IR@PKUHSC  > 北京大学口腔医学院  > 牙周科
学科主题口腔医学
Involvement of trigeminal ganglionic Na(v)1.7 in hyperalgesia of inflamed temporomandibular joint is dependent on ERK1/2 phosphorylation of glial cells in rats
Bi, R-Y.1; Kou, X-X.2; Meng, Z.3,4; Wang, X-D.2; Ding, Y.1; Gan, Y-H.3,4
刊名EUROPEAN JOURNAL OF PAIN
2013-08-01
DOI10.1002/j.1532-2149.2012.00262.x
17期:7页:983-994
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Anesthesiology ; Clinical Neurology ; Neurosciences
研究领域[WOS]Anesthesiology ; Neurosciences & Neurology
关键词[WOS]ADJUVANT-INDUCED INFLAMMATION ; SODIUM-CHANNEL NA(V)1.7 ; PROTEIN-KINASE ; SUBSTANCE-P ; OVARIECTOMIZED RATS ; PAIN ; ACTIVATION ; NEURONS ; SCN9A ; PATHWAY
英文摘要

Background: Inflammation is a major cause of temporomandibular disorder-related pain. The Na(v)1.7 sodium channel has a critical function in pain perceptions. However, whether and how Na(v)1.7 in the trigeminal ganglion is involved in temporomandibular joint (TMJ) inflammatory pain remains to be examined.

Methods: TMJ inflammation was induced by complete Freund′s adjuvant in female rats. The expression of trigeminal ganglionic Na(v)1.7 and other sodium channels was examined using real-time polymerase chain reaction or Western blotting. Immunohistofluorescence with fluorescent retrograde neuronal tracer DiI was used to confirm Na(v)1.7 in the trigeminal neurons innervating TMJ. The functions of trigeminal ganglionic Na(v)1.7 and extracellular signal-regulated kinase 1/2 (ERK1/2) phosphorylation were blocked with the microinjection of the Na(v)1.7 antibody or U0126 into the trigeminal ganglion. Head withdrawal threshold and food intake was measured to evaluate TMJ nociceptive responses.

Results: TMJ inflammation significantly up-regulated Na(v)1.7 mRNA and protein; however, the mRNA of Na(v)1.3 was not affected and those of Na(v)1.8 and Na(v)1.9 were only slightly up-regulated. TMJ inflammation specifically induced Na(v)1.7 in the neurons innervating TMJ. In addition, blocking the Na(v)1.7 function significantly attenuated the hyperalgesia of the inflamed TMJ. Moreover, TMJ inflammation up-regulated ERK1/2 phosphorylation only in the glials; blocking ERK1/2 phosphorylation in the glials blocked Na(v)1.7 up-regulation in the neurons and correspondingly attenuated the hyperalgesia of the inflamed TMJ.

Conclusions: Trigeminal ganglionic Na(v)1.7 has an important function in the hyperalgesia of the inflamed TMJ, which is dependent on the communication with the satellite glials.

语种英语
WOS记录号WOS:000321204100006
引用统计
被引频次:8[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/55579
专题北京大学口腔医学院_牙周科
北京大学临床肿瘤学院_药剂科
作者单位1.Peking Univ, Dent Ctr 3, Sch & Hosp Stomatol, Beijing 100871, Peoples R China
2.Peking Univ, Dept Orthodont, Sch & Hosp Stomatol, Beijing 100871, Peoples R China
3.Peking Univ, Cent Lab, Sch & Hosp Stomatol, Beijing 100871, Peoples R China
4.Peking Univ, Ctr Temporomandibular Disorders & Orofacial Pain, Sch & Hosp Stomatol, Beijing 100871, Peoples R China
推荐引用方式
GB/T 7714
Bi, R-Y.,Kou, X-X.,Meng, Z.,et al. Involvement of trigeminal ganglionic Na(v)1.7 in hyperalgesia of inflamed temporomandibular joint is dependent on ERK1/2 phosphorylation of glial cells in rats[J]. EUROPEAN JOURNAL OF PAIN,2013,17(7):983-994.
APA Bi, R-Y.,Kou, X-X.,Meng, Z.,Wang, X-D.,Ding, Y.,&Gan, Y-H..(2013).Involvement of trigeminal ganglionic Na(v)1.7 in hyperalgesia of inflamed temporomandibular joint is dependent on ERK1/2 phosphorylation of glial cells in rats.EUROPEAN JOURNAL OF PAIN,17(7),983-994.
MLA Bi, R-Y.,et al."Involvement of trigeminal ganglionic Na(v)1.7 in hyperalgesia of inflamed temporomandibular joint is dependent on ERK1/2 phosphorylation of glial cells in rats".EUROPEAN JOURNAL OF PAIN 17.7(2013):983-994.
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