ArticleCellular and molecular neurobiology2014
Enhanced slow inactivation of the human skeletal muscle sodium channel causing normokalemic periodic paralysis.
Article in Cellular and molecular neurobiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- Exercise and fatigue: integrating the role of KEuropean journal of applied physiology · 2023Review
- SCN4A p.R675Q Mutation Leading to Normokalemic Periodic Paralysis: A Family Report and Literature Review.Frontiers in neurology · 2019Article
- Familial Normokalemic Periodic Paralysis Associated With Mutation in theFrontiers in neurology · 2018Article
- A recessive Nav1.4 mutation underlies congenital myasthenic syndrome with periodic paralysis.Neurology · 2016Article
- Physiological and Pathophysiological Insights of Nav1.4 and Nav1.5 Comparison.Frontiers in pharmacology · 2015Review
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Normokalemic periodic paralysis (normoPP) is a type of skeletal muscle function disorder which is characterized by paralysis attack with concomitant normal serum potassium level. We previously reported that R675Q mutation of human skeletal muscle voltage-gated sodium channel α subunit (SCN4A) may be the novel mutation which caused normoPP in Chinese families. However, it is still not clear how this mutation affects the SCN4A channel function. In this study, we used patch-clamp recording to study the function of wild type (WT) and R675Q mutant of SCN4A channels expressed in human embryonic kidney (HEK293) cells. We found that R675Q mutation did not affect the voltage dependence of sodium channel activation. The fast inactivation was also not significantly affected by R675Q mutation. However, R675Q mutation of SCN4A channels exhibited an 11.1 mV hyperpolarized shift in the voltage dependence of slow inactivation and significantly prolonged the recovery from prolonged inactivation state. Our results thus indicate that SCN4A was functionally affected by R675Q mutation, suggesting a possible reason for causing normoPP in Chinese patients.
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