ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014
Schwann cells sense and control acetylcholine spillover at the neuromuscular junction by α7 nicotinic receptors and butyrylcholinesterase.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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34 citing papers in PubMed, 67 citations in OpenAlex.
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- Purinergic Tuning of the Tripartite Neuromuscular Synapse.Molecular neurobiology · 2023Review
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- Cholinergic blockade of neuroinflammation: from tissue to RNA regulators.Neuronal signaling · 2022Review
- Role of α7 Nicotinic Acetylcholine Receptors in Synaptic Transmission in Frog Neuromuscular Contacts.Bulletin of experimental biology and medicine · 2022Article
- Balanced modulation of neuromuscular synaptic transmission via M1 and M2 muscarinic receptors during inhibition of cholinesterases.Scientific reports · 2022Article
- Effects of 3,4-diaminopyridine on myasthenia gravis: Preliminary results of an open-label study.Frontiers in pharmacology · 2022Article
- hiPSC-Derived Schwann Cells Influence Myogenic Differentiation in Neuromuscular Cocultures.Cells · 2021Article
- Adrenoceptors Modulate Cholinergic Synaptic Transmission at the Neuromuscular Junction.International journal of molecular sciences · 2021Review
- Cholinesterases in Tripartite Neuromuscular Synapse.Frontiers in molecular neuroscience · 2021Review
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Authors and funding
12 authors at 9 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Terminal Schwann cells (TSCs) are key components of the mammalian neuromuscular junction (NMJ). How the TSCs sense the synaptic activity in physiological conditions remains unclear. We have taken advantage of the distinct localization of acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) at the NMJ to bring out the function of different ACh receptors (AChRs). AChE is clustered by the collagen Q in the synaptic cleft and prevents the repetitive activation of muscle nicotinic AChRs. We found that BChE is anchored at the TSC by a proline-rich membrane anchor, the small transmembrane protein anchor of brain AChE. When BChE was specifically inhibited, ACh release was significant depressed through the activation of α7 nAChRs localized on the TSC and activated by the spillover of ACh. When both AChE and BChE were inhibited, the spillover increased and induced a dramatic reduction of ACh release that compromised the muscle twitch triggered by the nerve stimulation. α7 nAChRs at the TSC may act as a sensor for spillover of ACh adjusted by BChE and may represent an extrasynaptic sensor for homeostasis at the NMJ. In myasthenic rats, selective inhibition of AChE is more effective in rescuing muscle function than the simultaneous inhibition of AChE and BChE because the concomitant inhibition of BChE counteracts the positive action of AChE inhibition. These results show that inhibition of BChE should be avoided during the treatment of myasthenia and the pharmacological reversal of residual curarization after anesthesia.
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