Statistics from Altmetric.com
If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.
The spectrum of sodium (Na+) channel-associated pain disorders is expanding, with mutations in the Na+ channel isoforms Nav1.7, Nav1.8 and Nav1.9 all associated with human syndromes.1 ,2 However, the characterisation of clinical and electrophysiological properties of mutations in Nav1.9 has trailed behind those of Nav1.7 and Nav1.8. Identification of the functional role of Nav1.9 in sensory neurons followed the documentation of a persistent Na+ current with ultraslow activation that was not eliminated by Nav1.8 knockout,3 although the gene functionality in neurons was not proven until Nav1.9 was painstakingly heterologously expressed in murine Nav1.9 knockout neurons.4 Almost 10 years …
Competing interests None declared.
Provenance and peer review Commissioned; internally peer reviewed.