NaV1.7: A central role in pain

Loss of function of sodium channel NaV1.7 produces pain insensitivity. In this issue, Deng et al. 1 Deng L. Dourado M. Reese R.M. Huang K. Shields S.D. Stark K.L. Maksymetz J. Lin H. Kaminker J.S. Jung M. et al. Nav1.7 is essential for nociceptor action potentials in the mouse in a manner independent of endogenous opioids. Neuron. 2023; 111: 2642-2659https://doi.org/10.1016/j.neuron.2023.05.024 Abstract Full Text Full Text PDF Scopus (2) Google Scholar 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. Loss of function of sodium channel NaV1.7 produces pain insensitivity. In this issue, Deng et al. 1 Deng L. Dourado M. Reese R.M. Huang K. Shields S.D. Stark K.L. Maksymetz J. Lin H. Kaminker J.S. Jung M. et al. Nav1.7 is essential for nociceptor action potentials in the mouse in a manner independent of endogenous opioids. Neuron. 2023; 111: 2642-2659https://doi.org/10.1016/j.neuron.2023.05.024 Abstract Full Text Full Text PDF Scopus (2) Google Scholar 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. Nav1.7 is essential for nociceptor action potentials in the mouse in a manner independent of endogenous opioidsDeng et al.NeuronJune 22, 2023In BriefDeng et al. show that genetic removal or selective inhibition of Nav1.7 blocks nociceptor action potentials, highlighting the essential role Nav1.7 plays in initiating such APs and explaining the resulting analgesia. Enkephalin overexpression, previously thought to drive analgesia in Nav1.7 knockout mice, was found to play a limited role, if any. Full-Text PDF Open Access