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Kinetic Model of Nav1.5 Channel Provides a Subtle Insight into Slow Inactivation Associated Excitability in Cardiac Cells

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  • Zheng Zhang
  • Zhiwen Zhao
  • Yongfeng Liu
  • Wei Wang
  • Ying Wu
  • Jiuping Ding

Abstract

Voltage-gated sodium channel Nav1.5 has been linked to the cardiac cell excitability and a variety of arrhythmic syndromes including long QT, Brugada, and conduction abnormalities. Nav1.5 exhibits a slow inactivation, corresponding to a duration-dependent bi-exponential recovery, which is often associated with various arrhythmia syndromes. However, the gating mechanism of Nav1.5 and the physiological role of slow inactivation in cardiac cells remain elusive. Here a 12-state two-step inactivation Markov model was successfully developed to depict the gating kinetics of Nav1.5. This model can simulate the Nav1.5 channel in not only steady state processes, but also various transient processes. Compared with the simpler 8-state model, this 12-state model is well-behaved in simulating and explaining the processes of slow inactivation and slow recovery. This model provides a good framework for further studying the gating mechanism and physiological role of sodium channel in excitable cells.

Suggested Citation

  • Zheng Zhang & Zhiwen Zhao & Yongfeng Liu & Wei Wang & Ying Wu & Jiuping Ding, 2013. "Kinetic Model of Nav1.5 Channel Provides a Subtle Insight into Slow Inactivation Associated Excitability in Cardiac Cells," PLOS ONE, Public Library of Science, vol. 8(5), pages 1-8, May.
    • Handle: RePEc:plo:pone00:0064286
    DOI: 10.1371/journal.pone.0064286
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    Cited by:

    1. Pietro Balbi & Paolo Massobrio & Jeanette Hellgren Kotaleski, 2017. "A single Markov-type kinetic model accounting for the macroscopic currents of all human voltage-gated sodium channel isoforms," PLOS Computational Biology, Public Library of Science, vol. 13(9), pages 1-29, September.
    2. Colin H Peters & Alec Yu & Wandi Zhu & Jonathan R Silva & Peter C Ruben, 2017. "Depolarization of the conductance-voltage relationship in the NaV1.5 mutant, E1784K, is due to altered fast inactivation," PLOS ONE, Public Library of Science, vol. 12(9), pages 1-29, September.

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