Роль мутаций потенциалзависимых натриевых каналов в патогенезе нейропатической боли
Аннотация
Многие подтипы натриевых каналов локализуются в клетках периферической нервной системы и играют важную роль в формировании потенциала действия и возбудимости периферической нервной системы. Набор этих каналов важен для получения ощущения любого типа боли. Четыре изоформы натриевых каналов Na+ 1.3, 1.7, 1.8 и 1.9 могут быть вовлечены в патогенез нейропатической боли. Последние генетические исследования человека и трансгенных животных показывают, что натриевые каналы связаны с различными типами боли и могут являться мишенями для терапевтического воздействия, в том числе при нейропатической боли.
Об авторах
М. М. Петрова
Красноярский государственный медицинский университет им. проф. В.Ф. Войно-Ясенецкого
Россия
Россия
Е. А. Пронина
Красноярский государственный медицинский университет им. проф. В.Ф. Войно-Ясенецкого
Россия
Россия
Н. А. Шнайдер
Красноярский государственный медицинский университет им. проф. В.Ф. Войно-Ясенецкого
Россия
Россия
Д. В. Дмитренко
Красноярский государственный медицинский университет им. проф. В.Ф. Войно-Ясенецкого
Россия
Россия
М. В. Строганова
Красноярский государственный медицинский университет им. проф. В.Ф. Войно-Ясенецкого
Россия
Россия
О. П. Боброва
Красноярский государственный медицинский университет им. проф. В.Ф. Войно-Ясенецкого
Россия
Россия
Список литературы
1. Димитриев ДА, Сапёрова ЕВ. Электрофизиология кардиомиоцита: учеб. Пособие. Чебоксары:Чуваш. гос. пед. ун-т; 2009. 102 с.
2. Салмина АБ, Шнайдер НА, Михуткина СВ Современные представления об ионных каналах и каналопатиях (обзор литературы). Сибирское медицинское обозрение. 2005;(1):75-78.
3. Benarroch EE. Sodium channels and pain. Neurology 2007;68(3):233-6. 10.1212/01.wnl.0000252951.48745.a1
4. Devor M Sodium channels and mechanisms of neuropathic pain. J Pain. 2006; 7:S3-S12. DOI:10.1016/j.jpain.2005.09.006
5. Liu M, Wood JN The roles of sodium channels in nociception: implications for mechanisms of neuropathic pain. Pain Med. 2011 Jul;12 Suppl 3:S93-9. doi: 10.1111/j.1526-4637.2011.01158.x
6. Misawa S Pathophysiology of neuropathic pain: Na+ channel and hyperexcitability of primary afferents Brain Nerve. 2012 Nov;64(11):1249-53. PMID:23131735
7. Shou WT, Zhang SH, Chen Z Role of voltage-sodium channels in neuropathic pain. Zhejiang Da Xue Xue Bao Yi Xue Ban. 2011 Mar;40(2):217-21. PMID:21488221
8. Бокерия ОЛ, Ахобеков АА Ионные каналы и их роль в развитии нарушений ритма сердца. Анналы аритмологии. 2014;(3):176-184. Bockeria OL, Akhobekov AA. Ion channels and their role in the development of arrhythmias. Annaly aritmologii. 2014; 11(3): 176-184. doi:10.15275/annaritmol.2014.3.6
9. Дмитренко ДВ, Шнайдер НА, Мартынова ГП и др. Мутации натриевых каналов как генетический предиктор фебрильных приступов у детей Современные проблемы науки и образования. 2015;(5). Dmitrenko DV, Shnayder NA, Martynova G.P. et al. Sodium channel mutations as genetics predictors of febrile seizures in children. Problems of Modern Science and Education. 2015;(5). http://www.science-education.ru/ru/article/view?id=22774
10. Wood JN, Boorman JP, Okuse K, Baker MD. Voltage-gated sodium channels and pain pathways. J Neurobiol 2004;61(1):55-71. doi:10.1002/neu.20094
11. Minett MS, Nassar MA, Clark AK, et al. Distinct Nav1.7-dependent pain sensations require different sets of sensory and sympathetic neurons Nat Commun. 2012 April 24; 3:791. DOI:10.1038/ncomms1795
12. Black JA, Liu S, Tanaka M, et al. Changes in the expression of tetrodotoxinsensitive sodium channels within dorsal root ganglia neurons in inflammatory pain. Pain. 2004; 108:237-247. doi:10.1016/j.pain.2003.12.035
13. Nassar MA, Stirling LC, Forlani G, et al. Nociceptorspecific gene deletion reveals a major role for Nav1.7 (PN1) in acute and inflammatory pain. Proc Natl Acad Sci U S A. 2004; 101:12706-12711. doi: 10.1073/pnas.0404915101
14. Chattopadhyay M, Mata M, Fink DJ. Vector-mediated release of GABA attenuates pain-related behaviors and reduces Na(V)1.7 in DRG neurons. Eur J Pain. 2011 Oct;15(9):913-20. doi:10.1016/j.ejpain.2011.03.007
15. Chattopadhyay M, Mata M, Fink DJ Continuous delta opioid receptor activation reduces neuronal voltage gated sodium channel (NaV1.7) levels through activation of protein kinase C in painful diabetic neuropathy J Neurosci. 2008 June 25;28(26):6652-6658. doi: 10.1523/JNEUROSCI.5530-07.2008
16. Hong S, Morrow TJ, Paulson PE, et al. Early painful diabetic neuropathy is associated with differential changes in tetrodotoxin-sensitive and -resistant sodium channels in dorsal root ganglion neurons in the rat. J Biol Chem. 2004;279:29341-29350. doi: 10.1074/jbc.M404167200
17. Cox JJ, Reimann F, Nicholas AK, et al. An SCN9A channelopathy causes congenital inability to experience pain. Nature. 2006 Dec 14;444(7121):894-8. doi: 10.1038/nature05413
18. Choi JS, Dib-Hajj SD, Waxman SG. Inherited erythermalgia: limb pain from an S4 charge-neutral Na channelopathy. Neurology. 2006; 67:1563-1567. doi:10.1212/01.wnl.0000231514.33603.1e
19. Dib-Hajj SD, Rush AM, Cummins TR, et al. Gain-of-function mutation in Nav1.7 in familial erythromelalgia induces bursting of sensory neurons. Brain. 2005;128:1847-1854. doi:10.1093/brain/awh514
20. Yang Y, Wang Y, Li S, et al. Mutations in SCN9A, encoding a sodium channel alpha subunit, in patients with primary erythermalgia. J Med Genet. 2004; 41:171-174. PMCID:PMC1735695
21. Dib-Hajj SD, Yang Y, Waxman SG Genetics and molecular pathophysiology of Na(v)1.7-related pain syndromes. Adv Genet. 2008;63:85-110. doi: 10.1016/S0065-2660(08)01004-3
22. Fertleman CR, Baker MD, Parker KA, et al.SCN9A mutations in paroxysmal extreme pain disorder: allelic variants underlie distinct channel defects and phenotypes. Neuron. 2006; 52:767-774 doi:10.1016/j.neuron.2006.10.006
23. Dib-Hajj SD, Black JA, Waxman SC. Voltage-gated sodium cannels: therapeutic targets for pain. Pain Med. 2009;10:1260-1269. doi: 10.1111/j.1526-4637.2009.00719.x
24. Orstavik K., Jorum E. Microneurographic findings of relevance to pain in patients with erythromelalgia and patients with diabetic neuropathy. Neurosci Lett. 2010;470:108-114. doi:10.1016/j.neulet.2009.05.061
25. Orstavik K., Weidner C., Schmidt R. et al. Pathological C-fibres in patients with a chronic painful condition. Brain. 2003;126:567-578. PMID:12566278
26. Слободин ТН. Патогенез и современные подходы к лечению хронической боли Украiнський вiсник психоневрологii. 2012;20(73):106-113.
27. Tang Z, Chen Z, Tang B, Jiang H Primary erythromelalgia: a review. Orphanet J Rare Dis. 2015 Sep 30;10:127. doi: 10.1186/s13023-015-0347-1. doi:10.1186/s13023-015-0347-1
28. Faber CG, Hoeijmakers JG, Ahn HS et al. Gain of function Na(V)1.7 mutations in idiopathic small fiber neuropathy. Ann Neurol 2012; 71: 26-39. doi: 10.1002/ana.22485
29. Hoeijmakers JG, Merkies IS, Gerrits MM, et al. Genetic aspects of sodium channelopathy in small fiber neuropathy. Clin Genet. 2012 Oct;82(4):351-8. doi: 10.1111/j.1399-0004.2012.01937.x
30. Reimann F, Cox JJ, Belfer I et al. Pain perception is altered by a nucleotide polymorphism in SCN9A. Proc Natl Acad Sci U S A 2010; 107: 5148-5153. doi:10.1073/pnas.0913181107
31. Valdes AM, Arden NK, Vaughn FL et al. Role of the Nav1.7 R1150Wamino acid change in susceptibility to symptomatic knee osteoarthritis and multiple regional pain. Arthritis Care Res (Hoboken) 2011; 63: 440-444. doi:10.1002/acr.20375
32. Holliday KL, Thomson W, Neogi T, et al. The non-synonymous SNP, R1150W, in SCN9A is not associated with chronic widespread pain susceptibility. Mol Pain. 2012 Sep 24;8:72. doi: 10.1186/1744-8069-8-72.
33. Vargas-Alarcon G, Alvarez-Leon E, Fragoso JM, et al. A SCN9A gene-encoded dorsal root ganglia sodium channel polymorphism associated with severe fibromyalgia. BMC Musculoskelet Disord. 2012 Feb 20;13:23. doi: 10.1186/1471-2474-13-23.
34. Li QS, Cheng P, Favis R, et al. SCN9A Variants May Implicated in Neuropathic Pain Associated With Diabetic Peripheral Neuropathy andPain Severity. Clin J Pain. 2015 Nov;31(11):976-82. doi: 10.1097/AJP.0000000000000205.
35. Duan G, Guo S, Zhang Y et al. The Effect of SCN9A Variation on Basal Pain Sensitivity in the General Population: An Experimental Study in Young Women. J Pain. 2015 Oct;16(10):971-80. doi: 10.1016/j.jpain.2015.06.011.
36. Zhang Q, Chibalina MV, Bengtsson M, et al. Na+ current properties in islet a- and b-cells reflect cell-specific Scn3a and Scn9a expression J Physiol. 2014 November 1;592(Pt 21): 4677-4696. doi:10.1113/jphysiol.2014.274209
37. Shields SD, Ahn HS, Yang Y, et al. Nav1.8 expression is not restricted to nociceptors in mouse peripheral nervous system. Pain. 2012 Oct;153(10):2017-30. doi: 10.1016/j.pain.2012.04.022.
38. Renganathan M, Cummins TR, Waxman SG Contribution of Na(v)1.8 sodium channels to action potential electrogenesis in DRG neurons. J Neurophysiol. 2001 Aug; 86(2):629-40. PMID:11495938
39. Rush AM, Dib-Hajj SD, Liu S, et al. A single sodium channel mutation produces hyper- or hypoexcitability in different types of neurons. Proc Natl Acad Sci U S A. 2006 May 23; 103(21):8245-50. doi: 10.1073/pnas.0602813103
40. Abrahamsen B, Zhao J, Asante CO, et al. The cell and molecular basis of mechanical, cold, and inflammatory pain. Science 2008;321(5889):702-5. doi:10.1126/science.1156916
41. Zimmermann K, Leffler A, Babes A, et al. Sensory neuron sodium channel Nav1.8 is essential for pain at low temperatures. Nature. 2007 Jun 14; 447(7146):855-8. doi:10.1038/nature05880
42. Akopian AN, Souslova V, England S, et al. The tetrodotoxin-resistant sodium channel SNS has a specialized function in pain pathways. Nat Neurosci 1999;2(6):541-8. doi:10.1038/9195
43. Laird JM, Souslova V, Wood JN, Cervero F. Deficits in visceral pain and referred hyperalgesia in Nav1.8 (SNS/PN3)-null mice. J Neurosci 2002;22(19):8352-6. PMID:12351708
44. Lai J, Gold MS, Kim CS, et al. Inhibition of neuropathic pain by decreased expression of the tetrodotoxin-resistant sodium channel, NaV1.8. Pain 2002;95(1-2):143-52. PMID:11790477
45. Roza C, Laird JM, Souslova V, et al. 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(Pt:921-6. doi:10.1113/jphysiol.2003.046110
46. Faber CG, Lauria G, Merkies IS, et al. Gain-of-function Nav1.8 mutations in painful neuropathy. Proc Natl Acad Sci U S A. 2012 Nov 20;109(47):19444-9. doi: 10.1073/pnas.1216080109
47. Duan G, Han C, Wang Q et al. A SCN10A SNP biases human pain sensitivity. Mol Pain. 2016 Sep 2;12 pii: 1744806916666083 doi:10.1177/1744806916666083
48. Rugiero F, Mistry M, Sage D, et al. Selective expression of a persistent tetrodotoxin-resistant Na+ current and NaV1.9 subunit in myenteric sensory neurons. J Neurosci. 2003 Apr 1; 23(7):2715-25. PMID:12684457
49. Fang X, Djouhri L, McMullan S, et al. Intense isolectin-B4 binding in rat dorsal root ganglion neurons distinguishes C-fiber nociceptors with broad action potentials and high Nav1.9 expression. J Neurosci. 2006 Jul 5; 26(27):7281-92. doi: 10.1523/JNEUROSCI.1072-06.2006
50. Padilla F, Couble ML, Coste B, et al. Expression and localization of the Nav1.9 sodium channel in enteric neurons and in trigeminal sensory endings: implication for intestinal reflex function and orofacial pain. Mol Cell Neurosci. 2007 May; 35(1):138-52. doi:10.1016/j.mcn.2007.02.008
51. Dib-Hajj SD, Tyrrell L, Black JA, Waxman SG NaN, a novel voltage-gated Na channel, is expressed preferentially in peripheral sensory neurons and down-regulated after axotomy. Proc Natl Acad Sci U S A. 1998 Jul 21; 95(15):8963-8. PMCID:PMC21185
52. Ostman JA, Nassar MA, Wood JN, Baker MD. GTP up-regulated persistent Na+ current and enhanced nociceptor excitability require NaV1.9. J Physiol 2008;586(4):1077-87. doi:10.1113/jphysiol.2007.147942
53. Maingret F, Coste B, Padilla F, et al. Inflammatory mediators increase Nav1.9 current and excitability in nociceptors through a coincident detection mechanism. J Gen Physiol. 2008;131(3):211-25. doi:10.1085/jgp.200709935
54. Ritter AM, Martin WJ, Thorneloe KS. The voltage-gated sodium channel Nav1.9 is required for inflammation-based urinary bladder dysfunction. Neurosci Lett. 2009;452(1):28-32 doi:10.1016/j.neulet.2008.12.051
55. Leo S, D’Hooge R, Meert T. Exploring the role of nociceptor-specific sodium channels in pain transmission using Nav1.8 and Nav1.9 knockout mice. Behav Brain Res. 2010;208(1):149-57. doi: 10.1016/j.bbr.2009.11.023
56. Huang J, Han C, Estacion M, et al. Gain-of-function mutations in sodium channel Na(v)1.9 in painful neuropathy Brain. 2014 Jun;137(Pt 6):1627-42. doi:10.1093/brain/awu079
57. Han C, Yang Y, de Greef BTA et al. The Domain II S4-S5 Linker in Nav1.9: A Missense Mutation Enhances Activation, Impairs Fast Inactivation, and Produces Human Painful Neuropathy. Neuromolecular Med. 2015 Jun;17(2):158-69 doi: 10.1007/s12017-015-8347-9
58. Zhang XY, Wen J, Yang W et al. Gain of-Function mutations in SCN11A cause familial episodic pain. Am J Hum Genet 2013;93:957-66. doi: 10.1016/j.ajhg.2013.09.016
59. Spillane J, Kullmann, DM, Hanna MG. Genetic neurological channelopathies: molecular genetics and clinical phenotypes. J Neurol Neurosurg Psychiatry. 2016 Jan;87(1):37-48. doi:10.1136/jnnp-2015-311233
Рецензия
Для цитирования:
Петрова М.М., Пронина Е.А., Шнайдер Н.А., Дмитренко Д.В., Строганова М.В., Боброва О.П. Роль мутаций потенциалзависимых натриевых каналов в патогенезе нейропатической боли. Медицинская генетика. 2017;16(1):3-10.
For citation:
Petrova M.M., Pronina E.A., Shnayder N.A., Dmytrenko D.V., Stroganova M.V., Bobrova O.P. The roles of voltage-gated sodium channels mutations in mechanisms of neuropathic pain. Medical Genetics. 2017;16(1):3-10. (In Russ.)
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