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Cited by 127Mitochondrial Function and PathologyMetabolism, Diabetes, and CancerIon Transport and Channel Regulation

The DOI matches its Crossref record; 78 of the 78 references it cites were found in a registry or an index.

Non-Canonical Control of Neuronal Energy Status by the Na+ Pump

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Baeza-Lehnert, Felipe, Saab, Aiman S., Gutiérrez, Robin, Larenas, Valeria, Díaz, Esteban, Horn, Melanie, Vargas, Miriam, Hösli, Ladina, Stobart, Jillian, Hirrlinger, Johannes, Weber, Bruno, Barros, L. Felipe·2019·Cell Metabolism
DOI 10.1016/j.cmet.2018.11.005
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Abstract

Neurons have limited intracellular energy stores but experience acute and unpredictable increases in energy demand. To better understand how these cells repeatedly transit from a resting to active state without undergoing metabolic stress, we monitored their early metabolic response to neurotransmission using ion-sensitive probes and FRET sensors in vitro and in vivo. A short theta burst triggered immediate Na+ entry, followed by a delayed stimulation of the Na+/K+ ATPase pump. Unexpectedly, cytosolic ATP and ADP levels were unperturbed across a wide range of physiological workloads, revealing strict flux coupling between the Na+ pump and mitochondria. Metabolic flux measurements revealed a "priming" phase of mitochondrial energization by pyruvate, whereas glucose consumption coincided with delayed Na+ pump stimulation. Experiments revealed that the Na+ pump plays a permissive role for mitochondrial ATP production and glycolysis. We conclude that neuronal energy homeostasis is not mediated by adenine nucleotides or by Ca 2+, but by a mechanism commanded by the Na+ pump.

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Crossref · 10.1016/j.cmet.2018.11.005

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Metadata

Authors
Baeza-Lehnert, F., Saab, A. S., Gutiérrez, R., Larenas, V., Díaz, E., Horn, M., Vargas, M., Hösli, L., Stobart, J., Hirrlinger, J., Weber, B., & Barros, L. F.
Affiliations
  • University of Zurich (CH)
  • Austral University of Chile (CL)
  • Centro de Estudios Científicos (CL)
  • Max Planck Institute of Experimental Medicine (DE)
Corresponding author
Barros, L. Felipe
ORCID
Venue
Cell Metabolism
Publisher
Elsevier BV
Published
2019-03
Volume
29
Issue
3
Pages
668-680.e4
ISSN
1550-4131 (ISSN-L)
DOI
10.1016/j.cmet.2018.11.005
OpenAlex
W2904685632
Cited by
126
References
78
Citations by year
2026: 10 · 2025: 19 · 2024: 25 · 2023: 21 · 2022: 12 · 2021: 12 · 2020: 13 · 2019: 14
FWCI
3.47
Type
journal article
Language
en
Open access
Licence
Locations
  • Cell Metabolism (publishedVersion)
  • PubMed (publishedVersion)
  • Zurich Open Repository and Archive (University of Zurich) (submittedVersion)
Funders
  • FONDECYT (1160317)
  • University of Zurich
  • National Science Foundation
  • Centro de Estudios Científicos
  • Chilean Government
  • CONICYT
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion Transport and Channel Regulation
Keywords
Na+/K+-ATPase, mitochondrial energization, pyruvate, glycolysis, glucose utilization, ATP production, neurotransmission, theta burst stimulation, FRET biosensor, ion sensitive probe
MeSH terms
Sodium-Potassium-Exchanging ATPase, Adenosine Triphosphate, Animals, Astrocytes, Energy Metabolism, Glucose, Glycolysis, Homeostasis, Mice, Inbred C57BL, Mitochondria, Neurons

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