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Background  Voltage-gated sodium channel Na v 1.7 is preferentially expressed in dorsal root ganglion (DRG) and sympathetic neurons within the peripheral nervous system. Homozygous or compound heterozygous loss-of-function mutations in  SCN9A , the gene which encodes Na v 1.7, cause congenital insensitivity to pain (CIP) accompanied by anosmia. Global knock-out of Na v 1.7 in mice is neonatal lethal reportedly from starvation, suggesting anosmia. These findings led us to hypothesize that Na v 1.7 is the main sodium channel in the peripheral olfactory sensory neurons (OSN, also known as olfactory receptor neurons).    Methods  We used multiplex PCR-restriction enzyme polymorphism,  in situ  hybridization and immunohistochemistry to determine the identity of sodium channels in rodent OSNs.    Results  We show here that Na v 1.7 is the predominant sodium channel transcript, with low abundance of other sodium channel transcripts, in olfactory epithelium from rat and mouse. Our  in situ  hybridization data show that Na v 1.7 transcripts are present in rat OSNs. Immunostaining of Na v 1.7 and Na v 1.6 channels in rat shows a complementary accumulation pattern with Na v 1.7 in peripheral presynaptic OSN axons, and Na v 1.6 primarily in postsynaptic cells and their dendrites in the glomeruli of the olfactory bulb within the central nervous system.    Conclusions  Our data show that Na v 1.7 is the dominant sodium channel in rat and mouse OSN, and may explain anosmia in Na v 1.7 null mouse and patients with Na v 1.7-related CIP.

Nav1.7 is the Predominant Sodium Channel in Rodent Olfactory Sensory Neurons

Na_v1.7 is the Predominant Sodium Channel in Rodent Olfactory Sensory Neurons