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      Glutamate uptake into astrocytes stimulates aerobic glycolysis: a mechanism coupling neuronal activity to glucose utilization.

      Proceedings of the National Academy of Sciences of the United States of America

      Aerobiosis, Animals, Animals, Newborn, Astrocytes, drug effects, metabolism, Biological Transport, Brain, physiology, radionuclide imaging, Cells, Cultured, Cerebral Cortex, Deoxyglucose, Excitatory Amino Acid Antagonists, pharmacology, Glutamic Acid, Glycolysis, Lactates, Mice, Models, Neurological, Neurons, Sodium-Potassium-Exchanging ATPase, Tritium

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          Abstract

          Glutamate, released at a majority of excitatory synapses in the central nervous system, depolarizes neurons by acting at specific receptors. Its action is terminated by removal from the synaptic cleft mostly via Na(+)-dependent uptake systems located on both neurons and astrocytes. Here we report that glutamate, in addition to its receptor-mediated actions on neuronal excitability, stimulates glycolysis--i.e., glucose utilization and lactate production--in astrocytes. This metabolic action is mediated by activation of a Na(+)-dependent uptake system and not by interaction with receptors. The mechanism involves the Na+/K(+)-ATPase, which is activated by an increase in the intracellular concentration of Na+ cotransported with glutamate by the electrogenic uptake system. Thus, when glutamate is released from active synapses and taken up by astrocytes, the newly identified signaling pathway described here would provide a simple and direct mechanism to tightly couple neuronal activity to glucose utilization. In addition, glutamate-stimulated glycolysis is consistent with data obtained from functional brain imaging studies indicating local nonoxidative glucose utilization during physiological activation.

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          7938003
          45074

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