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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
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.
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.
