Please use this identifier to cite or link to this item: https://www.um.edu.mt/library/oar/handle/123456789/26718
Title: β2-adrenergic receptors protect axons during energetic stress but do not influence basal glio-axonal lactate shuttling in mouse white matter
Authors: Laureys, Guy
Valentino, Mario
Demol, Frauke
Zammit, Christian
Muscat, Richard
Cambron, Melissa
Kooijman, Ron
Keyser, Jacques de
Keywords: Glucose
Adrenergic beta agonists in animal nutrition
Adrenergic beta blockers -- Physiological effect
Lactic acid
Beta adrenoceptors
Glutamic acid
Axons -- Physiology
Issue Date: 2014
Publisher: Pergamon Press
Citation: Laureys, G., Valentino, M., Demol, F., Zammit, C., Muscat, R., Cambron, M., ... & De Keyser, J. (2014). β2-adrenergic receptors protect axons during energetic stress but do not influence basal glio-axonal lactate shuttling in mouse white matter. Neuroscience, 277, 367-374.
Abstract: In vitro studies have demonstrated that b2-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 b2-adrenergic receptors. In two-photon imaging experiments on ex vivo mouse corpus callosum subjected to aglycemia, b2-adrenergic activation rescued axons, whereas inhibition of axonal lactate uptake by a-cyano-4-hydroxycinnamic acid (4-CIN) was associated with severe axonal loss. Our results suggest that axonal protective effects of glial b2-adrenergic receptor activation are not mediated by enhanced lactate production.
URI: https://www.um.edu.mt/library/oar//handle/123456789/26718
Appears in Collections:Scholarly Works - FacM&SAna
Scholarly Works - FacM&SPB

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