ArticleMolecular pain2016
A SCN10A SNP biases human pain sensitivity.
Article in Molecular pain, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03164161 (The Relationship Between Saliva β-endorphins Levels, Sensitivity and Tolerance to Cold Pain and Perception of Pain in Oral Surgery Procedures in Adult Patients), which is not on this map. Cited by 34 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.
The Relationship Between Saliva β-endorphins Levels, Sensitivity and Tolerance to Cold Pain and Perception of Pain in Oral Surgery Procedures in Adult Patients
Who cites it
34 citing papers in PubMed, 55 citations in OpenAlex.
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- Targeting Supramolecular Active Complexes of NaAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Association between voltage-gated sodium channel gene polymorphisms and chronic oxaliplatin-induced peripheral neuropathy in Japanese patients with colorectal cancer.Journal of pharmaceutical health care and sciences · 2026Article
- Selective NaV1.8 Inhibition for Pain Management: Current Evidence and Future Potential of Suzetrigine.Current pain and headache reports · 2026Review
- Shaping the Action Potential in Dorsal Root and Trigeminal Ganglia Neurons: Relevance to Pain Mechanisms.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Review
- Targeting sodium channels - challenges for acute pain and the leap to chronic pain.Nature reviews. Neurology · 2025Review
- Inhibiting Nav1.8 for pain: Lessons from patients and from neurons.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Nav1.8 and Chronic Pain: From Laboratory Animals to Clinical Patients.Biomolecules · 2025Review
- Structural basis of inhibition of human NaNature communications · 2025Article
- Pain in idiopathic scoliosis not associated with known genetic variants for pain.Pain reports · 2025Article
- SCN10A gene polymorphism is associated with pain sensitivity and postoperative analgesic effects in patients undergoing gynecological laparoscopy.European journal of medical research · 2025Article
- Impact of SCN10A Polymorphism on Abdominal Pain Perception and Visceral Hypoalgesia in Crohn's Disease and Ulcerative Colitis.Clinical and translational gastroenterology · 2024Article
- Structural basis of inhibition of human NabioRxiv : the preprint server for biology · 2024Article
- Heterologous expression of the human wild-type and variant NaNeurogastroenterology and motility · 2024Article
- Insights into the voltage-gated sodium channel, NaFrontiers in pharmacology · 2024Review
- The role of nociceptive neurons in allergic rhinitis.Frontiers in immunology · 2024Review
- Peripheral temperature dysregulation associated with functionally altered NaPflugers Archiv : European journal of physiology · 2023Article
- Ectopic expression of Nav1.7 in spinal dorsal horn neurons induced by NGF contributes to neuropathic pain in a mouse spinal cord injury model.Frontiers in molecular neuroscience · 2023Article
- Article
- Potential therapeutic targets for the treatment of opioid abuse and pain.Advances in pharmacology (San Diego, Calif.) · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNav1.8 sodium channels, encoded by SCN10A, are preferentially expressed in nociceptive neurons and play an important role in human pain. Although rare gain-of-function variants in SCN10A have been identified in individuals with painful peripheral neuropathies, whether more common variants in SCN10A can have an effect at the channel level and at the dorsal root ganglion, neuronal level leading to a pain disorder or an altered normal pain threshold has not been determined.
resultsCandidate single nucleotide polymorphism association approach together with experimental pain testing in human subjects was used to explore possible common SCN10A missense variants that might affect human pain sensitivity. We demonstrated an association between rs6795970 (G > A; p.Ala1073Val) and higher thresholds for mechanical pain in a discovery cohort (496 subjects) and confirmed it in a larger replication cohort (1005 female subjects). Functional assessments showed that although the minor allele shifts channel activation by -4.3 mV, a proexcitatory attribute, it accelerates inactivation, an antiexcitatory attribute, with the net effect being reduced repetitive firing of dorsal root ganglion neurons, consistent with lower mechanical pain sensitivity.
conclusionsAt the association and mechanistic levels, the SCN10A single nucleotide polymorphism rs6795970 biases human pain sensitivity.
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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.