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First published online May 26, 2006
Journal of Experimental Biology 209, 2304-2311 (2006)
Published by The Company of Biologists 2006
doi: 10.1242/jeb.02208
Review Article: Phenotypic Plasticity of the Brain |
Neuron–glia metabolic coupling and plasticity
Brain Mind Institute, Ecole Polytechnique Fédérale de Lausanne (EPFL), Switzerland and Centre de Neurosciences Psychiatriques, CHUV, Departement de Psychiatrie, Site de Cery, CH1008 Prilly/Lausanne, Switzerland
e-mail: pierre.magistretti{at}unil.ch
Accepted 14 March 2006
Summary
The coupling between synaptic activity and glucose utilization (neurometabolic coupling) is a central physiological principle of brain function that has provided the basis for 2-deoxyglucose-based functional imaging with positron emission tomography (PET). Astrocytes play a central role in neurometabolic coupling, and the basic mechanism involves glutamate-stimulated aerobic glycolysis; the sodium-coupled reuptake of glutamate by astrocytes and the ensuing activation of the Na-K-ATPase triggers glucose uptake and processing via glycolysis, resulting in the release of lactate from astrocytes. Lactate can then contribute to the activity-dependent fuelling of the neuronal energy demands associated with synaptic transmission. An operational model, the `astrocyte–neuron lactate shuttle', is supported experimentally by a large body of evidence, which provides a molecular and cellular basis for interpreting data obtained from functional brain imaging studies. In addition, this neuron–glia metabolic coupling undergoes plastic adaptations in parallel with adaptive mechanisms that characterize synaptic plasticity. Thus, distinct subregions of the hippocampus are metabolically active at different time points during spatial learning tasks, suggesting that a type of metabolic plasticity, involving by definition neuron–glia coupling, occurs during learning. In addition, marked variations in the expression of genes involved in glial glycogen metabolism are observed during the sleep–wake cycle, with in particular a marked induction of expression of the gene encoding for protein targeting to glycogen (PTG) following sleep deprivation. These data suggest that glial metabolic plasticity is likely to be concomitant with synaptic plasticity.
Key words: neuro-metabolic coupling, plasticity, astrocyte, glia, sleep–wake cycle
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