ArticleThe Journal of physiology2006
The human adult subtype ACh receptor channel has high Ca2+ permeability and predisposes to endplate Ca2+ overloading.
Article in The Journal of physiology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.
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Who cites it
29 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.
- Pharmacological Strategy for Congenital Myasthenic Syndrome with CHRNE Mutations: A Meta-Analysis of Case Reports.Current neuropharmacology · 2021Pooled it
- Reduction of the CaFrontiers in cellular neuroscience · 2025Review
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- Donepezil inhibits neuromuscular junctional acetylcholinesterase and enhances synaptic transmission and function in isolated skeletal muscle.British journal of pharmacology · 2022Article
- "Calcium bombs" as harbingers of synaptic pathology and their mitigation by magnesium at murine neuromuscular junctions.Frontiers in molecular neuroscience · 2022Article
- The Structure, Function, and Physiology of the Fetal and Adult Acetylcholine Receptor in Muscle.Frontiers in molecular neuroscience · 2020Review
- The Distribution of Charged Amino Acid Residues and the CaFrontiers in molecular neuroscience · 2017Article
- Mutations Causing Slow-Channel Myasthenia Reveal That a Valine Ring in the Channel Pore of Muscle AChR is Optimized for Stabilizing Channel Gating.Human mutation · 2016Article
- Article
- Bispyridinium Compounds Inhibit Both Muscle and Neuronal Nicotinic Acetylcholine Receptors in Human Cell Lines.PloS one · 2015Article
- Tracking the molecular evolution of calcium permeability in a nicotinic acetylcholine receptor.Molecular biology and evolution · 2014Article
- A mutation in the extracellular domain of the α7 nAChR reduces calcium permeability.Pflugers Archiv : European journal of physiology · 2014Article
- Functional and genetic characterization of clinical malignant hyperthermia crises: a multi-centre study.Orphanet journal of rare diseases · 2014Article
- Exploring the central modulation hypothesis: do ancient memory mechanisms underlie the pathophysiology of trigger points?Current pain and headache reports · 2013Review
- Cholinergic receptors: functional role of nicotinic ACh receptors in brain circuits and disease.Pflugers Archiv : European journal of physiology · 2013Review
- CC4, a dimer of cytisine, is a selective partial agonist at α4β2/α6β2 nAChR with improved selectivity for tobacco smoking cessation.British journal of pharmacology · 2013Article
- Functional α7 nicotinic ACh receptors on astrocytes in rat hippocampal CA1 slices.Journal of molecular neuroscience : MN · 2012Article
- Riluzole blocks human muscle acetylcholine receptors.The Journal of physiology · 2012Article
- Physiological characterization of human muscle acetylcholine receptors from ALS patients.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Skeletal muscle IP3R1 receptors amplify physiological and pathological synaptic calcium signals.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 3 countries.
Funding
Abstract
Slow-channel congenital myasthenic syndrome, caused by mutations in subunits of the endplate ACh receptor (AChR), results in prolonged synaptic currents and excitotoxic injury of the postsynaptic region by Ca2+ overloading. The Ca2+ overloading could be due entirely to the prolonged openings of the AChR channel or could be abetted by enhanced Ca2+ permeability of the mutant channels. We therefore measured the fractional Ca2+ current, defined as the percentage of the total ACh-evoked current carried by Ca2+ ions (Pf), for AChRs harbouring the alphaG153S or the alphaV249F slow-channel mutation, and for wild-type human AChRs in which Pf has not yet been determined. Experiments were performed in transiently transfected GH4C1 cells and human myotubes with simultaneous recording of ACh-evoked whole-cell currents and fura-2 fluorescence signals. We found that the Pf of the wild-type human endplate AChR was unexpectedly high (Pf approximately 7%), but neither the alphaV249F nor the alphaG153S mutation altered Pf. Fetal human AChRs containing either the wild-type or the mutated alpha subunit had a much lower Pf (2-3%). We conclude that the Ca2+ permeability of human endplate AChRs is higher than that reported for any other human nicotinic AChR, with the exception of alpha7-containing AChRs (Pf > 10%); and that neither the alphaG153S nor the alphaV249F mutations affect the Pf of fetal or adult endplate AChRs. However, the intrinsically high Ca2+ permeability of human AChRs probably predisposes to development of the endplate myopathy when opening events of the AChR channel are prolonged by altered AChR-channel kinetics.
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