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Bidirectional astrocytic GLUT1 activation by elevated extracellular K +
Author(s) -
FernándezMoncada Ignacio,
RoblesMaldonado Daniel,
Castro Pablo,
Alegría Karin,
Epp Robert,
Ruminot Iván,
Barros Luis Felipe
Publication year - 2021
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/glia.23944
Subject(s) - glut1 , glucose transporter , glycolysis , biology , astrocyte , stimulation , extracellular , glucose transporter type 1 , transporter , neuroglia , monocarboxylate transporter , biochemistry , cellular respiration , glucose uptake , microbiology and biotechnology , biophysics , medicine , endocrinology , metabolism , mitochondrion , central nervous system , gene , insulin
The acute rise in interstitial K + that accompanies neural activity couples the energy demand of neurons to the metabolism of astrocytes. The effects of elevated K + on astrocytes include activation of aerobic glycolysis, inhibition of mitochondrial respiration and the release of lactate. Using a genetically encoded FRET glucose sensor and a novel protocol based on 3‐ O ‐methylglucose trans‐acceleration and numerical simulation of glucose dynamics, we report that extracellular K + is also a potent and reversible modulator of the astrocytic glucose transporter GLUT1. In cultured mouse astrocytes, the stimulatory effect developed within seconds, engaged both the influx and efflux modes of the transporter, and was detected even at 1 mM incremental K + . The modulation of GLUT1 explains how astrocytes are able to maintain their glucose pool in the face of strong glycolysis stimulation. We propose that the stimulation of GLUT1 by K + supports the production of lactate by astrocytes and the timely delivery of glucose to active neurons.