Astrocyte-neuron metabolic cooperation shapes brain activity

The brain has almost no energy reserve, but its activity coordinates organismal function, a burden that requires precise coupling between neurotransmission and energy metabolism. Deciphering how the brain accomplishes this complex task is crucial to understand central facets of human physiology and...

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Bibliographic Details
Published inCell metabolism Vol. 33; no. 8; pp. 1546 - 1564
Main Authors Bonvento, Gilles, Bolaños, Juan P.
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 03.08.2021
Elsevier
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Summary:The brain has almost no energy reserve, but its activity coordinates organismal function, a burden that requires precise coupling between neurotransmission and energy metabolism. Deciphering how the brain accomplishes this complex task is crucial to understand central facets of human physiology and disease mechanisms. Each type of neural cell displays a peculiar metabolic signature, forcing the intercellular exchange of metabolites that serve as both energy precursors and paracrine signals. The paradigm of this biological feature is the astrocyte-neuron couple, in which the glycolytic metabolism of astrocytes contrasts with the mitochondrial oxidative activity of neurons. Astrocytes generate abundant mitochondrial reactive oxygen species and shuttle to neurons glycolytically derived metabolites, such as L-lactate and L-serine, which sustain energy needs, conserve redox status, and modulate neurotransmitter-receptor activity. Conversely, early disruption of this metabolic cooperation may contribute to the initiation or progression of several neurological diseases, thus requiring innovative therapies to preserve brain energetics. In this review, Bonvento and Bolaños examine how a partnership between neurons and astrocytes coordinates the energy needs of neurotransmission, preserves the redox balance, and modulates neurotransmitter-receptor activity in the healthy brain. They suggest that disruption of this metabolic cooperation contributes to the initiation or progression of several neurological diseases.
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ISSN:1550-4131
1932-7420
1932-7420
DOI:10.1016/j.cmet.2021.07.006