ArticleMolecular pain2011
Nav1.7 is the predominant sodium channel in rodent olfactory sensory neurons.
Article in Molecular pain, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 61 citations in OpenAlex.
- Safety, Tolerability, and Pharmacokinetics of GDC-0276, a Novel NaClinical drug investigation · 2019Trial
- Chasing the Wrong Door for 30 Years: Is Suzetrigine the Key to Selective Pain Relief?Medicina (Kaunas, Lithuania) · 2026Review
- Targeting Supramolecular Active Complexes of NaAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Suzetrigine: A promising analgesic targeting voltage-gated sodium channel.Indian journal of pharmacology · 2026Review
- Immature olfactory sensory neurons are intrinsically excitable and show maturation-dependent changes in voltage-gated NaPflugers Archiv : European journal of physiology · 2026Article
- Voltage-gated sodium channels in excitable cells as drug targets.Nature reviews. Drug discovery · 2025Review
- Post-operative analgesic regime in a patient with congenital indifference to pain.Journal of surgical case reports · 2025Article
- Ion Channels in Odor Information Processing of Neural Circuits of the Vertebrate Olfactory Bulb.International journal of molecular sciences · 2024Review
- Shining a Light on Venom-Peptide Receptors: Venom Peptides as Targeted Agents for In Vivo Molecular Imaging.Toxins · 2024Review
- Pain, Smell, and Taste in Adults: A Narrative Review of Multisensory Perception and Interaction.Pain and therapy · 2021Review
- Article
- HDAC6: A Key Link Between Mitochondria and Development of Peripheral Neuropathy.Frontiers in molecular neuroscience · 2021Review
- Status of peripheral sodium channel blockers for non-addictive pain treatment.Nature reviews. Neurology · 2020Review
- Application of Pharmacokinetic-Pharmacodynamic Modeling to Inform Translation of In Vitro NaV1.7 Inhibition to In Vivo Pharmacological Response in Non-human Primate.Pharmaceutical research · 2020Article
- A Comparison of the Primary Sensory Neurons Used in Olfaction and Vision.Frontiers in cellular neuroscience · 2020Review
- SCN9A Epileptic Encephalopathy Mutations Display a Gain-of-function Phenotype and Distinct Sensitivity to Oxcarbazepine.Neuroscience bulletin · 2020Article
- Challenges and Opportunities for Therapeutics Targeting the Voltage-Gated Sodium Channel Isoform NaJournal of medicinal chemistry · 2019Review
- Insensitivity to Pain upon Adult-Onset Deletion of Nav1.7 or Its Blockade with Selective Inhibitors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- DRG Voltage-Gated Sodium Channel 1.7 Is Upregulated in Paclitaxel-Induced Neuropathy in Rats and in Humans with Neuropathic Pain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Modulation of Ion Channels in the Superior Cervical Ganglion Neurons by Myocardial Ischemia and Fluvastatin Treatment.Frontiers in physiology · 2018Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundVoltage-gated sodium channel Nav1.7 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 Nav1.7, cause congenital insensitivity to pain (CIP) accompanied by anosmia. Global knock-out of Nav1.7 in mice is neonatal lethal reportedly from starvation, suggesting anosmia. These findings led us to hypothesize that Nav1.7 is the main sodium channel in the peripheral olfactory sensory neurons (OSN, also known as olfactory receptor neurons).
methodsWe used multiplex PCR-restriction enzyme polymorphism, in situ hybridization and immunohistochemistry to determine the identity of sodium channels in rodent OSNs.
resultsWe show here that Nav1.7 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 Nav1.7 transcripts are present in rat OSNs. Immunostaining of Nav1.7 and Nav1.6 channels in rat shows a complementary accumulation pattern with Nav1.7 in peripheral presynaptic OSN axons, and Nav1.6 primarily in postsynaptic cells and their dendrites in the glomeruli of the olfactory bulb within the central nervous system.
conclusionsOur data show that Nav1.7 is the dominant sodium channel in rat and mouse OSN, and may explain anosmia in Nav1.7 null mouse and patients with Nav1.7-related CIP.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.