ArticleNature communications2012
Distinct Nav1.7-dependent pain sensations require different sets of sensory and sympathetic neurons.
Article in Nature communications, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 158 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
158 citing papers in PubMed, 276 citations in OpenAlex.
- Safety and Efficacy of a Topical Sodium Channel Inhibitor (TV-45070) in Patients With Postherpetic Neuralgia (PHN): A Randomized, Controlled, Proof-of-Concept, Crossover Study, With a Subgroup Analysis of the Nav1.7 R1150W Genotype.The Clinical journal of pain · 2017Trial
- Behavioral genomics identifies Creld1 as a cross-modal regulator of somatosensation.Nature neuroscience · 2026Article
- Chasing the Wrong Door for 30 Years: Is Suzetrigine the Key to Selective Pain Relief?Medicina (Kaunas, Lithuania) · 2026Review
- Functional and molecular diversity of human C-fibers in pain modulation.Current opinion in supportive and palliative care · 2026Review
- Repurposing FDA-Approved Drugs as Nav1.7 Channel Modulators: An Integrated Structure-Based Virtual Screening and Molecular Dynamics Study.International journal of molecular sciences · 2026Article
- Targeting Supramolecular Active Complexes of NaAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Article
- Molecular determinant of low-voltage dependence of human NaNature communications · 2026Article
- Peripheral Nerve Transection Predominantly Drives Sympathetic Nerve Sprouting in Mouse Dorsal Root Ganglia.bioRxiv : the preprint server for biology · 2025Article
- Targeting sodium channels - challenges for acute pain and the leap to chronic pain.Nature reviews. Neurology · 2025Review
- Nociceptors use multiple neurotransmitters to drive pain.bioRxiv : the preprint server for biology · 2025Article
- Efficacy and safety of transcutaneous auricular vagus nerve stimulation plus pregabalin for radiotherapy-related neuropathic pain in patients with head and neck cancer (RELAX): a phase 2 randomised trial.EClinicalMedicine · 2025Article
- Sensory neuron-expressed FGF13 controls nociceptive signaling in diabetic neuropathy models.The Journal of clinical investigation · 2025Article
- Preclinical Animal Models to Investigate the Role of NaLife (Basel, Switzerland) · 2025Review
- Synergistic Inhibition of Nav1.7 and NCX1: A Novel Strategy for Treating Cancer-Induced Bone Pain by Modulating Pain Sensitization and Neuronal Inflammation.CNS neuroscience & therapeutics · 2025Article
- Article
- Electroacupuncture Regulates Sympathetic Nerve Through the NTSCNS neuroscience & therapeutics · 2025Article
- Optimizing Nav1.7-Targeted Analgesics: Revealing Off-Target Effects of Spider Venom-Derived Peptide Toxins and Engineering Strategies for Improvement.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Advancing Pain Understanding and Drug Discovery: Insights from Preclinical Models and Recent Research Findings.Pharmaceuticals (Basel, Switzerland) · 2024Review
- A Novel Antigen Design Strategy to Isolate Single-Domain Antibodies that Target Human Nav1.7 and Reduce Pain in Animal Models.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
98 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 5 institutions in 2 countries.
Funding
Abstract
Human acute and inflammatory pain requires the expression of voltage-gated sodium channel Nav1.7 but its significance for neuropathic pain is unknown. Here we show that Nav1.7 expression in different sets of mouse sensory and sympathetic neurons underlies distinct types of pain sensation. Ablating Nav1.7 gene (SCN9A) expression in all sensory neurons using Advillin-Cre abolishes mechanical pain, inflammatory pain and reflex withdrawal responses to heat. In contrast, heat-evoked pain is retained when SCN9A is deleted only in Nav1.8-positive nociceptors. Surprisingly, responses to the hotplate test, as well as neuropathic pain, are unaffected when SCN9A is deleted in all sensory neurons. However, deleting SCN9A in both sensory and sympathetic neurons abolishes these pain sensations and recapitulates the pain-free phenotype seen in humans with SCN9A loss-of-function mutations. These observations demonstrate an important role for Nav1.7 in sympathetic neurons in neuropathic pain, and provide possible insights into the mechanisms that underlie gain-of-function Nav1.7-dependent pain conditions.
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Registered trials
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.