NaV1.7: A central role in pain
- PMID: 37678164
- DOI: 10.1016/j.neuron.2023.08.011
NaV1.7: A central role in pain
Abstract
Loss of function of sodium channel NaV1.7 produces pain insensitivity. In this issue, Deng et al.1 show that analgesia after NaV1.7 removal or pharmacological blockade is not driven by enkephalin overexpression. These results underscore the essential role, independent of endogenous opioids, of NaV1.7 for nociceptor firing and pain.
Copyright © 2023 Elsevier Inc. All rights reserved.
Conflict of interest statement
Declaration of interests S.G.W. has served as a paid advisor to Olipass Therapeutics, Sangamo Pharma, Exicure Research, Envida Biopharma, Chromocell, Third Rock Bioventures, MedTronic, and Alnylam. He holds stocks in Navega Therapeutics and Site One Therapeutics. S.D.H. received consulting fees from Alnaylum and holds stocks in Pfizer Pharmaceuticals.
Comment on
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Nav1.7 is essential for nociceptor action potentials in the mouse in a manner independent of endogenous opioids.Neuron. 2023 Sep 6;111(17):2642-2659.e13. doi: 10.1016/j.neuron.2023.05.024. Epub 2023 Jun 22. Neuron. 2023. PMID: 37352856
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