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  Oligodendroglial NMDA receptors regulate glucose import and axonal energy metabolism.

Saab, A. S., Tzvetavona, I. D., Trevisiol, A., Baltan, S., Dibaj, P., K, K., et al. (2016). Oligodendroglial NMDA receptors regulate glucose import and axonal energy metabolism. Neuron, 91(1), 119-132. doi:10.1016/j.neuron.2016.05.016.

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Item Permalink: http://hdl.handle.net/11858/00-001M-0000-002B-34F5-E Version Permalink: http://hdl.handle.net/11858/00-001M-0000-002D-1882-4
Genre: Journal Article

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 Creators:
Saab, A. S., Author
Tzvetavona, I. D., Author
Trevisiol, A., Author
Baltan, S., Author
Dibaj, P., Author
K, Kusch, Author
Möbius, W., Author
Goetze, B., Author
Jahn, H. M., Author
Huang, W., Author
Steffens, H.1, Author              
Schoburg, E. D., Author
Pérez-Samartín, A., Author
Pérez-Cerdá, F., Author
Bakhtiari, D.2, Author              
Matute, C., Author
Löwel, S., Author
Griesinger, C.2, Author              
Hirrlinger, J., Author
Kirchhoff, F., Author
Nave, K. A., Author more..
Affiliations:
1Department of NanoBiophotonics, MPI for biophysical chemistry, Max Planck Society, ou_578627              
2Department of NMR-based Structural Biology, MPI for biophysical chemistry, Max Planck Society, ou_578567              

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 Abstract: Oligodendrocytes make myelin and support axons metabolically with lactate. However, it is unknown how glucose utilization and glycolysis are adapted to the different axonal energy demands. Spiking axons release glutamate and oligodendrocytes express NMDA receptors of unknown function. Here we show that the stimulation of oligodendroglial NMDA receptors mobilizes glucose transporter GLUT1, leading to its incorporation into the myelin compartment in vivo. When myelinated optic nerves from conditional NMDA receptor mutants are challenged with transient oxygen-glucose deprivation, they show a reduced functional recovery when returned to oxygen-glucose but are indistinguishable from wild-type when provided with oxygen-lactate. Moreover, the functional integrity of isolated optic nerves, which are electrically silent, is extended by preincubation with NMDA, mimicking axonal activity, and shortened by NMDA receptor blockers. This reveals a novel aspect of neuronal energy metabolism in which activity-dependent glutamate release enhances oligodendroglial glucose uptake and glycolytic support of fast spiking axons.

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Language(s): eng - English
 Dates: 2016-06-092016-07-06
 Publication Status: Published in print
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 Rev. Method: Peer
 Identifiers: DOI: 10.1016/j.neuron.2016.05.016
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Title: Neuron
Source Genre: Journal
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Pages: - Volume / Issue: 91 (1) Sequence Number: - Start / End Page: 119 - 132 Identifier: -