The nutritive function of glia is regulated by signals released by neurons

• Published in: Glia 1997-09, Vol.21 (1), p.84-91
• Main Authors: Tsacopoulos, Marco, Poitry-Yamate, Carol L., Poitry, Serge, Perrottet, Philippe, Veuthey, Anne-Lise
• Format: Article
• Language: English
• Subjects: Alanine - metabolism; Ammonia - metabolism; Animals; Apis mellifera; Bees; fluorescence imaging; Glucose - metabolism; glutamate; glutamate transport; Glutamic Acid - metabolism; In Vitro Techniques; Male; Models, Biological; NAD - metabolism; NADP - metabolism; Neuroglia - physiology; Neurons - physiology; NH4+ transport; Photoreceptor Cells, Invertebrate - physiology; Proline - metabolism; Retina - physiology; Signal Transduction
• ISSN: 0894-1491; 1098-1136
• DOI: 10.1002/(SICI)1098-1136(199709)21:1<84::AID-GLIA9>3.0.CO;2-1

The idea of a metabolic coupling between neurons and astrocytes in the brain has been entertained for about 100 years. The use recently of simple and well‐compartmentalized nervous systems, such as the honeybee retina or purified preparations of neurons and glia, provided strong support for a nutritive function of glial cells: glial cells transform glucose to a fuel substrate taken up and used by neurons. Particularly, in the honeybee retina, photoreceptor‐neurons consume alanine supplied by glial cells and exogenous proline. NH4+ and glutamate are transported into glia by functional plasma membrane transport systems. During increased activity 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]. Quantitative biochemistry showed that this is due to activation of glycolysis in glial cells by the direct action of NH4+ and of glutamate, probably on the enzymatic reactions controlled by phosphofructokinase alanine aminotransferase and glutamate dehydrogenase. This activation leads to a massive increase in the production and release of alanine by glia. This constitutes an intracellular signal and it depends upon the rate of conversion of NH4+ and of glutamate to alanine and α‐ketoglutarate, respectively, in the glial cells. Alanine and α‐ketoglutarate are released extracellularly and then taken up by neurons where they contribute to the maintenance of the mitochondrial redox potential. This signaling raises the novel hypothesis of a tight regulation of the nutritive function of glia. GLIA 21:84–91, 1997. © 1997 Wiley‐Liss, Inc.