Key result
Increased late sodium current due to disrupted channel inactivation leads to repetitive action potentials and prolonged action potential duration, contributing to seizures, arrhythmias, and pain.
Why the study?
Disruption of sodium channel inactivation leads to increased late sodium current, a common defect across neurological, muscular, and cardiac disorders.
This review highlights the pathophysiological role of increased late sodium current across multiple organ systems, including its contribution to cardiac arrhythmias.
Answers are grounded in this paper and cite their sources.
Late Na current from inactivation defects may promote arrhythmias; leaves open selective inhibition as targeted therapy.
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.
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Fouda et al. (2022) conducted a review in Sodium channelopathies. Late sodium current was evaluated. Increased late sodium current due to disrupted channel inactivation leads to repetitive action potentials and prolonged action potential duration, contributing to seizures, arrhythmias, and pain.
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