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    Channel-Mediated Lactate Release by K+-Stimulated Astrocytes

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    Type
    Article
    Authors
    Sotelo-Hitschfeld, T.
    Niemeyer, M. I.
    Machler, P.
    Ruminot, I.
    Lerchundi, R.
    Wyss, M. T.
    Stobart, J.
    Fernandez-Moncada, I.
    Valdebenito, R.
    Garrido-Gerter, P.
    Contreras-Baeza, Y.
    Schneider, B. L.
    Aebischer, P.
    Lengacher, S.
    San Martin, A.
    Le Douce, J.
    Bonvento, G.
    Magistretti, Pierre J. cc
    Sepulveda, F. V.
    Weber, B.
    Barros, L. F.
    KAUST Department
    Biological and Environmental Sciences and Engineering (BESE) Division
    Bioscience Program
    Date
    2015-03-11
    Online Publication Date
    2015-03-11
    Print Publication Date
    2015-03-11
    Permanent link to this record
    http://hdl.handle.net/10754/579843
    
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    Abstract
    Excitatory 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.
    Citation
    Channel-Mediated Lactate Release by K+-Stimulated Astrocytes 2015, 35 (10):4168 Journal of Neuroscience
    Publisher
    Society for Neuroscience
    Journal
    Journal of Neuroscience
    DOI
    10.1523/JNEUROSCI.5036-14.2015
    PubMed ID
    25762664
    Additional Links
    http://www.jneurosci.org/cgi/doi/10.1523/JNEUROSCI.5036-14.2015
    ae974a485f413a2113503eed53cd6c53
    10.1523/JNEUROSCI.5036-14.2015
    Scopus Count
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    Articles; Biological and Environmental Science and Engineering (BESE) Division; Bioscience Program

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