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Related Experiment Videos

Voltage-dependent sodium channel function is regulated through membrane mechanics.

A Shcherbatko1, F Ono, G Mandel

  • 1Department of Neurobiology and Behavior, State University of New York at Stony Brook, Stony Brook, New York 11794 USA. ashcherb@brain.neurobio.sunysb.edu

Biophysical Journal
|October 8, 1999
PubMed
Summary

Mechanical forces influence sodium channel kinetics. Disruption of the cytoskeleton shifts sodium channel (Na+) inactivation to faster speeds, suggesting mechanical destabilization is key.

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Biophysics

Background:

  • Sodium channels (Na+) are crucial for electrical signaling in nerve and muscle.
  • Previous studies indicated slow inactivation kinetics in cut-open Xenopus oocyte recordings.
  • The role of mechanical forces and cytoskeleton in Na+ channel function remained unclear.

Purpose of the Study:

  • To investigate the impact of different electrophysiological recording configurations on Na+ channel kinetics.
  • To explore the influence of mechanical forces and cytoskeleton on Na+ channel inactivation and activation.
  • To determine the potential role of the Na+ channel beta1 subunit in mediating these mechanical effects.

Main Methods:

  • Electrophysiological recordings (cut-open, macropatch, cell-attached) from Xenopus oocytes expressing nerve (PN1) and skeletal muscle (SkM1) Na+ channel alpha subunits.

Related Experiment Videos

  • Application of pressure (positive and negative) to cell-attached patch electrodes.
  • Pharmacological disruption of microtubule formation.
  • Simultaneous electrophysiological recording and video imaging.
  • Investigation of Na+ channel alpha subunit function with and without the beta1 subunit.

    • Main Results:

    • Macropatch recordings showed a negative shift in voltage-dependence and faster inactivation/activation kinetics compared to cut-open recordings.
    • Patch excision and microtubule disruption accelerated the shift to fast inactivation.
    • Negative pressure induced fast inactivation, while positive pressure prevented it.
    • Pressure-induced shifts correlated with cytoskeleton attachment disruption.
    • The beta1 subunit mimicked these mechanical effects on Na+ channel alpha subunit function.

    Conclusions:

    • Mechanical destabilization, potentially via cytoskeleton interaction, may underlie the fast kinetics and negative voltage-dependence of endogenous Na+ channels.
    • The Na+ channel beta1 subunit might mediate these effects through cytoskeletal interactions.
    • These findings highlight the importance of mechanical forces in regulating ion channel function.