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• W1582582842 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 Ca 2+ overloading. The Ca 2+ overloading could be due entirely to the prolonged openings of the AChR channel or could be abetted by enhanced Ca 2+ permeability of the mutant channels. We therefore measured the fractional Ca 2+ current, defined as the percentage of the total ACh‐evoked current carried by Ca 2+ ions ( P f ), for AChRs harbouring the αG153S or the αV249F slow‐channel mutation, and for wild‐type human AChRs in which P f 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 P f of the wild‐type human endplate AChR was unexpectedly high ( P f ∼7%), but neither the αV249F nor the αG153S mutation altered P f . Fetal human AChRs containing either the wild‐type or the mutated α subunit had a much lower P f (2–3%). We conclude that the Ca 2+ permeability of human endplate AChRs is higher than that reported for any other human nicotinic AChR, with the exception of α7‐containing AChRs ( P f > 10%); and that neither the αG153S nor the αV249F mutations affect the P f of fetal or adult endplate AChRs. However, the intrinsically high Ca 2+ 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." @default.
• W1582582842 created "2016-06-24" @default.
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• W1582582842 date "2006-05-09" @default.
• W1582582842 modified "2023-10-15" @default.
• W1582582842 title "The human adult subtype ACh receptor channel has high Ca²⁺permeability and predisposes to endplate Ca²⁺overloading" @default.
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• W1582582842 doi "https://doi.org/10.1113/jphysiol.2006.108092" @default.
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