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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

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