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

Original publication

DOI

10.4161/chan.19484

Type

Journal article

Journal

Channels (austin)

Publication Date

03/2012

Volume

6

Pages

103 - 110

Keywords

Animals, Axons, CHO Cells, Cricetinae, Cricetulus, Humans, Immunohistochemistry, Male, Monocytes, NAV1.7 Voltage-Gated Sodium Channel, Olfactory Bulb, Olfactory Mucosa, Rats, Rats, Sprague-Dawley, Smell, Sodium Channels, Vomeronasal Organ