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Related Experiment Videos

Ca2+/calmodulin modulates TRPV1 activation by capsaicin.

Tamara Rosenbaum1, Ariela Gordon-Shaag, Mika Munari

  • 1Department of Physiology and Biophysics, University of Washington, Seattle, WA 98195-7290, USA.

The Journal of General Physiology
|December 31, 2003
PubMed
Summary
This summary is machine-generated.

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TRPV1 channels, activated by heat and capsaicin, mediate pain. Calcium influx through TRPV1 may inhibit channel activity, potentially explaining pain desensitization over time.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Ion Channel Physiology

Background:

  • TRPV1 ion channels are crucial for sensing painful heat, acidosis, and capsaicin.
  • These channels are expressed in sensory nerves, contributing to pain perception.
  • TRPV1 channels are nonselective cation channels with high calcium permeability, important for pain response and desensitization.

Purpose of the Study:

  • To investigate the role of Ca2+/calmodulin in regulating TRPV1 channel activity.
  • To determine the mechanism by which Ca2+ influx influences TRPV1 channel gating.
  • To explore the potential involvement of this mechanism in capsaicin-induced pain desensitization.

Main Methods:

  • Utilized inside-out excised patches from Xenopus oocytes and HEK 293 cells expressing TRPV1.

Related Experiment Videos

  • Investigated the effect of Ca2+/calmodulin on capsaicin-activated TRPV1 currents.
  • Employed coexpression of wild-type and mutant calmodulin with TRPV1.
  • Performed in vitro calmodulin-binding assays and experiments with GST-fusion proteins.

    • Main Results:

    • Ca2+/calmodulin inhibited capsaicin-activated TRPV1 currents, an effect mediated by decreased open probability and slowly reversible.
    • Increasing calmodulin concentration enhanced Ca2+-dependent inhibition.
    • TRPV1 binds calmodulin in a Ca2+-dependent manner within its NH2-terminal domain.
    • Ca2+ influx through TRPV1 may provide feedback inhibition of channel gating.

    Conclusions:

    • TRPV1 channel activity is regulated by Ca2+/calmodulin.
    • Ca2+ influx via TRPV1 can lead to feedback inhibition of channel gating.
    • This feedback mechanism may contribute to the desensitization of pain sensations.