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P2X3 和 P2X2/3 受体在三氯蔗糖诱导的大鼠炎性痛觉过敏中的作用。

Involvement of temporomandibular joint P2X3 and P2X2/3 receptors in carrageenan-induced inflammatory hyperalgesia in rats.

机构信息

Department of Physiological Sciences, Laboratory of Orofacial Pain, Piracicaba Dental School, State University of Campinas - UNICAMP, Piracicaba, Sao Paulo, Brazil.

出版信息

Eur J Pharmacol. 2010 Oct 25;645(1-3):79-85. doi: 10.1016/j.ejphar.2010.06.008. Epub 2010 Jun 15.

DOI:10.1016/j.ejphar.2010.06.008
PMID:20558155
Abstract

The aim of this study was to investigate the role of P2X3, P2X2/3 and P2X7 receptors in the development of TMJ hyperalgesia induced by carrageenan. We also investigated the expression of mRNA of P2X7 receptors in the trigeminal ganglia and the existence of functional P2X7 receptors in the rat's TMJ. The P2X1, P2X3 and P2X2/3 receptor antagonist TNP-ATP, but not the selective P2X7 receptor antagonist A-438079, significantly reduced carrageenan-induced TMJ inflammatory hyperalgesia. The qPCR assay showed that mRNA of P2X7 receptors are expressed in the trigeminal ganglia but this expression is not increased by the inflammation induced by carrageenan in the TMJ region. The P2X7 receptor agonist BzATP induced TMJ inflammatory hyperalgesia that was significantly reduced by pretreatment with dexamethasone. These results indicate that P2X3 and P2X2/3 but not P2X7 receptors are involved in carrageenan-induced TMJ inflammatory hyperalgesia. However, functional P2X7 receptors are expressed in the TMJ region. The activation of these receptors by BzATP sensitizes the primary afferent nociceptors in the TMJ through the previous release of inflammatory mediators. The findings of this study point out P2X3 and P2X2/3 receptors, but not P2X7 receptors, as potential targets for the development of new analgesic drugs to control TMJ inflammatory pain.

摘要

本研究旨在探讨 P2X3、P2X2/3 和 P2X7 受体在卡拉胶诱导的 TMJ 痛觉过敏发展中的作用。我们还研究了 P2X7 受体在三叉神经节中的 mRNA 表达以及功能性 P2X7 受体在大鼠 TMJ 中的存在。P2X1、P2X3 和 P2X2/3 受体拮抗剂 TNP-ATP,但不是选择性 P2X7 受体拮抗剂 A-438079,显著减轻了卡拉胶诱导的 TMJ 炎症性痛觉过敏。qPCR 检测表明,P2X7 受体的 mRNA 表达存在于三叉神经节中,但 TMJ 区域的卡拉胶诱导炎症并未增加这种表达。P2X7 受体激动剂 BzATP 诱导 TMJ 炎症性痛觉过敏,用地塞米松预处理可显著减轻。这些结果表明,P2X3 和 P2X2/3 受体而不是 P2X7 受体参与了卡拉胶诱导的 TMJ 炎症性痛觉过敏。然而,功能性 P2X7 受体在 TMJ 区域表达。BzATP 通过先前释放炎症介质,激活 TMJ 中的初级传入伤害感受器,使这些受体敏化。本研究的结果指出,P2X3 和 P2X2/3 受体而不是 P2X7 受体,可能成为开发新的镇痛药以控制 TMJ 炎症性疼痛的潜在靶点。

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