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

Loss-of-function mutations in the pore-forming α subunit of the voltage-gated sodium channel 1.7 (Na v 1.7) cause congenital indifference to pain and anosmia. We used immunohistochemical techniques to study Na v 1.7 localization in the rat olfactory system in order to better understand its role in o...

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Bibliographic Details
Published in:Channels (Austin, Tex.) Tex.), 2012-03, Vol.6 (2), p.103-110
Main Authors: Rupasinghe, Darshani B., Knapp, Oliver, Blomster, Linda V., Schmid, Annina B., Adams, David J., King, Glenn F., Ruitenberg, Marc J.
Format: Article
Language:English
Subjects:
Binding
Biology
Bioscience
Calcium
Cancer
Cell
Cycle
inflammation
injury
Landes
monocyte
Organogenesis
pain
Proteins
regeneration
sodium channel
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Summary:Loss-of-function mutations in the pore-forming α subunit of the voltage-gated sodium channel 1.7 (Na v 1.7) cause congenital indifference to pain and anosmia. We used immunohistochemical techniques to study Na v 1.7 localization in the rat olfactory system in order to better understand its role in olfaction. We confirm that Na v 1.7 is expressed on olfactory sensory axons and report its presence on vomeronasal axons, indicating an important role for Na v 1.7 in transmission of pheromonal cues. Following neuroepithelial injury, Na v 1.7 was transiently expressed by cells of monocytic lineage. These findings support an emerging role for Na v 1.7 in immune function. This sodium channel may provide an important pharmacological target for treatment of inflammatory injury and inflammatory pain syndromes.
ISSN:1933-6950
1933-6969
DOI:10.4161/chan.19484