Abstract
Neuron-glia interactions are essential for synaptic function, and glial glutamate (re)uptake plays a key role at glutamatergic synapses. In knockout mice, for either glial glutamate transporters, GLAST or GLT-1, a classical metabolic response to synaptic activation (i.e., enhancement of glucose utilization) is decreased at an early functional stage in the somatosensory barrel cortex following activation of whiskers. Investigation in vitro demonstrates that glial glutamate transport represents a critical step for triggering enhanced glucose utilization, but also lactate release from astrocytes through a mechanism involving changes in intracellular Na+ concentration. These data suggest that a metabolic crosstalk takes place between neurons and astrocytes in the developing cortex, which would be regulated by synaptic activity and mediated by glial glutamate transporters.
Original language | English (US) |
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Pages (from-to) | 275-286 |
Number of pages | 12 |
Journal | Neuron |
Volume | 37 |
Issue number | 2 |
DOIs | |
State | Published - Jan 23 2003 |
Externally published | Yes |
Bibliographical note
Funding Information:The authors acknowledge the expert technical assistance provided by Mauricette Maillard, Didier Foretay, Charles Quairiaux, and Angélique Regnier. They also thank Ruth Debernardi for preparing astrocyte culture homogenates for Western blotting, Jean-François Brunet for performing RT-PCR of glutamate transporters, and Sylvain Lengacher for setting up genotyping. We are also grateful to Igor Allaman and Karin Pierre for critically reading the manuscript. This work was supported by a Human Frontier Science Program grant number RG118/1998-B (to L.P. and G.B.).
ASJC Scopus subject areas
- General Neuroscience