Sodium signaling and astrocyte energy metabolism.

Détails

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Etat: Serval
Version: Author's accepted manuscript
ID Serval
serval:BIB_D88ECDA61995
Type
Article: article d'un périodique ou d'un magazine.
Sous-type
Synthèse (review): revue aussi complète que possible des connaissances sur un sujet, rédigée à partir de l'analyse exhaustive des travaux publiés.
Collection
Publications
Titre
Sodium signaling and astrocyte energy metabolism.
Périodique
Glia
Auteur(s)
Chatton J.Y., Magistretti P.J., Barros L.F.
ISSN
1098-1136 (Electronic)
ISSN-L
0894-1491
Statut éditorial
Publié
Date de publication
10/2016
Peer-reviewed
Oui
Volume
64
Numéro
10
Pages
1667-1676
Langue
anglais
Notes
Publication types: Journal Article ; Review
Publication Status: ppublish
Résumé
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.

Mots-clé
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
Oui
Création de la notice
09/04/2016 16:06
Dernière modification de la notice
09/05/2019 1:58
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