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- G Laureys, M Valentino, F Demol, C Zammit, R Muscat, M Cambron, R Kooijman, and J De Keyser.
- Department of Neurology, University Hospital Brussels, Center for Neurosciences, Vrije Universiteit Brussel, Laarbeeklaan 101, 1090 Brussels, Belgium. Electronic address: laureysg@hotmail.com.
- Neuroscience. 2014 Sep 26;277:367-74.
AbstractIn vitro studies have demonstrated that β2-adrenergic receptor activation stimulates glycogen degradation in astrocytes, generating lactate as a potential energy source for neurons. Using in vivo microdialysis in mouse cerebellar white matter we demonstrate continuous axonal lactate uptake and glial-axonal metabolic coupling of glutamate/lactate exchange. However, this physiological lactate production was not influenced by activation (clenbuterol) or blocking (ICI 118551) of β2-adrenergic receptors. In two-photon imaging experiments on ex vivo mouse corpus callosum subjected to aglycemia, β2-adrenergic activation rescued axons, whereas inhibition of axonal lactate uptake by α-cyano-4-hydroxycinnamic acid (4-CIN) was associated with severe axonal loss. Our results suggest that axonal protective effects of glial β2-adrenergic receptor activation are not mediated by enhanced lactate production.Copyright © 2014 IBRO. Published by Elsevier Ltd. All rights reserved.
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