Sodium signaling and astrocyte energy metabolism.

Details

Ressource 1Download: 27027636_PostPrint.pdf (1647.50 [Ko])
State: Public
Version: Author's accepted manuscript
Serval ID
serval:BIB_D88ECDA61995
Type
Article: article from journal or magazin.
Publication sub-type
Review (review): journal as complete as possible of one specific subject, written based on exhaustive analyses from published work.
Collection
Publications
Institution
Title
Sodium signaling and astrocyte energy metabolism.
Journal
Glia
Author(s)
Chatton J.Y., Magistretti P.J., Barros L.F.
ISSN
1098-1136 (Electronic)
ISSN-L
0894-1491
Publication state
Published
Issued date
10/2016
Peer-reviewed
Oui
Volume
64
Number
10
Pages
1667-1676
Language
english
Notes
Publication types: Journal Article ; Review
Publication Status: ppublish
Abstract
The Na(+) gradient across the plasma membrane is constantly exploited by astrocytes as a secondary energy source to regulate the intracellular and extracellular milieu, and discard waste products. One of the most prominent roles of astrocytes in the brain is the Na(+) -dependent clearance of glutamate released by neurons during synaptic transmission. The intracellular Na(+) load collectively generated by these processes converges at the Na,K-ATPase pump, responsible for Na(+) extrusion from the cell, which is achieved at the expense of cellular ATP. These processes represent pivotal mechanisms enabling astrocytes to increase the local availability of metabolic substrates in response to neuronal activity. This review presents basic principles linking the intracellular handling of Na(+) following activity-related transmembrane fluxes in astrocytes and the energy metabolic pathways involved. We propose a role of Na(+) as an energy currency and as a mediator of metabolic signals in the context of neuron-glia interactions. We further discuss the possible impact of the astrocytic syncytium for the distribution and coordination of the metabolic response, and the compartmentation of these processes in cellular microdomains and subcellular organelles. Finally, we illustrate future avenues of investigation into signaling mechanisms aimed at bridging the gap between Na(+) and the metabolic machinery. GLIA 2016;64:1667-1676.

Keywords
Animals, Astrocytes/physiology, Energy Metabolism/physiology, Signal Transduction/physiology, Sodium/metabolism, Na,K-ATPase, glycolysis, lactate, membrane transport, mitochondria, neuron-glia interactions, syncytium
Pubmed
Web of science
Open Access
Yes
Create date
09/04/2016 15:06
Last modification date
20/08/2019 15:58
Usage data