Glutamate Transport Decreases Mitochondrial pH and Modulates Oxidative Metabolism in Astrocytes.
Détails
Etat: Public
Version: de l'auteur⸱e
ID Serval
serval:BIB_1F0FA45DD911
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Glutamate Transport Decreases Mitochondrial pH and Modulates Oxidative Metabolism in Astrocytes.
Périodique
Journal of Neuroscience
ISSN
1529-2401[electronic], 0270-6474[linking]
Statut éditorial
Publié
Date de publication
2011
Peer-reviewed
Oui
Volume
31
Numéro
10
Pages
3550-3559
Langue
anglais
Notes
Publication types: Journal Article Publication Status: ppublish
Résumé
During synaptic activity, the clearance of neuronally released glutamate leads to an intracellular sodium concentration increase in astrocytes that is associated with significant metabolic cost. The proximity of mitochondria at glutamate uptake sites in astrocytes raises the question of the ability of mitochondria to respond to these energy demands. We used dynamic fluorescence imaging to investigate the impact of glutamatergic transmission on mitochondria in intact astrocytes. Neuronal release of glutamate induced an intracellular acidification in astrocytes, via glutamate transporters, that spread over the mitochondrial matrix. The glutamate-induced mitochondrial matrix acidification exceeded cytosolic acidification and abrogated cytosol-to-mitochondrial matrix pH gradient. By decoupling glutamate uptake from cellular acidification, we found that glutamate induced a pH-mediated decrease in mitochondrial metabolism that surpasses the Ca(2+)-mediated stimulatory effects. These findings suggest a model in which excitatory neurotransmission dynamically regulates astrocyte energy metabolism by limiting the contribution of mitochondria to the metabolic response, thereby increasing the local oxygen availability and preventing excessive mitochondrial reactive oxygen species production.
Pubmed
Web of science
Open Access
Oui
Création de la notice
11/03/2011 16:20
Dernière modification de la notice
20/08/2019 13:55