Participation of NK1 receptors in nociceptin-induced modulation of rat knee joint mechanosensitivity
Participation of NK1 receptors in nociceptin-induced modulation of rat knee joint mechanosensitivity
复制标题
NK1受体参与伤害感受素诱导的大鼠膝关节机械敏感性调节
作者：
J. McDougall;U. Hanesch;M. Pawlak;R. Schmidt
抽象的。众所周知，伤害感受肽在大鼠膝关节的外周发挥作用，调节关节机械敏感性，并且推测神经激肽-1 (NK1) 受体可能参与这一过程。为了检验这一假设，从膝关节初级传入神经对关节正常和极端旋转的反应中进行了单个单元的细胞外记录。在动脉内紧密注射 NK1 拮抗剂 RP67580，然后施用 20 nmol 伤害感受肽后，评估传入放电率。无论膝关节正常旋转还是过度旋转，伤害感受肽都无法引发其通常的机械调节作用，因此传入活动与对照组没有显着差异（对于关节正常旋转和过度旋转，分别为 P=0.7572 和 P=0.9182）。这些数据表明，伤害感受肽诱导的大鼠膝部机械敏感性变化取决于 NK1 受体激活，可能是通过 P 物质的二次释放实现的。
Abstract. Nociceptin is known to act peripherally in the rat knee joint to modulate articular mechanosensitivity and it has been postulated that neurokinin-1 (NK1) receptors may be involved in this process. To test this hypothesis, single unit extracellular recordings were made from knee joint primary afferents in response to normal and extreme rotation of the joint. Afferent firing rate was assessed following close intraarterial injection of the NK1 antagonist RP67580 followed by administration of 20 nmol nociceptin. With both normal and hyper-rotation of the knee, nociceptin was unable to elicit its usual mechanomodulatory effect such that afferent activity was not significantly different from control (P=0.7572 and P=0.9182 for normal and hyper-rotation of the joint, respectively). These data indicate that nociceptin-induced mechanosensitivity changes in the rat knee depend upon NK1 receptor activation possibly through secondary release of substance P.