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Late sodium current: incomplete inactivation triggers seizures, myotonias, arrhythmias, and pain syndromes
Author(s) -
Fouda Mohamed A.,
Ghovanloo MohammadReza,
Ruben Peter C.
Publication year - 2022
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jp282768
Subject(s) - sodium channel , myotonia , skeletal muscle , medicine , sodium , gating , erythromelalgia , endocrinology , cardiology , anesthesia , neuroscience , chemistry , biology , physiology , myotonic dystrophy , organic chemistry
Acquired and inherited dysfunction in voltage‐gated sodium channels underlies a wide range of diseases. In addition to defects in trafficking and expression, sodium channelopathies are caused by dysfunction in one or several gating properties, for instance activation or inactivation. Disruption of channel inactivation leads to increased late sodium current, which is a common defect in seizure disorders, cardiac arrhythmias skeletal muscle myotonia and pain. An increase in late sodium current leads to repetitive action potentials in neurons and skeletal muscles, and prolonged action potential duration in the heart. In this Topical Review, we compare the effects of late sodium current in brain, heart, skeletal muscle and peripheral nerves.