ArticleJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism2015
Physiology-based kinetic modeling of neuronal energy metabolism unravels the molecular basis of NAD(P)H fluorescence transients.
Article in Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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38 citing papers in PubMed, 57 citations in OpenAlex.
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- Mutant huntingtin impairs neurodevelopment in human brain organoids through CHCHD2-mediated neurometabolic failure.Nature communications · 2024Article
- Metabolic flexibility ensures proper neuronal network function in moderate neuroinflammation.Scientific reports · 2024Article
- Isoflurane lowers the cerebral metabolic rate of oxygen and prevents hypoxia during cortical spreading depolarizationJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024Article
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- Targeting the TCA cycle can ameliorate widespread axonal energy deficiency in neuroinflammatory lesions.Nature metabolism · 2023Article
- Proteomic phenotype of cerebral organoids derived from autism spectrum disorder patients reveal disrupted energy metabolism, cellular components, and biological processes.Molecular psychiatry · 2022Article
- Sevoflurane Effects on Neuronal Energy Metabolism Correlate with Activity States While Mitochondrial Function Remains Intact.International journal of molecular sciences · 2022Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Imaging of the cellular fluorescence of the reduced form of nicotinamide adenine dinucleotide (phosphate) (NAD(P)H) is one of the few metabolic readouts that enable noninvasive and time-resolved monitoring of the functional status of mitochondria in neuronal tissues. Stimulation-induced transient changes in NAD(P)H fluorescence intensity frequently display a biphasic characteristic that is influenced by various molecular processes, e.g., intracellular calcium dynamics, tricarboxylic acid cycle activity, the malate-aspartate shuttle, the glycerol-3-phosphate shuttle, oxygen supply or adenosine triphosphate (ATP) demand. To evaluate the relative impact of these processes, we developed and validated a detailed physiologic mathematical model of the energy metabolism of neuronal cells and used the model to simulate metabolic changes of single cells and tissue slices under different settings of stimulus-induced activity and varying nutritional supply of glucose, pyruvate or lactate. Notably, all experimentally determined NAD(P)H responses could be reproduced with one and the same generic cellular model. Our computations reveal that (1) cells with quite different metabolic status may generate almost identical NAD(P)H responses and (2) cells of the same type may quite differently contribute to aggregate NAD(P)H responses recorded in brain slices, depending on the spatial location within the tissue. Our computational approach reconciles different and sometimes even controversial experimental findings and improves our mechanistic understanding of the metabolic changes underlying live-cell NAD(P)H fluorescence transients.
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