A null mutation of the neuronal sodium channel NaV1.6 disrupts action potential propagation and excitation-contraction coupling in the mouse heart

Sodium channel gene family: epilepsy mutations, gene interactions and modifier effects

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Na+currents are required for efficient excitation-contraction coupling in rabbit ventricular myocytes: a possible contribution of neuronal Na+channels

(2010) Natalia S. Torres et al.   JOURNAL OF PHYSIOLOGY-LONDON

The ataxia3 Mutation in the N-Terminal Cytoplasmic Domain of Sodium Channel Nav1.6 Disrupts Intracellular Trafficking

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Nerve Supply of the Human Pulmonary Veins: An Anatomical Study

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Inherited Neuronal Ion Channelopathies: New Windows on Complex Neurological Diseases

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Functional properties and differential neuromodulation of Nav1.6 channels

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