Localization of Nav1.7 in the normal and injured rodent olfactory system indicates a critical role in olfaction, pheromone sensing and immune function

Abstract

Loss-of-function mutations in the pore-forming α subunit of the voltage-gated sodium channel 1.7 (Nav1.7) cause congenital indifference to pain and anosmia. We used immunohistochemical techniques to study Nav1.7 localization in the rat olfactory system in order to better understand its role in olfaction. We confirm that Nav1.7 is expressed on olfactory sensory axons and report its presence on vomeronasal axons, indicating an important role for Nav1.7 in transmission of pheromonal cues. Following neuroepithelial injury, Nav1.7 was transiently expressed by cells of monocytic lineage. These findings support an emerging role for Nav1.7 in immune function. This sodium channel may provide an important pharmacological target for treatment of inflammatory injury and inflammatory pain syndromes.