ArticleFrontiers in cellular neuroscience2016
ATP Released by Injured Neurons Activates Schwann Cells.
Article in Frontiers in cellular neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 41 citations in OpenAlex.
- New Insights into Neuromuscular Junction Biology: Evidence from Human and Animal Research.International journal of molecular sciences · 2026Review
- Article
- Schwann cell reprogramming via EMT-like program following peripheral nerve injury and during nerve regeneration.Frontiers in cell and developmental biology · 2025Review
- Agonists of melatonin receptors strongly promote the functional recovery from the neuroparalysis induced by neurotoxic snakes.PLoS neglected tropical diseases · 2024Article
- Mechanism of ERK/CREB pathway in pain and analgesia.Frontiers in molecular neuroscience · 2023Review
- Hydrogen peroxide induced by nerve injury promotes axon regeneration via connective tissue growth factor.Acta neuropathologica communications · 2022Article
- Models and methods to study Schwann cells.Journal of anatomy · 2022Review
- MAPK/ERK Pathway as a Central Regulator in Vertebrate Organ Regeneration.International journal of molecular sciences · 2022Review
- Neuronal activity-dependent ATP enhances the pro-growth effect of repair Schwann cell extracellular vesicles by increasing their miRNA-21 loading.Frontiers in cellular neuroscience · 2022Article
- hiPSC-Derived Schwann Cells Influence Myogenic Differentiation in Neuromuscular Cocultures.Cells · 2021Article
- Emerging roles of dysregulated adenosine homeostasis in brain disorders with a specific focus on neurodegenerative diseases.Journal of biomedical science · 2021Review
- Metabolic Transporters in the Peripheral Nerve-What, Where, and Why?Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021Review
- Pannexin 1, a large-pore membrane channel, contributes to hypotonicity-induced ATP release in Schwann cells.Neural regeneration research · 2021Article
- Signals Orchestrating Peripheral Nerve Repair.Cells · 2020Review
- Curse of the devil: molecular insights into the emergence of transmissible cancers in the Tasmanian devil (Sarcophilus harrisii).Cellular and molecular life sciences : CMLS · 2020Review
- Review
- CXCL12α/SDF-1 from perisynaptic Schwann cells promotes regeneration of injured motor axon terminals.EMBO molecular medicine · 2017Article
- Moving forward with the neuromuscular junction.Journal of neurochemistry · 2017Review
- Schwann cells are activated by ATP released from neurons in anDisease models & mechanisms · 2017Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Injured nerve terminals of neuromuscular junctions (NMJs) can regenerate. This remarkable and complex response is governed by molecular signals that are exchanged among the cellular components of this synapse: motor axon nerve terminal (MAT), perisynaptic Schwann cells (PSCs), and muscle fiber. The nature of signals that govern MAT regeneration is ill-known. In the present study the spider toxin α-latrotoxin has been used as tool to investigate the mechanisms underlying peripheral neuroregeneration. Indeed this neurotoxin induces an acute, specific, localized and fully reversible damage of the presynaptic nerve terminal, and its action mimics the cascade of events that leads to nerve terminal degeneration in injured patients and in many neurodegenerative conditions. Here we provide evidence of an early release by degenerating neurons of adenosine triphosphate as alarm messenger, that contributes to the activation of a series of intracellular pathways within Schwann cells that are crucial for nerve regeneration: Ca(2+), cAMP, ERK1/2, and CREB. These results contribute to define the cross-talk taking place among degenerating nerve terminals and PSCs, involved in the functional recovery of the NMJ.
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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.