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学科主题: 口腔医学
题名:
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
作者: 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
发表日期: 2013-08-01
DOI: 10.1002/j.1532-2149.2012.00262.x
卷: 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
所属项目编号: 81070849 ; 81271173
项目资助者: National Natural Science Foundation of China
WOS记录号: WOS:000321204100006
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/55579
Appears in Collections:北京大学口腔医学院_牙周科_期刊论文

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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

Recommended Citation:
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.
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