Abstract
In vitro studies have demonstrated that beta 2-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 beta 2-adrenergic receptors. In two-photon imaging experiments on ex vivo mouse corpus callosum subjected to aglycemia, beta 2-adrenergic activation rescued axons, whereas inhibition of axonal lactate uptake by alpha-cyano-4-hydroxycinnamic acid (4-CIN) was associated with severe axonal loss. Our results suggest that axonal protective effects of glial beta 2-adrenergic receptor activation are not mediated by enhanced lactate production. (C) 2014 IBRO. Published by Elsevier Ltd. All rights reserved.
Original language | English |
---|---|
Pages (from-to) | 367-374 |
Number of pages | 8 |
Journal | Neuroscience |
Volume | 277 |
DOIs | |
Publication status | Published - 26-Sept-2014 |
Keywords
- glucose
- lactate
- glutamate
- white matter
- axons
- beta 2-adrenergic receptors
- NEURONAL-ACTIVITY
- GLYCOLYSIS
- GLYCOGEN
- GLUCOSE
- ASTROCYTES
- INJURY