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• W2936955096 abstract "Although Ca2+ influx through muscle nAChR-channels has been described over the past 40 years, its functions remain still poorly understood. In this review we suggest possible roles of Ca2+ entry at all stages of muscle development, summarizing the evidence present in literature. nAChRs are expressed in myoblasts prior to fusion, and can be activated in the absence of an ACh-releasing nerve terminal, with Ca2+ influx likely contributing to regulate cell fusion. Upon establishment of nerve-muscle contact, Ca2+ influx contributes to orchestrate the signaling required for the correct formation of the neuromuscular junction. Finally, in the mature synapse, Ca2+ entry through postsynaptic nAChR-channels – highly Ca2+ permeable, in particular in humans – acts on K+ and Na+ channels to shape endplate excitability. However, when genetic defects cause excessive channel activation, Ca2+ influx becomes toxic and causes endplate myopathy. Throughout the review, we highlight how Ricardo Miledi has contributed to construct this whole body of knowledge, from the initial description of Ca2+ permeability of endplate nAChR channels, to the rationale for the treatment of endplate excitotoxic damage under pathological conditions. This article is part of a Special Issue entitled: SI: Honoring Ricardo Miledi - outstanding neuroscientist of XX-XXI centuries" @default.
• W2936955096 created "2019-04-25" @default.
• W2936955096 creator A5060520612 @default.
• W2936955096 creator A5064196678 @default.
• W2936955096 date "2020-07-01" @default.
• W2936955096 modified "2023-09-23" @default.
• W2936955096 title "Calcium influx through muscle nAChR-channels: One route, multiple roles" @default.
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• W2936955096 doi "https://doi.org/10.1016/j.neuroscience.2019.04.011" @default.
• W2936955096 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30999028" @default.
• W2936955096 hasPublicationYear "2020" @default.
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