Abstract
Loss of function of sodium channel NaV1.7 produces pain insensitivity. In this issue, Deng etal.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.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have