FERNANDEZ-MONCADA, Ignacio; ROBLES-MALDONADO, Daniel; CASTRO, Pablo; ALEGRIA, Karin; EPP, Robert; RUMINOT, Ivan; BARROS, Luis Felipe

doi:10.1002/glia.23944

Metadatos

Mostrar el registro completo del ítem

Licencia de uso del documento

FERNANDEZ-MONCADA, Ignacio
Neurocentre Magendie : Physiopathologie de la Plasticité Neuronale [U1215 Inserm - UB]

ROBLES-MALDONADO, Daniel

CASTRO, Pablo

Idioma

Article de revue

Este ítem está publicado en

Glia. 2021-04, vol. 69, n° 4, p. 1012-1021

Resumen en inglés

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.< Leer menos

Palabras clave en inglés

3-O-methylglucose

Fluorescence microscopy

Genetically encoded FRET sensor

Glucose transport

Metadatos

Compartir este ítem

Licencia de uso del documento

Bidirectional astrocytic GLUT1 activation by elevated extracellular K+

Idioma

Este ítem está publicado en

Resumen en inglés

Palabras clave en inglés

URI

DOI

Centros de investigación