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dc.rights.licenseopenen_US
hal.structure.identifierNeurocentre Magendie : Physiopathologie de la Plasticité Neuronale [U1215 Inserm - UB]
dc.contributor.authorSHERWOOD, Mark W.
hal.structure.identifierInterdisciplinary Institute for Neuroscience [Bordeaux] [IINS]
dc.contributor.authorARIZONO, Misa
hal.structure.identifierNeurocentre Magendie : Physiopathologie de la Plasticité Neuronale [U1215 Inserm - UB]
dc.contributor.authorPANATIER, Aude
hal.structure.identifierNeurocentre Magendie : Physiopathologie de la Plasticité Neuronale [U1215 Inserm - UB]
dc.contributor.authorOLIET, Stéphane
dc.contributor.authorMIKOSHIBA, Katsuhiko
dc.date.accessioned2021-12-21T15:35:57Z
dc.date.available2021-12-21T15:35:57Z
dc.date.issued2021-07-30
dc.identifier.issn1662-5102en_US
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/124297
dc.description.abstractEnAstrocytes are sensitive to ongoing neuronal/network activities and, accordingly, regulate neuronal functions (synaptic transmission, synaptic plasticity, behavior, etc.) by the context-dependent release of several gliotransmitters (e.g., glutamate, glycine, D-serine, ATP). To sense diverse input, astrocytes express a plethora of G-protein coupled receptors, which couple, via Gi/o and Gq, to the intracellular Ca2+ release channel IP3-receptor (IP3R). Indeed, manipulating astrocytic IP3R-Ca2+ signaling is highly consequential at the network and behavioral level: Depleting IP3R subtype 2 (IP3R2) results in reduced GPCR-Ca2+ signaling and impaired synaptic plasticity; enhancing IP3R-Ca2+ signaling affects cognitive functions such as learning and memory, sleep, and mood. However, as a result of discrepancies in the literature, the role of GPCR-IP3R-Ca2+ signaling, especially under physiological conditions, remains inconclusive. One primary reason for this could be that IP3R2 has been used to represent all astrocytic IP3Rs, including IP3R1 and IP3R3. Indeed, IP3R1 and IP3R3 are unique Ca2+ channels in their own right; they have unique biophysical properties, often display distinct distribution, and are differentially regulated. As a result, they mediate different physiological roles to IP3R2. Thus, these additional channels promise to enrich the diversity of spatiotemporal Ca2+ dynamics and provide unique opportunities for integrating neuronal input and modulating astrocyte-neuron communication. The current review weighs evidence supporting the existence of multiple astrocytic-IP3R isoforms, summarizes distinct sub-type specific properties that shape spatiotemporal Ca2+ dynamics. We also discuss existing experimental tools and future refinements to better recapitulate the endogenous activities of each IP3R isoform.
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.enCalcium
dc.subject.enGliotransmission
dc.subject.enGPCR
dc.subject.enInositol triphosphate (IP3) receptor
dc.subject.enIP3R subtypes
dc.subject.enTripartite synapse
dc.title.enAstrocytic IP3Rs: Beyond IP3R2
dc.title.alternativeFront Cell Neurosci.en_US
dc.typeArticle de revueen_US
dc.identifier.doi10.3389/fncel.2021.695817en_US
dc.subject.halSciences du Vivant [q-bio]/Neurosciences [q-bio.NC]en_US
dc.identifier.pubmed34393726en_US
bordeaux.journalFrontiers in Cellular Neuroscienceen_US
bordeaux.volume15en_US
bordeaux.hal.laboratoriesNeurocentre Magendie - UMR-S 1215en_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
bordeaux.identifier.funderIDTakeda Science Foundationen_US
bordeaux.identifier.funderIDRIKENen_US
bordeaux.identifier.funderIDJapan Science and Technology Agencyen_US
bordeaux.identifier.funderIDCentre National de la Recherche Scientifiqueen_US
bordeaux.identifier.funderIDInstitut National de la Santé et de la Recherche Médicaleen_US
hal.identifierhal-03447677
hal.version1
hal.exporttrue
dc.rights.ccCC BYen_US
bordeaux.COinSctx_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.jtitle=Frontiers%20in%20Cellular%20Neuroscience&rft.date=2021-07-30&rft.volume=15&rft.eissn=1662-5102&rft.issn=1662-5102&rft.au=SHERWOOD,%20Mark%20W.&ARIZONO,%20Misa&PANATIER,%20Aude&OLIET,%20St%C3%A9phane&MIKOSHIBA,%20Katsuhiko&rft.genre=article


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