Metabolic substrates other than glucose support axon function in central white matter
Article first published online: 30 NOV 2001
Copyright © 2001 Wiley-Liss, Inc.
Journal of Neuroscience Research
Volume 66, Issue 5, pages 839–843, 1 December 2001
How to Cite
Brown, A. M., Wender, R. and Ransom, B. R. (2001), Metabolic substrates other than glucose support axon function in central white matter. J. Neurosci. Res., 66: 839–843. doi: 10.1002/jnr.10081
- Issue published online: 30 NOV 2001
- Article first published online: 30 NOV 2001
- Manuscript Accepted: 22 SEP 2001
- Manuscript Revised: 21 SEP 2001
- Manuscript Received: 27 JUN 2001
- energy metabolism;
- rat optic nerve
We tested the hypothesis that non-glucose energy sources can support axon function in the rat optic nerve. Axon function was assessed by monitoring the stimulus-evoked compound action potential (CAP). CAP was maintained at full amplitude for 2 hr in 10 mM glucose. 20 mM lactate, 20 mM pyruvate, 10 mM fructose, or 10 mM mannose supported axon function as effectively as did glucose, and 10 mM glutamine provided partial support, but β-hydroxybutyrate, octanoate, sorbitol, alanine, aspartate, and glutamate failed to support axon function. Our results indicated that a variety of compounds can sustain function in CNS myelinated axons. Axons probably use lactate, pyruvate, and glutamine directly as energy substrates, whereas mannose and fructose could be shuttled through astrocytes to lactate, which is then exported to axons. © 2001 Wiley-Liss, Inc.