β₂-adrenergic receptors protect axons during energetic stress but do not influence basal glio-axonal lactate shuttling in mouse white matter.

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

Neuroscience

journal_title

Neuroscience

authors

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

doi

10.1016/j.neuroscience.2014.07.022

subject

Has Abstract

pub_date

2014-09-26 00:00:00

pages

367-74

eissn

0306-4522

issn

1873-7544

pii

S0306-4522(14)00585-5

journal_volume

277

pub_type

杂志文章