Participation of peripheral tachykinin NK1 receptors in the carrageenan-induced inflammation of the rat temporomandibular joint

被引:38
作者
Denadai-Souza, Alexandre [1 ]
Camargo, Livia de Lucca [1 ]
Ribela, Maria T. C. P. [2 ]
Keeble, Julie E. [3 ]
Costa, Soraia K. P. [1 ]
Muscara, Marcelo N. [1 ]
机构
[1] Univ Sao Paulo, Dept Pharmacol, Inst Biomed Sci, BR-05508900 Sao Paulo, Brazil
[2] IPEN CNEN, Dept Biotechnol, Sao Paulo, Brazil
[3] Kings Coll London, Pharmaceut Sci Res Div, London, England
基金
巴西圣保罗研究基金会; 英国生物技术与生命科学研究理事会;
关键词
Temporomandibular joint; NK1; receptors; Arthritis; Neurogenic inflammation; Substance P; NEUROPEPTIDE-LIKE IMMUNOREACTIVITY; TRIGEMINAL ROOT GANGLION; GENE-RELATED PEPTIDE; EXPRESS SUBSTANCE-P; JAW MUSCLE-ACTIVITY; TNF-ALPHA; NEUROGENIC INFLAMMATION; RHEUMATOID-ARTHRITIS; SYNOVIAL-FLUID; IN-VIVO;
D O I
10.1016/j.ejpain.2008.09.012
中图分类号
R614 [麻醉学];
学科分类号
100217 ;
摘要
Temporomandibular disorders represent one of the major challenges in dentistry therapeutics. This study was undertaken to evaluate the time course of carrageenan-induced inflammation in the rat temporomandibular joint (TMJ) and to investigate the role of tachykinin NK1 receptors. Inflammation was induced by a single intra-articular (i.art.) injection of carrageenan into the left TMJ (control group received sterile saline). Inflammatory parameters such as plasma extravasation, leukocyte influx and mechanical allodynia (measured as the head-withdrawal force threshold) and TNF alpha and IL-1 beta concentrations were measured in the TMJ lavages at selected time-points. The carrageenan-induced responses were also evaluated after treatment with the NK1 receptor antagonist SR140333. The i.art. injection of carrageenan into the TMJ caused a time-dependent plasma extravasation associated with mechanical allodynia, and a marked neutrophil accumulation between 4 and 24 h. Treatment with SR140333 substantially inhibited the increase in plasma extravasation and leukocyte influx at 4 and 24 h, as well as the production of TNF alpha and IL-1 beta into the joint cavity, but failed to affect changes in head-withdrawal threshold. The results obtained from the present TMJ-arthritis model provide, for the first time, information regarding the time course of this experimental inflammatory process. In addition, our data show that peripheral NK1 receptors mediate the production of both TNF alpha and IL-1 beta in the TMJ as well as some of the inflammatory signs, such as plasma extravasation and leukocyte influx, but not the nociceptive component. 2008 European Federation of Chapters of the International Association for the Study of Pain. Published by Elsevier Ltd. All rights reserved.
引用
收藏
页码:812 / 819
页数:8
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