Localization of Nav 1.7 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 (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.

• Authors: Darshani B Rupasinghe, Oliver Knapp, Linda V Blomster, Annina B Schmid, David J Adams, Glenn F King, Marc J Ruitenberg
• Journal: Channels (Austin, Tex.) (Channels (Austin)) 2012 Mar-Apr Vol. 6 Issue 2 Pg. 103-10 ISSN: 1933-6969 [Electronic] United States
• PMID: 22622154 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• NAV1.7 Voltage-Gated Sodium Channel
• Scn9a protein, rat
• Sodium Channels

Topics

• Animals
• Axons (metabolism)
• CHO Cells
• Cricetinae
• Cricetulus
• Humans
• Immunohistochemistry
• Male
• Monocytes (immunology, metabolism)
• NAV1.7 Voltage-Gated Sodium Channel
• Olfactory Bulb (cytology)
• Olfactory Mucosa (drug effects, innervation, metabolism)
• Rats
• Rats, Sprague-Dawley
• Smell (physiology)
• Sodium Channels (immunology, metabolism, physiology)
• Vomeronasal Organ (cytology, physiology)