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Glycogenolysis and Purinergic Signaling

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Glutamate and ATP at the Interface of Metabolism and Signaling in the Brain

Part of the book series: Advances in Neurobiology ((NEUROBIOL,volume 11))

Abstract

Both ATP and glutamate are on one hand essential metabolites in brain and on the other serve a signaling function as transmitters. However, there is the major difference that the flux in the pathway producing transmitter glutamate is comparable to the rate of glucose metabolism in brain, whereas that producing transmitter ATP is orders of magnitude smaller than the metabolic turnover between ATP and ADP. Moreover, de novo glutamate production occurs exclusively in astrocytes, whereas transmitter ATP is produced both in neurons and astrocytes. This chapter deals only with ATP and exclusively with its formation and release in astrocytes, and it focuses on potential associations with glycogenolysis, which is known to be indispensable for the synthesis of glutamate. Glycogenolysis is dependent upon an increase in free intracellular Ca2+ concentration (Ca2+]i). It can be further stimulated by cAMP, but in contrast to widespread beliefs, cAMP can on its own not induce glycogenolysis. Astrocytes generate ATP from accumulated adenosine, and this process does not seem to require glycogenolysis. A minor amount of the generated ATP is utilized as a transmitter, and its synthesis requires the presence of the mainly intracellular nucleoside transporter ENT3. Many transmitters as well as extracellular K+ concentrations high enough to open the voltage-sensitive L-channels for Ca2+ cause a release of transmitter ATP from astrocytes. Adenosine and ATP induce release of ATP by action at several different purinergic receptors. The release evoked by transmitters or elevated K+ concentrations is abolished by DAB, an inhibitor of glycogenolysis.

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Acknowledgment

The careful studies by Henry Matz of adenosine metabolism in cultured astrocytes and neurons 25 years ago are gratefully acknowledged.

Conflict of Interest The authors declare no conflict of interest.

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Authors and Affiliations

  1. Laboratory of Brain Metabolic Diseases, Institute of Metabolic Disease Research and Drug Development, China Medical University, Shenyang, P. R. China

    Leif Hertz M.D., D.Sc., D.Sc. hon., Junnan Xu & Liang Peng

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  1. Leif Hertz M.D., D.Sc., D.Sc. hon.
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  2. Junnan Xu
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  3. Liang Peng
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Correspondence to Leif Hertz M.D., D.Sc., D.Sc. hon. .

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Editors and Affiliations

  1. Department of Neurobiology CIRC 429, University of Alabama, Birmingham, Alabama, USA

    Vladimir Parpura

  2. Faculty of Health and Medical Sciences, Department of Drug Design and Pharmacology, University of Copenhagen, Copenhagen, Denmark

    Arne Schousboe

  3. Faculty of Life Sciences, The University of Manchester, Manchester, United Kingdom

    Alexei Verkhratsky

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Hertz, L., Xu, J., Peng, L. (2014). Glycogenolysis and Purinergic Signaling. In: Parpura, V., Schousboe, A., Verkhratsky, A. (eds) Glutamate and ATP at the Interface of Metabolism and Signaling in the Brain. Advances in Neurobiology, vol 11. Springer, Cham. https://doi.org/10.1007/978-3-319-08894-5_3

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