ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2001
Synapse-glia interactions at the mammalian neuromuscular junction.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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Who cites it
59 citing papers in PubMed, 144 citations in OpenAlex.
- Neuromuscular junction innervation and motor function are preserved by restoring muscarinic signaling in perisynaptic glia in ALS.iScience · 2026Article
- Chemogenetic Schwann cell activation impairs early myelination and triggers adult demyelination in the peripheral nervous system.Frontiers in cellular neuroscience · 2026Article
- An α7 nicotinic and GABAThe Journal of physiology · 2025Article
- Schwann Cells as Orchestrators of Nerve Repair: Implications for Tissue Regeneration and Pathologies.Cold Spring Harbor perspectives in biology · 2024Review
- Origin, identity, and function of terminal Schwann cells.Trends in neurosciences · 2024Review
- Purinergic Tuning of the Tripartite Neuromuscular Synapse.Molecular neurobiology · 2023Review
- TDP-43 dysregulation and neuromuscular junction disruption in amyotrophic lateral sclerosis.Translational neurodegeneration · 2022Review
- Article
- Structure and Function of the Mammalian Neuromuscular Junction.Comprehensive Physiology · 2022Article
- Morphology of Schwann Cell Processes Supports Renal Sympathetic Nerve Terminals With Local Distribution of Adrenoceptors.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2022Article
- Neuromuscular Junction Dysfunction in Amyotrophic Lateral Sclerosis.Molecular neurobiology · 2022Review
- Terminal Schwann Cell Aging: Implications for Age-Associated Neuromuscular Dysfunction.Aging and disease · 2021Review
- Cholinesterases in Tripartite Neuromuscular Synapse.Frontiers in molecular neuroscience · 2021Review
- Properties of Glial Cell at the Neuromuscular Junction Are Incompatible with Synaptic Repair in theThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Specific labeling of synaptic schwann cells reveals unique cellular and molecular features.eLife · 2020Article
- Calcium Signaling in Schwann cells.Neuroscience letters · 2020Review
- Perisynaptic Schwann cells phagocytose nerve terminal debris in a mouse model of Guillain-Barré syndrome.Journal of the peripheral nervous system : JPNS · 2020Article
- Blocking skeletal muscle DHPRs/Ryr1 prevents neuromuscular synapse loss in mutant mice deficient in type III Neuregulin 1 (CRD-Nrg1).PLoS genetics · 2019Article
- Roles for neuronal and glial autophagy in synaptic pruning during development.Neurobiology of disease · 2019Review
- Clinical relevance of terminal Schwann cells: An overlooked component of the neuromuscular junction.Journal of neuroscience research · 2018Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Perisynaptic Schwann cells (PSCs) play critical roles in regulating and stabilizing nerve terminals at the mammalian neuromuscular junction (NMJ). However, although these functions are likely regulated by the synaptic properties, the interactions of PSCs with the synaptic elements are not known. Therefore, our goal was to study the interactions between mammalian PSCs in situ and the presynaptic terminals using changes in intracellular Ca(2+) as an indicator of cell activity. Motor nerve stimulation induced an increase in intracellular Ca(2+) in PSCs, and this increase was greatly reduced when transmitter release was blocked. Furthermore, local application of acetylcholine induced Ca(2+) responses that were blocked by the muscarinic antagonist atropine and mimicked by the muscarinic agonist muscarine. The nicotinic antagonist alpha-bungarotoxin had no effect on Ca(2+) responses induced by acetylcholine. Local application of the cotransmitter ATP induced Ca(2+) responses that were unaffected by the P2 antagonist suramin, whereas local application of adenosine induced Ca(2+) responses that were greatly reduced by the A1 receptor antagonist 8-cyclopentyl-1,3-dimethylxanthine (CPT). However, the presence of the A1 antagonist in the perfusate did not block responses induced by ATP. Ca(2+) responses evoked by stimulation of the motor nerve were reduced in the presence of CPT, whereas atropine almost completely abolished them. Ca(2+) responses were further reduced when both antagonists were present simultaneously. Hence, PSCs at the mammalian NMJ respond to the release of neurotransmitter induced by stimulation of the motor nerve through the activation of muscarinic and adenosine A1 receptors.
Indexed as
Identifiers
11356870PMC6762689W2150860493What OpenQuestion holds
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.