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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 …
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