Pain behavior in SCN9A (Nav1.7) and SCN10A (Nav1.8) mutant rodent models

The two voltage gated sodium channels Nav1.7 and Nav1.8 are expressed in the peripheral nervous system involved various pain conditions including inflammatory neuropathic pain. Rodent models bearing deletions or mutations of corresponding genes, Scn9a Scn10a, were created order to understand role these pathophysiological mechanism underlying symptoms. This review summarizes behavior profiles reported Scn10a rodent models. complete loss-of-function knockout (KO) conditional KO (cKO) specific cell populations shown decrease sensitivity stimuli. Possum mutant mice a dominant hypermorphic mutation revealed higher noxious Several gain-of-function identified patients with painful small fiber neuropathy. Future knowledge obtained from preclinical will allow understanding how affect In addition, gives perspectives for creating that better mimic patients’ symptoms view developing novel analgesic strategies.