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Nav1.7 is required for normal C-low threshold mechanoreceptor function in humans and mice.

Steven J Middleton1, Irene Perini2,3, Andreas C Themistocleous1,4

  • 1Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford OX3 9DU, UK.

Brain : a Journal of Neurology
|December 27, 2021
PubMed
Summary

Congenital insensitivity to pain (CIP) patients with Nav1.7 mutations also show impaired affective touch. Nav1.7 channel is crucial for C-low threshold mechanoreceptor (C-LTMR) function, cool sensitivity, and tactile perception.

Keywords:
C-low threshold mechanoreceptorsNav1.7affective touchcongenital insensitivity to pain

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Area of Science:

  • Neuroscience
  • Sensory Physiology

Background:

  • Congenital insensitivity to pain (CIP) is linked to loss-of-function mutations in the Nav1.7 sodium channel.
  • Previously, low threshold mechanosensation was considered unaffected in CIP patients.

Purpose of the Study:

  • To investigate the role of Nav1.7 in affective touch encoding.
  • To determine if Nav1.7 is essential for C-low threshold mechanoreceptor (C-LTMR) function.

Main Methods:

  • Psychophysical testing in CIP patients and healthy controls.
  • Facial electromyography in CIP patients and healthy controls.
  • Genetic and pharmacological manipulation of Nav1.7 in mouse C-LTMRs.

Main Results:

  • CIP patients exhibited abnormalities in affective touch encoding.
  • Nav1.7 is highly expressed in mouse C-LTMRs.
  • Loss of Nav1.7 in C-LTMRs reduced sodium current, increased mechanical threshold, and decreased cooling sensitivity in mice.

Conclusions:

  • Nav1.7 is essential for normal pain perception.
  • Nav1.7 plays a critical role in C-LTMR function, including cool sensitivity and affective touch.
  • Nav1.7 mutations impact more than just pain sensation.