期刊文献+

外周代谢型谷氨酸受体5在颞下颌关节疼痛大鼠三叉神经节表达

The expression of metabtrophic glutamate receptor subtype 5 in the trigeminal ganglion of rats with temporomandibular joint pain
原文传递
导出
摘要 目的探讨外周代谢型谷氨酸受体5(m Glu R5)在颞下颌关节炎性疼痛中的作用。方法 SD大鼠36只,随机均分为6组,正常对照组(不做任何处理),阴性对照组(右侧颞下颌关节内注射50μl生理盐水),完全弗氏佐剂组(CFA组,右侧颞下颌关节内50μl CFA注射),MPEP-1组(1mm 2-甲基-6苯基乙炔嘧啶+50μl CFA),MPEP-2组(2.5mm MPEP+CFA),MPEP-3组(5mm MPEP+CFA)。将CFA注入右侧颞下颌关节腔内,诱导大鼠颞下颌关节疼痛。24h后检测各组大鼠的机械疼痛阈值,用Western-blot法和RT-PCR方法检测各组大鼠三叉神经节内m Glu R5和ERK1/2的蛋白和m RNA表达变化。结果 CFA组大鼠摆头阈值较正常组和阴性对照组明显下降(<0.01),MPEP-3组明显高于CFA组(<0.05)。三叉神经节内m Gu Rl 5和ERK1/2 m RNA及蛋白表达水平CFA组明显高于正常对照组和阴性对照组(<0.05),MPEP-3组明显低于CFA组(<0.05)。结论 m Glu R5参与颞下颌关节炎性疼痛,可能与ERK1/2信号通路相关。 Objective To study the expression of metabtrophic glutamate receptor subtype 5(mGluR5) in the trigeminal ganglion of rat with temporomandibular joint(TMJ) pain induced by CFA. Methods 36 rats were randomly divided into six groups averagely: normal control group (untreated), negative control group(0.9%NaCl injection), CFA group, MPEP-1 group (CFA + lmM MPEP), MPEP-2 group (CFA +2.5 mM MPEP), and MPEP-3 group (CFA + 5 mM MPEP). The head withdrawal threshold was measured 24h after injection of CFA into the TMJ. Western-blot and RT-PCR were used to detect the expressions of mGluR5 and p-ERK1/2 protein and mRNA respectively. Results The head withdrawal threshold was significandy decreased in all CFA-treated groups compared with the control groups(P〈0.05), but significantly increased in 5 mM MPEP group than in CFA group(P〈0.05).The expression levels of mGluR5 and ERK1/2 protein and mRNA in the trigeminal ganglion showed a marked increase in CFA group than in control groups(P 〈0.05), but decreased in 5 mM MPEP than in CFA group(P〈0.05). Conclusion The involvement of mGluR5 in the temporomandibular joint pain might be related to ERK1/2 signal pathway.
出处 《解剖科学进展》 CAS 2015年第5期527-530,共4页 Progress of Anatomical Sciences
基金 辽宁省自然科学基金(No.2013021094)
关键词 疼痛 代谢型谷氨酸受体5 代谢型谷氨酸受体5拮抗剂 ERK1/2 完全弗氏佐剂 pain metabtrophic glutamate receptor subtype 5 2-methyl-6-(phenylethynyl)-pyridine ERK1/2 complete Freund' s adjuvant
  • 相关文献

参考文献11

  • 1Lobbezoo F,Drangbholt M,Peck C,et al.Topical review:new insights into the pathlogy and diagnosis of disorders of the temporomandibular joint[J].J Orofacial Pain,2004,18(3):181-191.
  • 2Chen JJ,Johnson EJ.Targeting the bradykimin B1 receptor to reduce pain[J].Expert Opin Ther Targets,2007,11(1):21-35.
  • 3Finneru PNB,Jensen TS.Mechanisms of diseases:mechanism-based classification of neuropachic pain—a critical analysis[J].Nat Clin Pract Neurol,2006,2(2):107-115.
  • 4Bhave G,Karim F,Carlton SM,et al.peripheral group I metabotropic glutamate receptors modulate nociception in mice[J].Nat Neurosci,2001,4(4):417-423.
  • 5傅开元.颞下颌关节及口颌面疼痛的治疗[J].中国实用口腔科杂志,2009,2(3):139-143. 被引量:9
  • 6Liang YC,Huang CC,Hsu KS.Characterization of long-term potentiation of primary transmission at trigeminal synapses of juvenile rats:essential role of subtype 5 metabotropic glutamate receptors[J].Pain,2005,114(3):417-428.
  • 7Ahn DK,Jung CY,Lee HJ,et al.Peripheral glutamate receptors participate in interleukin-1 beta induced mechanical allodynia in the orofacial area of rats[J].Neurosci Lett,2004,357(3):203-206.
  • 8李红莲,王小丽,张亦农,等.第五型代谢型谷氨酸受体(m Glu R5)与一级传入C纤维关系的免疫组织化学研究[J].解剖科学进展,1999,5(4):381.
  • 9Lee JS,Ro JY.Peripheral metabotropic glutamate receptor 5 mediates mechanical hypersensitivity in craniofacial muscle via protein kinase C dependent mechanisms[J].Neuroscience,2007b,146:375–338.
  • 10朱东望,李长义,张健,刘洪臣.口颌面部炎性疼痛对大鼠三叉神经脊束核p38信号转导的影响[J].中华口腔医学杂志,2012,47(1):14-18. 被引量:1

二级参考文献29

  • 1董研,刘洪臣,王新木,刘大庆,武胜昔.咬合创伤对三叉神经脊束核敏化作用的研究[J].中华口腔医学杂志,2004,39(5):418-420. 被引量:7
  • 2Obata T, Brown GE, Yaffe MB. MAP kinase pathways activated by stress: the p38 MAPK pathway. Cril Care Ned, 2000, 28(4 Suppl) : N67-N77.
  • 3Imbe H, Okamoto K, Aikawa F, et al. Effects of peripheral inflammation on aciivalion of p3g mitogen-aclivaled prolein kinase in the mstral ventrumedial medulla. Brain Res. 2007, 1134 (1) : 131-139.
  • 4Sweitzer SM, Peters MC, Ma JY, et al. Peripheral and cenlral p38 MAPK mediales eapsaiein-induced hyperalgesia. Pain, 2004, 111 ( 3 ) :278-285.
  • 5Slleth K, Friel J, Nolan B, el al. Inhibition of p38 mitogen activated protein kinase increases lipopolysaeeharide induced inhibition of apoplosis in neutrophils by activating extracellular signal-regulated kinase. Surgery, 2001 , 130(2) : 242-248.
  • 6Yamanaka O, Saika S, Ohnishi Y, el al. Inhibilion of p38MAP kinase suppresses fibrogenie reaction in conjunetiva in mice. Mol Vis, 2007, 13: 1730-1739.
  • 7Svensson CI, Fitzsimmons B, Azizi S, et al. Spinal p38bela isofonn mediales tissue injury-induced hyperalgesia and spinal sensitization. J Neurochem, 2005, 92(6): 1508-1520.
  • 8Ro JY, Capra NF, Masri R. Contribution of peripheral N-methyl- D-aspartate receptors to e-fos expression in the trigeminal spinal nucleus following acute masseteric inflammation. Neuroscience, 2004. 125( I ) : 213-219.
  • 9Takeshila S, Hirata H, Bereiter DA. Intensiry coding by TMJ-responsive neurons in superficial laminae of caudal medullary dorsal horn of Ihe rat. J Neurophysiol. 2001 , 86(5 ) : 2393-2404.
  • 10Zhuang ZY. Gerner P, Woolf CJ, el al. ERK is sequentially activaled in neurons, mieroglia, and astrocytes by spinal nerve ligation and contributes to mechanical allodynia in this neuropathic pain model. Pain, 2005. 114(1-2) : 149-159.

共引文献8

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部