Bidirectional astrocytic GLUT1 activation by elevated extracellular K+

Ignacio Fernández‐Moncada, Daniel Robles‐Maldonado, Pablo Castro, Karin Alegría, Robert Epp, Iván Ruminot, Luis Felipe Barros
Glia. 2020-12-05; 69(4): 1012-1021
DOI: 10.1002/glia.23944

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Fernández-Moncada I(1)(2), Robles-Maldonado D(1)(3), Castro P(1), Alegría K(1), Epp R(4), Ruminot I(1), Barros LF(1).

Author information:
(1)Centro de Estudios Científicos, Valdivia, Chile.
(2)INSERM U1215 NeuroCentre Magendie, Bordeaux, France.
(3)Universidad Austral de Chile, Valdivia, Chile.
(4)Institute of Fluid Dynamics, ETH Zurich, Zurich, Switzerland.

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 s-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.


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