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.