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dc.rights.licenseopenen_US
hal.structure.identifierNeurocentre Magendie : Physiopathologie de la Plasticité Neuronale [U1215 Inserm - UB]
dc.contributor.authorFERNANDEZ-MONCADA, Ignacio
dc.contributor.authorROBLES-MALDONADO, Daniel
dc.contributor.authorCASTRO, Pablo
dc.contributor.authorALEGRIA, Karin
dc.contributor.authorEPP, Robert
dc.contributor.authorRUMINOT, Ivan
dc.contributor.authorBARROS, Luis Felipe
dc.date.accessioned2022-03-15T17:14:27Z
dc.date.available2022-03-15T17:14:27Z
dc.date.issued2021-04
dc.identifier.issn1098-1136en_US
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/136469
dc.description.abstractEnThe acute rise in interstitial K+ that accompanies neural activity couples the energy demand of neurons to the metabolism of astrocytes. The effects of elevated K+ on astrocytes include activation of aerobic glycolysis, inhibition of mitochondrial respiration and the release of lactate. Using a genetically encoded FRET glucose sensor and a novel protocol based on 3-O-methylglucose trans-acceleration and numerical simulation of glucose dynamics, we report that extracellular K+ is also a potent and reversible modulator of the astrocytic glucose transporter GLUT1. In cultured mouse astrocytes, the stimulatory effect developed within seconds, engaged both the influx and efflux modes of the transporter, and was detected even at 1 mM incremental K+. The modulation of GLUT1 explains how astrocytes are able to maintain their glucose pool in the face of strong glycolysis stimulation. We propose that the stimulation of GLUT1 by K+ supports the production of lactate by astrocytes and the timely delivery of glucose to active neurons.
dc.language.isoENen_US
dc.subject.en3-O-methylglucose
dc.subject.enFluorescence microscopy
dc.subject.enGenetically encoded FRET sensor
dc.subject.enGlucose transport
dc.title.enBidirectional astrocytic GLUT1 activation by elevated extracellular K+
dc.typeArticle de revueen_US
dc.identifier.doi10.1002/glia.23944en_US
dc.subject.halSciences du Vivant [q-bio]/Neurosciences [q-bio.NC]en_US
dc.identifier.pubmed33277953en_US
bordeaux.journalGliaen_US
bordeaux.page1012-1021en_US
bordeaux.volume69en_US
bordeaux.hal.laboratoriesNeurocentre Magendie - UMR-S 1215en_US
bordeaux.issue4en_US
bordeaux.institutionUniversité de Bordeauxen_US
bordeaux.institutionINSERMen_US
bordeaux.peerReviewedouien_US
bordeaux.inpressnonen_US
hal.identifierhal-03609721
hal.version1
hal.date.transferred2022-03-15T17:14:29Z
hal.exporttrue
dc.rights.ccPas de Licence CCen_US
bordeaux.COinSctx_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.jtitle=Glia&rft.date=2021-04&rft.volume=69&rft.issue=4&rft.spage=1012-1021&rft.epage=1012-1021&rft.eissn=1098-1136&rft.issn=1098-1136&rft.au=FERNANDEZ-MONCADA,%20Ignacio&ROBLES-MALDONADO,%20Daniel&CASTRO,%20Pablo&ALEGRIA,%20Karin&EPP,%20Robert&rft.genre=article


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