Neuronal culture microenvironments determine preferences in bioenergetic pathway use
Open accessAbstract
In the brain, metabolic supply and demand is directly coupled to neuronal activation. Methods for culturing primary rodent brain cells have come of age and are geared toward sophisticated modeling of human brain physiology and pathology. However, the impact of the culture microenvironment on neuronal function is rarely considered. Therefore, we investigated the role of different neuronal culture supplements for neuronal survival and metabolic activity in a model of metabolic deprivation of neurons using oxygen deprivation, glucose deprivation, as well as live cell metabolic flux analysis. We demonstrate the impact of neuronal culture conditions on metabolic function and neuronal survival under conditions of metabolic stress. In particular, we find that the common neuronal cell culture supplement B27 protects neurons from cell death under hypoxic conditions and inhibits glycolysis. Furthermore, we present data that B27 as well as the alternative neuronal culture supplement N2 restrict neuronal glucose metabolism. On the contrary, we find that the more modern supplement GS21 promotes neuronal energy metabolism. Our data support the notion that careful control of the metabolic environment is an essential component in modeling brain function and the cellular and molecular pathophysiology of brain disease in culture.
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In vitro glycolytic behavior can change with choice of culture media and astrocyte coculture.
“In vitro glycolytic behavior can change with choice of culture media (Sünwoldt et al., 2017) and astrocyte coculture (Mamczur et al., 2015), but gene expression data from acutely dissociated brain cells indicate that neurons are well equipped for glycolysis, with higher levels of mRNA expression than astrocytes for most glycolytic enzymes (Fig. 1, left).”
From Fueling thought: Management of glycolysis and oxidative phosphorylation in neuronal metabolism (2018) · cites this paper as Sünwoldt et al., 2017
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- Authors
- Sünwoldt, J., Bosche, B., Meisel, A., & Mergenthaler, P.
- Affiliations
- Charité – Universitätsmedizin Berlin (DE)
- St. Michael's Hospital (CA)
- NeuroCure Cluster of Excellence (DE)
- Berlin Institute of Health at Charité - Universitätsmedizin Berlin (DE)
- Corresponding author
- Mergenthaler, Philipp
- Venue
- Frontiers in Molecular Neuroscience
- Publisher
- Frontiers Media SA
- Published
- 2017-09-29
- Volume
- 10
- Pages
- 305-305
- ISSN
- 1662-5099 (ISSN-L)
- PMC
- PMC5649214
- OpenAlex
- W2757938599
- Cited by
- 34
- References
- 58
- Citations by year
- 2026: 1 · 2025: 8 · 2024: 4 · 2023: 2 · 2022: 3 · 2021: 4 · 2020: 6 · 2019: 1 · 2018: 5
- FWCI
- 1.61
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Frontiers in Molecular Neuroscience (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Refubium (Universitätsbibliothek der Freien Universität Berlin) (submittedVersion, cc-by)
- Universitätsbibliothek der FU Berlin Hochschulschriftenstelle u. Dokumentenserver (cc-by)
- Funders
- FP7 People: Marie-Curie Actions (627951)
- Deutscher Akademischer Austauschdienst (57212163)
- Deutsche Forschungsgemeinschaft (Exc257, TR43, BO4229/1-1, BO4229/2-1)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Keywords
- N2, neuronal survival, metabolic stress, hypoxia, glucose deprivation, glycolysis, neuronal energy metabolism
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
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