ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2008
Mitochondrial membrane potential in axons increases with local nerve growth factor or semaphorin signaling.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 papers.
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Who cites it
100 citing papers in PubMed, 146 citations in OpenAlex.
- Metabolism Controls the Timing of Human Brain Development and Maturation.Journal of inherited metabolic disease · 2026Review
- Imaging mitochondrial membrane potential via concentration-dependent fluorescence lifetime changes.Nature communications · 2025Article
- Spinal motor neuron development and metabolism are transcriptionally regulated by nuclear factor IA.Science advances · 2025Article
- Genetically encoded biosensors of metabolic function for the study of neurodegeneration, a review and perspective.Neurophotonics · 2025Review
- Vimentin Intermediate Filaments Maintain Membrane Potential of Mitochondria in Growing Neurites.Biology · 2024Article
- The Axonal Actin Filament Cytoskeleton: Structure, Function, and Relevance to Injury and Degeneration.Molecular neurobiology · 2024Review
- Sema3A secreted by sensory nerve induces bone formation under mechanical loads.International journal of oral science · 2024Article
- 3D Reconstruction of the Mitochondrial Network within the Neuronal Soma from SBF-SEM Volume Data.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Mitochondrial dysfunction as a target in spinal cord injury: intimate correlation between pathological processes and therapeutic approaches.Neural regeneration research · 2023Review
- Actin cytoskeletal dynamics do not impose an energy drain on growth cone bioenergetics.Journal of cell science · 2023Article
- Mitochondria as central hubs in synaptic modulation.Cellular and molecular life sciences : CMLS · 2023Review
- Mitofusin 2 Sustains the Axonal Mitochondrial Network to Support Presynaptic CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Mitophagy regulation in aging and neurodegenerative disease.Biophysical reviews · 2023Review
- Decorin evokes reversible mitochondrial depolarization in carcinoma and vascular endothelial cells.American journal of physiology. Cell physiology · 2022Article
- The ANC-1 (Nesprin-1/2) organelle-anchoring protein functions through mitochondria to polarize axon growth in response to SLT-1.PLoS genetics · 2022Article
- The compartmentalised nature of neuronal mitophagy: molecular insights and implications.Expert reviews in molecular medicine · 2022Review
- Mitochondrial function in spinal cord injury and regeneration.Cellular and molecular life sciences : CMLS · 2022Review
- Inhibition of MicroRNA-182/183 Cluster Ameliorates Schizophrenia by Activating the Axon Guidance Pathway and Upregulating DCC.Oxidative medicine and cellular longevity · 2022Article
- Mitochondria and Other Organelles in Neural Development and Their Potential as Therapeutic Targets in Neurodegenerative Diseases.Frontiers in neuroscience · 2022Review
- SARM1 Suppresses Axon Branching Through Attenuation of Axonal Cytoskeletal Dynamics.Frontiers in molecular neuroscience · 2022Article
40 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Neurons concentrate mitochondria at sites in the cell that have a high demand for ATP and/or calcium buffering. To accomplish this, mitochondrial transport and docking are thought to respond to intracellular signaling pathways. However, the cell might also concentrate mitochondrial function by locally modulating mitochondrial activity. We tested this hypothesis by measuring the membrane potential of individual mitochondria throughout the axons of chick sensory neurons using the dye tetramethylrhodamine methylester (TMRM). We found no difference in the TMRM mitochondrial-to-cytoplasmic fluorescence ratio (F(m)/F(c)) among three functionally distinct regions: axonal branch points, distal axons, and the remaining axon shaft. In addition, we found no difference in F(m)/F(c) among stationary, retrogradely moving, or anterogradely moving mitochondria. However, F(m)/F(c) was significantly higher in the lamellipodia of growth cones, and among a small fraction of mitochondria throughout the axon. To identify possible signals controlling membrane potential, we used beads covalently coupled to survival and guidance cues to provide a local stimulus along the axon shaft. NGF- or semaphorin 3A-coupled beads caused a significant increase in F(m)/F(c) in the immediately adjacent region of axon, and this was diminished in the presence of the PI3 (phosphatidylinositol-3) kinase inhibitor LY294002 [2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one] or the MAP (mitogen-activated protein) kinase inhibitor U0126 (1,4-diamino-2,3-dicyano-1,4-bis[2-amino-phenylthio]butadiene), demonstrating that signaling pathways downstream of both ligands affect the DeltaPsi(m) of mitochondria. In addition, general inhibition of receptor tyrosine kinase activity produced a profound global decrease in F(m)/F(c). Thus, two guidance molecules that exert different effects on growth cone motility both elicit local, receptor-mediated increases in membrane potential.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.