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dc.contributor.authorSotelo-Hitschfeld, T.
dc.contributor.authorNiemeyer, M. I.
dc.contributor.authorMachler, P.
dc.contributor.authorRuminot, I.
dc.contributor.authorLerchundi, R.
dc.contributor.authorWyss, M. T.
dc.contributor.authorStobart, J.
dc.contributor.authorFernandez-Moncada, I.
dc.contributor.authorValdebenito, R.
dc.contributor.authorGarrido-Gerter, P.
dc.contributor.authorContreras-Baeza, Y.
dc.contributor.authorSchneider, B. L.
dc.contributor.authorAebischer, P.
dc.contributor.authorLengacher, S.
dc.contributor.authorSan Martin, A.
dc.contributor.authorLe Douce, J.
dc.contributor.authorBonvento, G.
dc.contributor.authorMagistretti, Pierre J.
dc.contributor.authorSepulveda, F. V.
dc.contributor.authorWeber, B.
dc.contributor.authorBarros, L. F.
dc.date.accessioned2015-10-18T14:42:32Z
dc.date.available2015-10-18T14:42:32Z
dc.date.issued2015-03-11
dc.identifier.citationChannel-Mediated Lactate Release by K+-Stimulated Astrocytes 2015, 35 (10):4168 Journal of Neuroscience
dc.identifier.issn0270-6474
dc.identifier.issn1529-2401
dc.identifier.pmid25762664
dc.identifier.doi10.1523/JNEUROSCI.5036-14.2015
dc.identifier.urihttp://hdl.handle.net/10754/579843
dc.description.abstractExcitatory synaptic transmission is accompanied by a local surge in interstitial lactate that occurs despite adequate oxygen availability, a puzzling phenomenon termed aerobic glycolysis. In addition to its role as an energy substrate, recent studies have shown that lactate modulates neuronal excitability acting through various targets, including NMDA receptors and G-protein-coupled receptors specific for lactate, but little is known about the cellular and molecular mechanisms responsible for the increase in interstitial lactate. Using a panel of genetically encoded fluorescence nanosensors for energy metabolites, we show here that mouse astrocytes in culture, in cortical slices, and in vivo maintain a steady-state reservoir of lactate. The reservoir was released to the extracellular space immediately after exposure of astrocytes to a physiological rise in extracellular K+ or cell depolarization. Cell-attached patch-clamp analysis of cultured astrocytes revealed a 37 pS lactate-permeable ion channel activated by cell depolarization. The channel was modulated by lactate itself, resulting in a positive feedback loop for lactate release. A rapid fall in intracellular lactate levels was also observed in cortical astrocytes of anesthetized mice in response to local field stimulation. The existence of an astrocytic lactate reservoir and its quick mobilization via an ion channel in response to a neuronal cue provides fresh support to lactate roles in neuronal fueling and in gliotransmission.
dc.language.isoen
dc.publisherSociety for Neuroscience
dc.relation.urlhttp://www.jneurosci.org/cgi/doi/10.1523/JNEUROSCI.5036-14.2015
dc.rightsArchived with thanks to Journal of Neuroscience
dc.titleChannel-Mediated Lactate Release by K+-Stimulated Astrocytes
dc.typeArticle
dc.contributor.departmentBiological and Environmental Sciences and Engineering (BESE) Division
dc.contributor.departmentBioscience Program
dc.identifier.journalJournal of Neuroscience
dc.eprint.versionPublisher's Version/PDF
dc.contributor.institutionCentro de Estudios Científicos, Valdivia 5110466, Chile
dc.contributor.institutionInstitute of Pharmacology and Toxicology, University of Zürich, 8057 Zürich, Switzerland
dc.contributor.institutionNeuroscience Center Zürich, University and ETH Zürich, 8092 Zürich, Switzerland
dc.contributor.institutionUniversidad Austral de Chile, Valdivia, Chile
dc.contributor.institutionBrain Mind Institute, École Polytechnique Fédérale de Lausanne, CH-1015 Lausanne, Switzerland
dc.contributor.institutionCommissariat à l'Energie Atomique, Institut d'Imagerie Biomédicale, Molecular Imaging Research Center and Centre National de la Recherche Scientifique, Université Paris-Sud, Université Paris-Saclay, UMR 9199, F-92265 Fontenay-aux-Roses, France
dc.contributor.affiliationKing Abdullah University of Science and Technology (KAUST)
kaust.personMagistretti, Pierre J.
refterms.dateFOA2018-06-13T09:53:24Z
dc.date.published-online2015-03-11
dc.date.published-print2015-03-11


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