Intertwined ROS and Metabolic Signaling at the Neuron-Astrocyte Interface
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ORIGINAL PAPER
Intertwined ROS and Metabolic Signaling at the Neuron‑Astrocyte Interface Carlos Vicente‑Gutiérrez1,2 · Daniel Jiménez‑Blasco1,2,3 · Rubén Quintana‑Cabrera1,2,4 Received: 4 September 2019 / Revised: 3 January 2020 / Accepted: 16 January 2020 © Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Metabolism and redox signalling share critical nodes in the nervous system. In the last years, a series of major findings have challenged the current vision on how neural reactive oxygen species (ROS) are produced and handled in the nervous system. Once regarded as deleterious by-products, ROS are now shown to be essential for a metabolic and redox crosstalk. In turn, this coupling defines neural viability and function to control behaviour or leading to neurodegeneration when compromised. Findings like a different assembly of mitochondrial respiratory supercomplexes in neurons and astrocytes stands behind a divergent production of ROS in either cell type, more prominent in astrocytes. ROS levels are however tightly controlled by an antioxidant machinery in astrocytes, assumed as more efficient than that of neurons, to regulate redox signalling. By exerting this control in ROS abundance, metabolic functions are finely tuned in both neural cells. Further, a higher engagement of mitochondrial respiration and oxidative function in neurons, underpinned by redox equivalents supplied from the pentose phosphate pathway and from glia, differs from the otherwise strong glycolytic capacity of astrocytes. Here, we recapitulate major findings on how ROS and metabolism differ between neural cells but merge to define reciprocal signalling pathways, ultimately defining neural function and fate. Keywords Neuron · Astrocyte · Metabolism · Oxidative stress · Mitochondria · Neurodegeneration
Introduction Studies from one of the founders of modern neuroscience, Santiago Ramón y Cajal, on the characterization of the nervous system, have made part of every textbook the notion that neurons are indivisible cells not replaced by new ones. This view has long remained as a cornerstone in our Special Issue: In Honor of Professor Juan Bolanos. * Rubén Quintana‑Cabrera [email protected] 1
Institute of Functional Biology and Genomics (IBFG), University of Salamanca, CSIC, Salamanca, Spain
2
Institute of Biomedical Research of Salamanca (IBSAL), University Hospital of Salamanca, University of Salamanca, CSIC, Salamanca, Spain
3
Centro de Investigación Biomédica en Red sobre Fragilidad y Envejecimiento Saludable (CIBERFES), Instituto de Salud Carlos III, Madrid, Spain
4
Department of Biochemistry and Molecular Biology, University of Salamanca, Salamanca, Spain
understanding and search for strategies to overcome neurodegeneration, even if challenged -not without discussion [1]—over the last years by the finding and characterization of neurogenic niches [2–4]. Indeed, uncovering the mechanisms that lead to neuronal death in diseases such as Alzheimer, Parkinson or Huntington is still a matter
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