beta(2)-ADRENERGIC RECEPTORS PROTECT AXONS DURING ENERGETIC STRESS BUT DO NOT INFLUENCE BASAL GLIO-AXONAL LACTATE SHUTTLING IN MOUSE WHITE MATTER

G. Laureys*, M. Valentino, F. Demol, C. Zammit, R. Muscat, M. Cambron, R. Kooijman, J. De Keyser

*Corresponding author for this work

    Research output: Contribution to journalArticleAcademicpeer-review

    8 Citations (Scopus)

    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 languageEnglish
    Pages (from-to)367-374
    Number of pages8
    JournalNeuroscience
    Volume277
    DOIs
    Publication statusPublished - 26-Sept-2014

    Keywords

    • glucose
    • lactate
    • glutamate
    • white matter
    • axons
    • beta 2-adrenergic receptors
    • NEURONAL-ACTIVITY
    • GLYCOLYSIS
    • GLYCOGEN
    • GLUCOSE
    • ASTROCYTES
    • INJURY

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