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Acute feedback control of astrocytic glycolysis by lactate

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Autor Sotelo-Hitschfeld T.
Autor Fernandez-Moncada I.
Autor Barros L.F.
Fecha Ingreso 2014-04-05T00:14:35Z
Fecha Disponible 2014-04-05T00:14:35Z
Fecha en Repositorio 2014-04-04
dc.identifier 10.1002/glia.22304
dc.description.abstract Neuronal activity is accompanied by a rapid increase in interstitial lactate, which is hypothesized to serve as a fuel for neurons and a signal for local vasodilation. Using FRET microscopy, we report here that the rate of glycolysis in cultured mice astrocytes can be acutely modulated by physiological changes in extracellular lactate. Glycolytic inhibition by lactate was not accompanied by detectable variations in intracellular pH or intracellular ATP and was not dependent of mitochondrial function. Pyruvate was also inhibitory, suggesting that the effect of lactate is not mediated by the NADH/NAD + ratio. We propose that lactate serves as a fast negative feedback signal limiting its own production by astrocytes and therefore the amplitude of the lactate surge. The inhibition of glucose usage by lactate was much stronger in resting astrocytes than in K +-stimulated astrocytes, which suggests that lactate may also help diverting glucose from resting to active zones. © 2012 Wiley Periodicals, Inc. en_US
dc.source GLIA
Link Descarga dc.source.uri
Title dc.title Acute feedback control of astrocytic glycolysis by lactate en_US
Tipo dc.type Article
dc.description.keywords adenosine triphosphate; lactic acid; nicotinamide adenine dinucleotide; pyruvic acid; reduced nicotinamide adenine dinucleotide; animal cell; animal experiment; article; astrocyte; feedback system; fluorescence resonance energy transfer; glycolysis; male; microscopy; mitochondrion; mouse; nerve conduction; newborn; nonhuman; pH; priority journal; Adenosine Triphosphate; Analysis of Variance; Animals; Animals, Newborn; Astrocytes; Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone; Cells, Cultured; Cerebral Cortex; Cytochalasin B; Cytosol; Dose-Response Relationship, Drug; Enzyme Inhibitors; Extracellular Fluid; Feedback, Physiological; Glucose; Glycolysis; Hydrogen-Ion Concentration; Iodoacetic Acid; Lactic Acid; Male; Mice; Mice, Inbred C57BL; Mice, Inbred CBA; Potassium; Proton Ionophores; Rotenone en_US

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