Nav1.7 is the main sodium channel in rodent olfactory sensory neurons
Author Information
Author(s): Ahn Hye-Sook, Black Joel A, Zhao Peng, Tyrrell Lynda, Waxman Stephen G, Dib-Hajj Sulayman D
Primary Institution: Yale University School of Medicine
Hypothesis
Nav1.7 is the main sodium channel in the peripheral olfactory sensory neurons.
Conclusion
Nav1.7 is the dominant sodium channel in rat and mouse olfactory sensory neurons, which may explain anosmia in Nav1.7 null mice and patients with Nav1.7-related congenital insensitivity to pain.
Supporting Evidence
- Nav1.7 transcripts were found to be the predominant sodium channel in the olfactory epithelium of rats and mice.
- Immunostaining showed Nav1.7 in presynaptic axons of olfactory sensory neurons.
- Loss-of-function mutations in SCN9A, which encodes Nav1.7, lead to congenital insensitivity to pain and anosmia.
Takeaway
This study found that a specific sodium channel, Nav1.7, is very important for how smell works in rats and mice. If this channel doesn't work, it can lead to a loss of the ability to smell.
Methodology
Multiplex PCR-restriction enzyme polymorphism, in situ hybridization, and immunohistochemistry were used to identify sodium channels in rodent olfactory sensory neurons.
Limitations
The study primarily focuses on rodent models, which may not fully represent human physiology.
Participant Demographics
Adult male Sprague-Dawley rats and C57BL/6 mice were used in the study.
Digital Object Identifier (DOI)
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