β₂-adrenergic receptors protect axons during energetic stress but do not influence basal glio-axonal lactate shuttling in mouse white matter
| Autor: | G, Laureys, M, Valentino, F, Demol, C, Zammit, R, Muscat, M, Cambron, R, Kooijman, J, De Keyser |
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| Rok vydání: | 2014 |
| Předmět: |
Male
Coumaric Acids Glutamic Acid White Matter Axons Corpus Callosum Mice Inbred C57BL Propanolamines Adrenergic beta-2 Receptor Antagonists Stress Physiological Cerebellum Animals Clenbuterol Lactic Acid Receptors Adrenergic beta-2 Adrenergic beta-2 Receptor Agonists Neuroglia Central Nervous System Agents |
| Zdroj: | Neuroscience. 277 |
| ISSN: | 1873-7544 |
| Popis: | In 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. |
| Databáze: | OpenAIRE |
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