronale [U1215 Inserm - UB]
dc.contributor.authorPANATIER, Aude
dc.date.accessioned2022-01-05T11:57:20Z
dc.date.available2022-01-05T11:57:20Z
dc.date.issued2021-07-06
dc.identifier.issn1422-0067en_US
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/124322
dc.description.abstractEnSynaptic plasticity is an extensively studied cellular correlate of learning and memory in which NMDARs play a starring role. One of the most interesting features of NMDARs is their ability to act as a co-incident detector. It is unique amongst neurotransmitter receptors in this respect. Coincident detection is possible because the opening of NMDARs requires membrane depolarisation and the binding of glutamate. Opening of NMDARs also requires a co-agonist. Although the dynamic regulation of glutamate and membrane depolarization have been well studied in coincident detection, the role of the co-agonist site is unexplored. It turns out that non-neuronal glial cells, astrocytes, regulate co-agonist availability, giving them the ability to influence synaptic plasticity. The unique morphology and spatial arrangement of astrocytes at the synaptic level affords them the capacity to sample and integrate information originating from unrelated synapses, regardless of any pre-synaptic and post-synaptic commonality. As astrocytes are classically considered slow re-sponders, their influence at the synapse is widely recognized as modulatory. The aim herein is to reconsider the potential of astrocytes to participate directly in ongoing synaptic NMDAR activity and co-incident detection.
dc.description.sponsorshipContribution des récepteurs IP3 et du réticulum endoplasmique à la signalisation Ca2+ dans les astrocytes - ANR-17-CE16-0002en_US
dc.description.sponsorshipExploration fonctionnelle du domaine astrocytaire - ANR-16-CE16-0001en_US
dc.language.isoENen_US
dc.rightsAttribution 3.0 United States*
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/us/*
dc.subject.enAstrocyte
dc.subject.enCoincident detection
dc.subject.enD-serine
dc.subject.enGliotransmission
dc.subject.enGlycine
dc.subject.enNeuron
dc.subject.enNMDAR
dc.subject.enSynapse cluster
dc.subject.enTrip-partite synapse
dc.title.enNMDARs, coincidence detectors of astrocytic and neuronal activities
dc.title.alternativeInt J Mol Scien_US
dc.typeArticle de revueen_US
dc.identifier.doi10.3390/ijms22147258en_US
dc.subject.halSciences du Vivant [q-bio]/Neurosciences [q-bio.NC]en_US
dc.identifier.pubmed34298875en_US
bordeaux.journalInternational journal of molecular sciencesen_US
bordeaux.volume22en_US
bordeaux.hal.laboratoriesNeurocentre Magendie - UMR-S 1215en_US
bordeaux.issue14en_US
bordeaux.institutionUniversité de Bordeauxen_US
bordeaux.institutionCNRSen_US
bordeaux.institutionINSERMen_US
bordeaux.peerReviewedouien_US
bordeaux.inpressnonen_US
bordeaux.identifier.funderIDLabEx BRAINen_US
bordeaux.identifier.funderIDAgence Nationale de la Rechercheen_US
hal.exportfalse
dc.rights.ccCC BYen_US
bordeaux.COinSctx_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.jtitle=International%20journal%20of%20molecular%20sciences&rft.date=2021-07-06&rft.volume=22&rft.issue=14&rft.eissn=1422-0067&rft.issn=1422-0067&rft.au=SHERWOOD,%20Mark%20W.&OLIET,%20St%C3%A9phane&PANATIER,%20Aude&rft.genre=article


Fichier(s) constituant ce document

Thumbnail
Thumbnail

Ce document figure dans la(les) collection(s) suivante(s)

Afficher la notice abrégée