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首页> 外文期刊>Pain. >Peripheral mechanisms underlying the essential role of P2X3,2/3 receptors in the development of inflammatory hyperalgesia.
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Peripheral mechanisms underlying the essential role of P2X3,2/3 receptors in the development of inflammatory hyperalgesia.

机译：在炎症性痛觉过敏的发展中，P2X3,2 / 3受体至关重要的外围机制。

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Activation of P2X3,2/3 receptors by endogenous ATP contributes to the development of inflammatory hyperalgesia. Given the clinical importance of mechanical hyperalgesia in inflammatory states, we hypothesized that the activation of P2X3,2/3 receptors by endogenous ATP contributes to carrageenan-induced mechanical hyperalgesia and that this contribution is mediated by an indirect and/or a direct sensitization of the primary afferent nociceptors. Co-administration of the selective P2X3,2/3 receptors antagonist A-317491, or the non-selective P2X3 receptor antagonist, TNP-ATP, with carrageenan blocked the mechanical hyperalgesia induced by carrageenan, and significantly reduced the increased concentration of tumor necrosis factor alpha (TNF-alpha) and chemokine-induced chemoattractant-1 (CINC-1) but not of interleukin-1 beta (IL-1 beta) induced by carrageenan. Co-administration of the selective P2X3,2/3 receptors antagonist A-317491 with carrageenan did not affect the neutrophil migration induced by carrageenan. Intrathecal administration of oligonucleotides antisense against P2X3 receptors for seven days significantly reduced the expression of P2X3 receptors in the saphenous nerve and significantly reduced the mechanical hyperalgesia induced by carrageenan. We concluded that the activation of P2X3,2/3 receptors by endogenous ATP is essential to the development of the mechanical hyperalgesia induced by carrageenan. Furthermore, we showed that this essential role of P2X3,2/3 receptors in the development of carrageenan-induced mechanical hyperalgesia is mediated by an indirect sensitization of the primary afferent nociceptors dependent on the previous release of TNF-alpha and by a direct sensitization of the primary afferent nociceptors.
机译：内源性ATP激活P2X3,2 / 3受体有助于发炎性痛觉过敏。鉴于机械性痛觉过敏在炎症状态的临床重要性，我们假设内源性ATP激活P2X3,2 / 3受体会导致角叉菜胶诱导的机械性痛觉过敏，并且这种作用是由间接和/或直接致敏性介导的。原发传入伤害感受器。选择性P2X3,2 / 3受体拮抗剂A-317491或非选择性P2X3受体拮抗剂TNP-ATP与角叉菜胶的共同给药可阻断角叉菜胶诱导的机械性痛觉过敏，并显着降低肿瘤坏死因子浓度的增加α（TNF-α）和趋化因子诱导的chemoattractant-1（CINC-1），但不是由角叉菜胶诱导的白介素1 beta（IL-1 beta）。选择性P2X3,2 / 3受体拮抗剂A-317491与角叉菜胶的共同给药不影响角叉菜胶诱导的嗜中性白细胞迁移。鞘内施用针对P2X3受体的反义寡核苷酸7天显着降低了隐神经中P2X3受体的表达，并显着降低了角叉菜胶诱导的机械性痛觉过敏。我们得出结论，内源性ATP激活P2X3,2 / 3受体对于由角叉菜胶诱导的机械性痛觉过敏的发展至关重要。此外，我们表明，P2X3,2 / 3受体在角叉菜胶诱导的机械性痛觉过敏的发展中的这种基本作用是由依赖于先前释放的TNF-α的主要传入伤害感受器的间接敏化和对TNF-α的直接敏化介导的主要传入伤害感受器。

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