Gene Symbol: Scn10a
Description: sodium channel, voltage-gated, type X, alpha
Alias: Nav1.8, PN3, SNS, sodium channel protein type 10 subunit alpha, peripheral nerve sodium channel 3, sensory neuron sodium channel, sodium channel protein type X subunit alpha, voltage gated sodium channel, voltage-gated sodium channel Nav1.8 variant a, voltage-gated sodium channel Nav1.8 variant b, voltage-gated sodium channel subunit alpha Nav1.8
Species: mouse
Products:     Scn10a

Top Publications

  1. Eijkelkamp N, Linley J, Torres J, Bee L, Dickenson A, Gringhuis M, et al. A role for Piezo2 in EPAC1-dependent mechanical allodynia. Nat Commun. 2013;4:1682 pubmed publisher
    ..These data indicate that the Epac1-Piezo2 axis has a role in the development of mechanical allodynia during neuropathic pain. ..
  2. Lagerström M, Rogoz K, Abrahamsen B, Lind A, Olund C, Smith C, et al. A sensory subpopulation depends on vesicular glutamate transporter 2 for mechanical pain, and together with substance P, inflammatory pain. Proc Natl Acad Sci U S A. 2011;108:5789-94 pubmed publisher
    ..These data define sets of primary afferents associated with specific modalities and provide useful genetic tools with which to analyze the pathways that are activated by functionally distinct neuronal populations and transmitters. ..
  3. Raouf R, Rugiero F, Kiesewetter H, Hatch R, Hummler E, Nassar M, et al. Sodium channels and mammalian sensory mechanotransduction. Mol Pain. 2012;8:21 pubmed publisher
    ..DEG/ENaC sodium channels are not mechanosensors in mouse sensory neurons. ..
  4. Eijkelkamp N, Wang H, Garza Carbajal A, Willemen H, Zwartkruis F, Wood J, et al. Low nociceptor GRK2 prolongs prostaglandin E2 hyperalgesia via biased cAMP signaling to Epac/Rap1, protein kinase Cepsilon, and MEK/ERK. J Neurosci. 2010;30:12806-15 pubmed publisher
    ..8+ nociceptors (SNS-GRK2+/- mice)...
  5. Chen X, Pang R, Shen K, Zimmermann M, Xin W, Li Y, et al. TNF-? enhances the currents of voltage gated sodium channels in uninjured dorsal root ganglion neurons following motor nerve injury. Exp Neurol. 2011;227:279-86 pubmed publisher
    ..These data suggest that the increase in sodium currents in uninjured DRG neurons following nerve injury might be mediated by over-production of TNF-?. ..
  6. Vetter I, Touska F, Hess A, Hinsbey R, Sattler S, Lampert A, et al. Ciguatoxins activate specific cold pain pathways to elicit burning pain from cooling. EMBO J. 2012;31:3795-808 pubmed publisher
  7. Gaveriaux Ruff C, Nozaki C, Nadal X, Hever X, Weibel R, Matifas A, et al. Genetic ablation of delta opioid receptors in nociceptive sensory neurons increases chronic pain and abolishes opioid analgesia. Pain. 2011;152:1238-48 pubmed publisher
    ..The conditional knockout of delta-opioid receptor in primary afferent Na(V)1.8 neurons augmented mechanical allodynia in persistent pain models and abolished delta opioid analgesia in these models. ..
  8. Gautron L, Sakata I, Udit S, Zigman J, Wood J, Elmquist J. Genetic tracing of Nav1.8-expressing vagal afferents in the mouse. J Comp Neurol. 2011;519:3085-101 pubmed publisher
    ..8-expressing vagal neurons in gastrointestinal functions. ..
  9. Stirling L, Forlani G, Baker M, Wood J, Matthews E, Dickenson A, et al. Nociceptor-specific gene deletion using heterozygous NaV1.8-Cre recombinase mice. Pain. 2005;113:27-36 pubmed
    ..These data demonstrate that the heterozygous NaV1.8-Cre mouse line is a useful tool to analyse the effects of deleting floxed genes on pain behaviour. ..

More Information


  1. Nassar M, Levato A, Stirling L, Wood J. Neuropathic pain develops normally in mice lacking both Na(v)1.7 and Na(v)1.8. Mol Pain. 2005;1:24 pubmed
    Two voltage gated sodium channel alpha-subunits, Nav1.7 and Nav1.8, are expressed at high levels in nociceptor terminals and have been implicated in the development of inflammatory pain...
  2. Lagerström M, Rogoz K, Abrahamsen B, Persson E, Reinius B, Nordenankar K, et al. VGLUT2-dependent sensory neurons in the TRPV1 population regulate pain and itch. Neuron. 2010;68:529-42 pubmed publisher
    ..This study establishes that VGLUT2 is a major player in TRPV1 thermal nociception and also serves to regulate a normal itch response. ..
  3. Patrick Harty T, Waxman S. Inactivation properties of sodium channel Nav1.8 maintain action potential amplitude in small DRG neurons in the context of depolarization. Mol Pain. 2007;3:12 pubmed
    ..We conclude that the presence of Nav1.8 allows AP amplitude to be maintained in DRG neurons and their centrally projecting axons even when depolarized within the dorsal horn. ..
  4. Nassar M, Stirling L, Forlani G, Baker M, Matthews E, Dickenson A, et al. Nociceptor-specific gene deletion reveals a major role for Nav1.7 (PN1) in acute and inflammatory pain. Proc Natl Acad Sci U S A. 2004;101:12706-11 pubmed
    ..7 in inflammatory pain. Nociceptor-specific gene ablation should prove useful in understanding the role of other broadly expressed genes in pain pathways. ..
  5. Shields S, Ahn H, Yang Y, Han C, Seal R, Wood J, et al. Nav1.8 expression is not restricted to nociceptors in mouse peripheral nervous system. Pain. 2012;153:2017-30 pubmed publisher
    ..Our results indicate that Na(v)1.8 underlies electrical activity of sensory neurons subserving multiple functional modalities, and call for cautious interpretation of the phenotypes of Na(v)1.8-Cre-driven conditional knockout mice. ..
  6. Akopian A, Souslova V, England S, Okuse K, Ogata N, Ure J, et al. The tetrodotoxin-resistant sodium channel SNS has a specialized function in pain pathways. Nat Neurosci. 1999;2:541-8 pubmed
    ..Here we examined the role of the sensory-neuron-specific (SNS) TTX-resistant sodium channel alpha subunit in nociception and pain by constructing sns-null mutant mice...
  7. Shields S, Cheng X, Gasser A, Saab C, Tyrrell L, Eastman E, et al. A channelopathy contributes to cerebellar dysfunction in a model of multiple sclerosis. Ann Neurol. 2012;71:186-94 pubmed publisher
    ..8-selective blocker. Our results add to the evidence that a channelopathy contributes to cerebellar dysfunction in MS. Our data suggest that Nav1.8-specific blockers, when available for humans, merit study in MS. ..
  8. Minett M, Falk S, Santana Varela S, Bogdanov Y, Nassar M, Heegaard A, et al. Pain without nociceptors? Nav1.7-independent pain mechanisms. Cell Rep. 2014;6:301-12 pubmed publisher
    ..8-positive nociceptors. Thus, similar pain phenotypes arise through distinct cellular and molecular mechanisms. Therefore, rational analgesic drug therapy requires patient stratification in terms of mechanisms and not just phenotype. ..
  9. Zhao J, Seereeram A, Nassar M, Levato A, Pezet S, Hathaway G, et al. Nociceptor-derived brain-derived neurotrophic factor regulates acute and inflammatory but not neuropathic pain. Mol Cell Neurosci. 2006;31:539-48 pubmed
    ..Nociceptor-derived BDNF thus plays an important role in regulating inflammatory pain thresholds and secondary hyperalgesia, but BDNF released only from nociceptors plays no role in the development of neuropathic pain. ..
  10. Kerr B, Souslova V, McMahon S, Wood J. A role for the TTX-resistant sodium channel Nav 1.8 in NGF-induced hyperalgesia, but not neuropathic pain. Neuroreport. 2001;12:3077-80 pubmed
    ..Neuropathic pain behaviours were unchanged in Nav 1.8 -/- mice indicating that this channel is not involved in the alteration of sensory thresholds following peripheral nerve injury. ..
  11. Abrahamsen B, Zhao J, Asante C, Cendan C, Marsh S, Martinez Barbera J, et al. The cell and molecular basis of mechanical, cold, and inflammatory pain. Science. 2008;321:702-5 pubmed publisher
    ..These data demonstrate that Na(v)1.8-expressing neurons are essential for mechanical, cold, and inflammatory pain but not for neuropathic pain or heat sensing. ..
  12. Zimmermann K, Leffler A, Babes A, Cendan C, Carr R, Kobayashi J, et al. Sensory neuron sodium channel Nav1.8 is essential for pain at low temperatures. Nature. 2007;447:855-8 pubmed
    ..Our data present strong evidence for a specialized role of Na(v)1.8 in nociceptors as the critical molecule for the perception of cold pain and pain in the cold. ..
  13. Nassar M, Baker M, Levato A, Ingram R, Mallucci G, McMahon S, et al. Nerve injury induces robust allodynia and ectopic discharges in Nav1.3 null mutant mice. Mol Pain. 2006;2:33 pubmed
    ..3 in global knock-out mice. Our data demonstrate that Nav1.3 is neither necessary nor sufficient for the development of nerve-injury related pain. ..
  14. Puhl H, Ikeda S. Identification of the sensory neuron specific regulatory region for the mouse gene encoding the voltage-gated sodium channel NaV1.8. J Neurochem. 2008;106:1209-24 pubmed publisher
    ..The type one VGSC family includes the tetrodotoxin insensitive sodium channel, Na(V)1.8, encoded by the Scn10a gene. Na(V)1...
  15. Minett M, Nassar M, Clark A, Passmore G, Dickenson A, Wang F, et al. Distinct Nav1.7-dependent pain sensations require different sets of sensory and sympathetic neurons. Nat Commun. 2012;3:791 pubmed publisher
    ..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. ..
  16. Chen C, Broom D, Liu Y, de Nooij J, Li Z, Cen C, et al. Runx1 determines nociceptive sensory neuron phenotype and is required for thermal and neuropathic pain. Neuron. 2006;49:365-77 pubmed
    ..Moreover, mice lacking Runx1 exhibit specific defects in thermal and neuropathic pain. Thus, Runx1 coordinates the phenotype of a large cohort of nociceptors, a finding with implications for pain therapy. ..
  17. Roza C, Laird J, Souslova V, Wood J, Cervero F. The tetrodotoxin-resistant Na+ channel Nav1.8 is essential for the expression of spontaneous activity in damaged sensory axons of mice. J Physiol. 2003;550:921-6 pubmed
    ..8 null neuromas (51 and 46%, respectively). We conclude that Nav1.8 is essential for the expression of spontaneous activity in damaged sensory axons, and may also contribute to the development of ectopic mechanosensitivity. ..
  18. Renganathan M, Cummins T, Waxman S. Contribution of Na(v)1.8 sodium channels to action potential electrogenesis in DRG neurons. J Neurophysiol. 2001;86:629-40 pubmed
    ..8 (alpha-SNS) in action potential electrogenesis...
  19. Eijkelkamp N, Heijnen C, Willemen H, Deumens R, Joosten E, Kleibeuker W, et al. GRK2: a novel cell-specific regulator of severity and duration of inflammatory pain. J Neurosci. 2010;30:2138-49 pubmed publisher
    ..Thus, we identified completely novel cell-specific roles of GRK2 in regulating acute and chronic inflammatory hyperalgesia. ..
  20. Shields S, Butt R, Dib Hajj S, Waxman S. Oral administration of PF-01247324, a subtype-selective Nav1.8 blocker, reverses cerebellar deficits in a mouse model of multiple sclerosis. PLoS ONE. 2015;10:e0119067 pubmed publisher
    ..These preclinical proof-of-concept data suggest that PF-01247324, its derivatives, or other Nav1.8-selective blockers merit further study for providing symptomatic therapy for cerebellar dysfunction in MS and related disorders. ..
  21. Rush A, Craner M, Kageyama T, Dib Hajj S, Waxman S, Ranscht B. Contactin regulates the current density and axonal expression of tetrodotoxin-resistant but not tetrodotoxin-sensitive sodium channels in DRG neurons. Eur J Neurosci. 2005;22:39-49 pubmed
  22. Moldovan M, Rosberg M, Alvarez S, Klein D, Martini R, Krarup C. Aging-associated changes in motor axon voltage-gated Na(+) channel function in mice. Neurobiol Aging. 2016;39:128-39 pubmed publisher
    ..8 null mice, and they were counteracted in WT mice by a Nav1.8 blocker. Our data suggest that alteration in voltage-gated Na(+) channel isoform expression contributes to changes in motor axon function during aging. ..
  23. Kozak C, Sangameswaran L. Genetic mapping of the peripheral sodium channel genes, Scn9a and Scn10a, in the mouse. Mamm Genome. 1996;7:787-8 pubmed
  24. Ebbinghaus M, Natura G, Segond von Banchet G, Hensellek S, Böttcher M, Hoffmann B, et al. Interleukin-17A is involved in mechanical hyperalgesia but not in the severity of murine antigen-induced arthritis. Sci Rep. 2017;7:10334 pubmed publisher
    ..Furthermore, in isolated DRG neurones most IL-17 isoforms increased tetrodotoxin- (TTX-) resistant sodium currents which indicate a role of IL-17 members in inflammation-evoked sensitization of sensory nociceptive neurones. ..
  25. Laird J, Souslova V, Wood J, Cervero F. Deficits in visceral pain and referred hyperalgesia in Nav1.8 (SNS/PN3)-null mice. J Neurosci. 2002;22:8352-6 pubmed
    ..We conclude that there is an essential role for Nav1.8 in mediating spontaneous activity in sensitized nociceptors. ..
  26. Zhao Z, Liu X, Jeffry J, Karunarathne W, Li J, Munanairi A, et al. Descending control of itch transmission by the serotonergic system via 5-HT1A-facilitated GRP-GRPR signaling. Neuron. 2014;84:821-34 pubmed publisher
    ..Thus, our studies demonstrate that the descending 5-HT system facilitates GRP-GRPR signaling via 5-HT1A to augment itch-specific outputs, and a disruption of crosstalk between 5-HT1A and GRPR may be a useful antipruritic strategy. ..
  27. van den Boogaard M, Smemo S, Burnicka Turek O, Arnolds D, van de Werken H, Klous P, et al. A common genetic variant within SCN10A modulates cardiac SCN5A expression. J Clin Invest. 2014;124:1844-52 pubmed publisher
    Variants in SCN10A, which encodes a voltage-gated sodium channel, are associated with alterations of cardiac conduction parameters and the cardiac rhythm disorder Brugada syndrome; however, it is unclear how SCN10A variants promote ..
  28. Fricker F, Zhu N, Tsantoulas C, Abrahamsen B, Nassar M, Thakur M, et al. Sensory axon-derived neuregulin-1 is required for axoglial signaling and normal sensory function but not for long-term axon maintenance. J Neurosci. 2009;29:7667-78 pubmed publisher
    ..Sensory neuronal survival and axonal maintenance, however, are not dependent on axon-derived neuregulin-1 signaling in adulthood. ..
  29. Weibel R, Reiss D, Karchewski L, Gardon O, Matifas A, Filliol D, et al. Mu opioid receptors on primary afferent nav1.8 neurons contribute to opiate-induced analgesia: insight from conditional knockout mice. PLoS ONE. 2013;8:e74706 pubmed publisher
    ..Previous pharmacology suggests that peripheral opiates may be clinically useful, and our data further demonstrate that Nav1.8 neuron-associated mu opioid receptors are feasible targets to alleviate some forms of persistent pain. ..
  30. Gallo R, Kim K, Bernfield M, Kozak C, Zanetti M, Merluzzi L, et al. Identification of CRAMP, a cathelin-related antimicrobial peptide expressed in the embryonic and adult mouse. J Biol Chem. 1997;272:13088-93 pubmed
    ..These data suggest that inflammatory cells in the mouse can use a nonoxidative mechanism for microbial killing and permit use of the mouse to study the role such peptides play in host defense and wound repair. ..
  31. Craner M, Kataoka Y, Lo A, Black J, Baker D, Waxman S. Temporal course of upregulation of Na(v)1.8 in Purkinje neurons parallels the progression of clinical deficit in experimental allergic encephalomyelitis. J Neuropathol Exp Neurol. 2003;62:968-75 pubmed
    ..8 expression. These results provide evidence that the expression of sodium channel Na(v)1.8 contributes to the development of clinical deficits in an in vivo model of neuroinflammatory disease...
  32. Tang H, Shiba E, Li Y, Morioka N, Zheng T, Ogata N, et al. Involvement of voltage-gated sodium channel Na(v)1.8 in the regulation of the release and synthesis of substance P in adult mouse dorsal root ganglion neurons. J Pharmacol Sci. 2008;108:190-7 pubmed
    ..8 knock-out mice. These findings suggest that Na(v)1.8 is involved in the regulation of the release and synthesis of SP in the DRG neurons of wild-type mice. ..
  33. Hillsley K, Lin J, Stanisz A, Grundy D, Aerssens J, Peeters P, et al. Dissecting the role of sodium currents in visceral sensory neurons in a model of chronic hyperexcitability using Nav1.8 and Nav1.9 null mice. J Physiol. 2006;576:257-67 pubmed
    ..8(-/-) mice, but is still present in Na(v)1.9(-/-) mice. It is not clear whether hyperexcitability is due to a change in the function of Na(v)1.8 channels or a change in the number of Na(v)1.8 channels. ..
  34. Montersino A, Brachet A, Ferracci G, Fache M, Angles d Ortoli S, Liu W, et al. Tetrodotoxin-resistant voltage-gated sodium channel Nav 1.8 constitutively interacts with ankyrin G. J Neurochem. 2014;131:33-41 pubmed publisher
    ..The constitutive binding of Nav 1.8 with ankG could contribute to the pathological aspects of illnesses where Nav 1.8 is ectopically expressed in CNS neurons. ..
  35. Yu J, Fang Q, Lou G, Shou W, Yue J, Tang Y, et al. Histamine modulation of acute nociception involves regulation of Nav 1.8 in primary afferent neurons in mice. CNS Neurosci Ther. 2013;19:649-58 pubmed publisher
    ..The regulation of Nav 1.8 expression and the excitability of nociceptive primary afferent neurons may be involved in the underlying mechanisms. ..
  36. Fischer B, Ho C, Kuzin I, Bottaro A, O Leary M. Chronic exposure to tumor necrosis factor in vivo induces hyperalgesia, upregulates sodium channel gene expression and alters the cellular electrophysiology of dorsal root ganglion neurons. Neurosci Lett. 2017;653:195-201 pubmed publisher
    ..Together, these data suggest that increases in the expression of Nav1.8 channels, regulatory β1 subunits and TNFR1 contribute to increased nociceptor excitability and hyperalgesia in the TNFtg mice. ..
  37. Kerr N, Holmes F, Wynick D. Novel isoforms of the sodium channels Nav1.8 and Nav1.5 are produced by a conserved mechanism in mouse and rat. J Biol Chem. 2004;279:24826-33 pubmed
    ..1 kilobases of genomic DNA spanning exons 16-18 of Scn10a. A novel cDNA isoform was identified, designated Na(v)1...
  38. Yu Y, Barry D, Hao Y, Liu X, Chen Z. Molecular and neural basis of contagious itch behavior in mice. Science. 2017;355:1072-1076 pubmed publisher
    ..The findings may have implications for our understanding of neural circuits that control socially contagious behaviors. ..
  39. Persson A, Kim I, Zhao P, Estacion M, Black J, Waxman S. Sodium channels contribute to degeneration of dorsal root ganglion neurites induced by mitochondrial dysfunction in an in vitro model of axonal injury. J Neurosci. 2013;33:19250-61 pubmed publisher
  40. de Lartigue G, Ronveaux C, Raybould H. Deletion of leptin signaling in vagal afferent neurons results in hyperphagia and obesity. Mol Metab. 2014;3:595-607 pubmed publisher
    ..Crucially Nav1.8/LepR (l/fl) mice did not gain further weight in response to a high fat diet. We conclude that disruption of leptin signaling in VAN is sufficient and necessary to promote hyperphagia and obesity. ..
  41. Renganathan M, Cummins T, Hormuzdiar W, Waxman S. alpha-SNS produces the slow TTX-resistant sodium current in large cutaneous afferent DRG neurons. J Neurophysiol. 2000;84:710-8 pubmed
    In this study, we used sensory neuron specific (SNS) sodium channel gene knockout (-/-) mice to ask whether SNS sodium channel produces the slow Na(+) current ("slow") in large (>40 microm diam) cutaneous afferent dorsal root ganglion ..
  42. Smith B, Côté P, Tremblay F. Contribution of Nav1.8 sodium channels to retinal function. Neuroscience. 2017;340:279-290 pubmed publisher
    ..8 plays a role in modulating specific aspects of the retinal physiology and that SBACs are a fundamental cellular contributor to the OPs in mice, a clear demonstration of the dichotomy between ERG b-wave and OPs. ..
  43. Yang T, Atack T, Stroud D, Zhang W, Hall L, Roden D. Blocking Scn10a channels in heart reduces late sodium current and is antiarrhythmic. Circ Res. 2012;111:322-32 pubmed publisher
    Although the sodium channel locus SCN10A has been implicated by genome-wide association studies as a modulator of cardiac electrophysiology, the role of its gene product Nav1.8 as a modulator of cardiac ion currents is unknown...
  44. Hodgdon K, Hingtgen C, Nicol G. Dorsal root ganglia isolated from Nf1+/- mice exhibit increased levels of mRNA expression of voltage-dependent sodium channels. Neuroscience. 2012;206:237-44 pubmed publisher
  45. Isensee J, Krahé L, Moeller K, Pereira V, Sexton J, Sun X, et al. Synergistic regulation of serotonin and opioid signaling contributes to pain insensitivity in Nav1.7 knockout mice. Sci Signal. 2017;10: pubmed publisher
    ..7 controls the efficacy and balance of GPCR-mediated pro- and antinociceptive intracellular signaling, such that without Nav1.7, the balance is shifted toward antinociception, resulting in lifelong endogenous analgesia. ..
  46. Zhao J, Yuan G, Cendan C, Nassar M, Lagerström M, Kullander K, et al. Nociceptor-expressed ephrin-B2 regulates inflammatory and neuropathic pain. Mol Pain. 2010;6:77 pubmed publisher
    ..Presynaptic ephrin-B2 expression thus plays an important role in regulating inflammatory pain through the regulation of synaptic plasticity in the dorsal horn and is also involved in the pathogenesis of some types of neuropathic pain. ..
  47. Foulkes T, Nassar M, Lane T, Matthews E, Baker M, Gerke V, et al. Deletion of annexin 2 light chain p11 in nociceptors causes deficits in somatosensory coding and pain behavior. J Neurosci. 2006;26:10499-507 pubmed
    ..A significant deficit in neuropathic pain behavior was also apparent in the conditional-null mice. These results confirm an important role for p11 in nociceptor function. ..
  48. Emery E, Young G, Berrocoso E, Chen L, McNaughton P. HCN2 ion channels play a central role in inflammatory and neuropathic pain. Science. 2011;333:1462-6 pubmed publisher
    ..After a nerve lesion, these mice showed no neuropathic pain in response to thermal or mechanical stimuli. Neuropathic pain is therefore initiated by HCN2-driven action potential firing in Na(V)1.8-expressing nociceptors. ..
  49. Stroud D, Yang T, Bersell K, Kryshtal D, Nagao S, Shaffer C, et al. Contrasting Nav1.8 Activity in Scn10a-/- Ventricular Myocytes and the Intact Heart. J Am Heart Assoc. 2016;5: pubmed
    Genome-wide association studies have implicated variants in SCN10A, which encodes Nav1.8, as modulators of cardiac conduction. Follow-up work has indicated the SCN10A sequence includes an intronic enhancer for SCN5A...
  50. Lin S, Cheng Y, Banks R, Min M, Bewick G, Chen C. Evidence for the involvement of ASIC3 in sensory mechanotransduction in proprioceptors. Nat Commun. 2016;7:11460 pubmed publisher
    ..We conclude that, at least in mouse, ASIC3 is a molecular determinant contributing to dynamic mechanosensitivity in proprioceptors. ..
  51. Fong S, Lin H, Wu M, Chen C, Huang Y. CPEB3 Deficiency Elevates TRPV1 Expression in Dorsal Root Ganglia Neurons to Potentiate Thermosensation. PLoS ONE. 2016;11:e0148491 pubmed publisher
    ..CPEB3-regulated translation of TRPV1 RNA may play a role in fine-tuning thermal sensitivity of nociceptors. ..
  52. Blasius A, Dubin A, Petrus M, Lim B, Narezkina A, Criado J, et al. Hypermorphic mutation of the voltage-gated sodium channel encoding gene Scn10a causes a dramatic stimulus-dependent neurobehavioral phenotype. Proc Natl Acad Sci U S A. 2011;108:19413-8 pubmed publisher
    ..Sequence variants of human Na(v)1.8 have been linked to altered cardiac conduction. We identified an allele of Scn10a encoding the ?-subunit of Na(v)1.8 among mice homozygous for N-ethyl-N-nitrosourea-induced mutations...
  53. Ma Q, Fode C, Guillemot F, Anderson D. Neurogenin1 and neurogenin2 control two distinct waves of neurogenesis in developing dorsal root ganglia. Genes Dev. 1999;13:1717-28 pubmed
    ..These data reveal remarkable parallels in the roles of bHLH factors during neurogenesis in the DRG, and myogenesis in the neighboring myotome. ..
  54. Shields S, Cheng X, Uceyler N, Sommer C, Dib Hajj S, Waxman S. Sodium channel Na(v)1.7 is essential for lowering heat pain threshold after burn injury. J Neurosci. 2012;32:10819-32 pubmed publisher
    ..Our results offer insights into the molecular and cellular mechanisms of modality-specific pain signaling, and suggest Na(v)1.7-blocking drugs may be effective in burn patients. ..
  55. van den Boogaard M, Wong L, Tessadori F, Bakker M, Dreizehnter L, Wakker V, et al. Genetic variation in T-box binding element functionally affects SCN5A/SCN10A enhancer. J Clin Invest. 2012;122:2519-30 pubmed publisher
    ..genes repressed by TBX3, including the clustered sodium channel genes Scn5a, essential for cardiac function, and Scn10a. We identified 2 enhancers in the Scn5a/Scn10a locus, which were regulated by TBX3 and its family member and ..
  56. Schirmeyer J, Szafranski K, Leipold E, Mawrin C, Platzer M, Heinemann S. Exon 11 skipping of SCN10A coding for voltage-gated sodium channels in dorsal root ganglia. Channels (Austin). 2014;8:210-5 pubmed
    The voltage-gated sodium channel Na(V)1.8 (encoded by SCN10A) is predominantly expressed in dorsal root ganglia(DRG) and plays a critical role in pain perception...
  57. Ren A, Wang K, Zhang H, Liu A, Ma X, Liang Q, et al. ZBTB20 regulates nociception and pain sensation by modulating TRP channel expression in nociceptive sensory neurons. Nat Commun. 2014;5:4984 pubmed publisher
    ..Our findings point to ZBTB20 as a critical regulator of nociception and pain sensation by modulating TRP channels expression in nociceptors. ..
  58. Tsunozaki M, Lennertz R, Vilceanu D, Katta S, Stucky C, Bautista D. A 'toothache tree' alkylamide inhibits A? mechanonociceptors to alleviate mechanical pain. J Physiol. 2013;591:3325-40 pubmed publisher
    ..These results suggest that sanshool targets voltage-gated sodium channels on A? mechanosensory nociceptors to dampen excitability and thus induce 'fast pain' analgesia. ..
  59. Lolignier S, Bonnet C, Gaudioso C, Noël J, Ruel J, Amsalem M, et al. The Nav1.9 channel is a key determinant of cold pain sensation and cold allodynia. Cell Rep. 2015;11:1067-78 pubmed publisher
    ..We conclude that Nav1.9 acts as a subthreshold amplifier in cold-sensitive nociceptive neurons and is required for the perception of cold pain under normal and pathological conditions. ..
  60. Yuan X, Huang Y, Shah S, Wu H, Gautron L. Levels of Cocaine- and Amphetamine-Regulated Transcript in Vagal Afferents in the Mouse Are Unaltered in Response to Metabolic Challenges. Eneuro. 2016;3: pubmed
    ..Moreover, prepro-MCH mRNA was undetectable in the nodose ganglion of fasted mice. In summary, this study showed that the perikarya and central terminals of vagal afferents are invariably enriched in CART and devoid of MCH. ..
  61. Zhao J, Lee M, Momin A, Cendan C, Shepherd S, Baker M, et al. Small RNAs control sodium channel expression, nociceptor excitability, and pain thresholds. J Neurosci. 2010;30:10860-71 pubmed publisher
    ..MicroRNA microarray and deep sequencing identified known and novel nociceptor microRNAs in mouse Nav1.8+ sensory neurons that may regulate nociceptor gene expression. ..
  62. Souslova V, Fox M, Wood J, Akopian A. Cloning and characterization of a mouse sensory neuron tetrodotoxin-resistant voltage-gated sodium channel gene, Scn10a. Genomics. 1997;41:201-9 pubmed
    ..clones encoding a mouse 129/SV genomic library, we have determined the detailed structure of the mouse SNS gene (Scn10a), including the location of exon-intron boundaries and the nucleotide sequence of the exons...
  63. Schirmeyer J, Szafranski K, Leipold E, Mawrin C, Platzer M, Heinemann S. A subtle alternative splicing event of the Na(V)1.8 voltage-gated sodium channel is conserved in human, rat, and mouse. J Mol Neurosci. 2010;41:310-4 pubmed publisher
    The voltage-gated sodium channel subtype Na(V)1.8 (SCN10A) is exclusively expressed in dorsal root ganglia (DRG) and plays a critical role in pain perception...
  64. Han Q, Kim Y, Wang X, Liu D, Zhang Z, Bey A, et al. SHANK3 Deficiency Impairs Heat Hyperalgesia and TRPV1 Signaling in Primary Sensory Neurons. Neuron. 2016;92:1279-1293 pubmed publisher
    ..Finally, partial knockdown of SHANK3 expression in human DRG neurons abrogates TRPV1 function. Our findings reveal a peripheral mechanism of SHANK3, which may underlie pain deficits in SHANK3-related ASDs. ..
  65. Lin S, Steinhoff M, Ikoma A, Chang Y, Cheng Y, Chandra Kopparaju R, et al. Involvement of TRPV1 and TDAG8 in Pruriception Associated with Noxious Acidosis. J Invest Dermatol. 2017;137:170-178 pubmed publisher
    ..Thus, protons could evoke pruriception by acting on TDAG8 to regulate TRPV1 activation with its mechanism of future therapeutic relevance. ..
  66. Riol Blanco L, Ordovas Montanes J, Perro M, Naval E, Thiriot A, Alvarez D, et al. Nociceptive sensory neurons drive interleukin-23-mediated psoriasiform skin inflammation. Nature. 2014;510:157-61 pubmed publisher
    ..These findings indicate that TRPV1(+)Nav1.8(+) nociceptors, by interacting with DDCs, regulate the IL-23/IL-17 pathway and control cutaneous immune responses. ..
  67. Wu D, Chandra D, McMahon T, Wang D, Dadgar J, Kharazia V, et al. PKC? phosphorylation of the sodium channel NaV1.8 increases channel function and produces mechanical hyperalgesia in mice. J Clin Invest. 2012;122:1306-15 pubmed publisher
    ..Moreover, a specific PKC? activator peptide, ??RACK, produced mechanical hyperalgesia in wild-type mice but not in Scn10a-/- mice, which lack NaV1.8 channels. These studies demonstrate that NaV1...
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    ..These findings indicate that loss of thermal sensitivity in aging animals may result from a decreased level of TRPV1 and Nav1.8 and decreased trophic support that inhibits efficient transport of channel proteins to peripheral afferents. ..
  70. Klein A, Vyshnevska A, Hartke T, De Col R, Mankowski J, Turnquist B, et al. Sodium Channel Nav1.8 Underlies TTX-Resistant Axonal Action Potential Conduction in Somatosensory C-Fibers of Distal Cutaneous Nerves. J Neurosci. 2017;37:5204-5214 pubmed publisher
    ..8 (NaV1.8). The functional prominence of NaV1.8 within the axonal compartment immediately proximal to its termination may affect strategies targeting pain of peripheral origin. ..
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    ..Close communication between inexcitable glial cells and excitable neural cells thus appears to be the basis of the central control of salt homeostasis. ..
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    ..Failure to conduct behavioural tests at different anatomical locations, stimulus intensities, and at different points in the circadian cycle may lead to a pain behavioural phenotype being misinterpreted, or missed altogether. ..