QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

HOME  |   SEARCH  |   ARCHIVE  |   SUBSCRIBE  |   CONTACT  |   HELP

This Article Full Text Full Text (PDF) Submit an eLetter Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (24) Citing Articles via Google Scholar Google Scholar Articles by Tsacopoulos, M. Articles by Poitry, S. Search for Related Content PubMed PubMed Citation Articles by Tsacopoulos, M. Articles by Poitry, S.

 Previous Article  |  Next Article 

Volume 17, Number 7, Issue of April 1, 1997 pp. 2383-2390
Copyright ©1997 Society for Neuroscience

Ammonium and Glutamate Released by Neurons Are Signals Regulating the Nutritive Function of a Glial Cell

Received Sept. 24, 1996; revised Dec. 17, 1996; accepted Jan. 17, 1997.

Marcos Tsacopoulos^{1, 2}, Carol L. Poitry-Yamate^{1, 2, 3}, and Serge Poitry^{1, 2}

¹ Experimental Ophthalmology Laboratory and Departments of ² Physiology and ³ Pharmacology, University of Geneva Medical School, 1211 Geneva 4, Switzerland

Glial cells transform glucose to a fuel substrate taken up and used by neurons. In the honeybee retina, photoreceptor neurons consume both alanine supplied by glial cells and exogenous proline. Ammonium (NH₄⁺) and glutamate, produced and released in a stimulus-dependent manner by photoreceptor neurons, contribute to the biosynthesis of alanine in glia. Here we report that NH₄⁺ and glutamate are transported into glia and that a transient rise in the intraglial concentration of NH₄⁺ or of glutamate causes a net increase in the level of reduced nicotinamide adenine dinucleotides [NAD(P)H]. Biochemical measurements indicate that this is attributable to activation of glycolysis in glial cells by the direct action of NH₄⁺ and glutamate on at least two enzymatic reactions: those catalyzed by phosphofructokinase (PFK; ATP:D-fructose-6-phosphotransferase, EC2.7.1.11) and glutamate dehydrogenase (GDH; L-glutamate:NAD oxidoreductase, deaminating; EC1.4.1.3). This activation leads to an increase in the production and release of alanine by glia. This signaling, which depends on the rate of conversion of NH₄⁺ and glutamate to alanine and -ketoglutarate, respectively, in the glial cells, raises the novel possibility of a tight regulation of the nutritive function of glia.

Key words: NADH; pH; fluorescence imaging; NH₄⁺ transport; glutamate transport; retina

This article has been cited by other articles:

				J. A. Coles, J.-L. Martiel, and K. Laskowska A glia-neuron alanine/ammonium shuttle is central to energy metabolism in bee retina J. Physiol., April 15, 2008; 586(8): 2077 - 2091. [Abstract] [Full Text] [PDF]

				L. Nybo, M. K Dalsgaard, A. Steensberg, K. Moller, and N. H Secher Cerebral ammonia uptake and accumulation during prolonged exercise in humans J. Physiol., February 15, 2005; 563(1): 285 - 290. [Abstract] [Full Text] [PDF]

				M. K. Dalsgaard, P. Ott, F. Dela, A. Juul, B. K. Pedersen, J. Warberg, J. Fahrenkrug, and N. H. Secher The CSF and arterial to internal jugular venous hormonal differences during exercise in humans Exp Physiol, May 1, 2004; 89(3): 271 - 277. [Abstract] [Full Text] [PDF]

				P. Marcaggi and J. A. Coles A Cl- Cotransporter Selective for Nh4+ over K+ in Glial Cells of Bee Retina J. Gen. Physiol., August 1, 2000; 116(2): 125 - 142. [Abstract] [Full Text] [PDF]

				S. Poitry, C. Poitry-Yamate, J. Ueberfeld, P. R. MacLeish, and M. Tsacopoulos Mechanisms of Glutamate Metabolic Signaling in Retinal Glial (Muller) Cells J. Neurosci., March 1, 2000; 20(5): 1809 - 1821. [Abstract] [Full Text] [PDF]

Home  |   Search  |   Archive  |   Subscribe  |   Contact  |   Help