Abstract:
: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.
journal_name
Neurosciencejournal_title
Neuroscienceauthors
Laureys G,Valentino M,Demol F,Zammit C,Muscat R,Cambron M,Kooijman R,De Keyser Jdoi
10.1016/j.neuroscience.2014.07.022subject
Has Abstractpub_date
2014-09-26 00:00:00pages
367-74eissn
0306-4522issn
1873-7544pii
S0306-4522(14)00585-5journal_volume
277pub_type
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