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Indirect mechanism of histamine-induced nociception in temporomandibular joint of rats.

机译：组胺诱发大鼠颞下颌关节痛的间接机制。

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A considerable amount of evidence suggests that temporomandibular joint (TMJ) pain associated with temporomandibular disorder results, at least in part, from an inflammatory episode. Although histamine can cause pain, it is not clear whether this mediator induces nociception in the TMJ. In this study, we investigated the contribution of endogenous histamine to formalin-induced nociception in the TMJ of rats. We also investigated whether the administration of histamine induces nociception in the TMJ and, if so, whether this effect is mediated by an indirect action on primary afferent nociceptors. Local administration of the H1-receptor antagonist pyrilamine prevented formalin-induced nociception in the TMJ in a dose-dependent manner. Local administration of histamine (250 microg) in the TMJ induced nociceptive behavior that was inhibited by co-administration of the lidocaine N-ethyl bromide quaternary salt QX-314 (2%) or the selective H1-receptor antagonist pyrilamine (400 microg). Nociception induced by histamine was also inhibited by pre-treatment with sodium cromoglycate (800 microg) and by co-administration of the 5-HT(3) receptor antagonist tropisetron (400 mug), while pyrilamine (400 mug) did not inhibit nociception induced by 5-hydroxytryptamine (5-HT, 250 microg) in the TMJ. Furthermore, histamine, in a dose that did not induce nociception by itself, strongly enhanced 5-HT-induced nociception. Finally, the administration of a sub-threshold dose of 5-HT (100 microg), but not of histamine (100 microg), elicited nociception in the TMJ previously challenged with the inflammatory agent carrageenan (100 microg). In conclusion, these data suggest that histamine induces TMJ nociception by an indirect mechanism involving endogenous release of 5-HT and activation of 5-HT(3) receptors on sensory afferents. It is proposed that histamine activates the H1 receptor to induce the release of 5-HT which depolarizes the nociceptor by activating 5-HT(3) receptor.
机译：大量证据表明与颞下颌疾病相关的颞下颌关节（TMJ）疼痛至少部分是由炎症发作引起的。尽管组胺会引起疼痛，但尚不清楚该介质是否在TMJ中引起伤害感受。在这项研究中，我们调查了内源性组胺对大鼠TMJ中福尔马林诱导的伤害感受的影响。我们还研究了组胺的施用是否在TMJ中诱导了伤害感受，如果是，这种作用是否由对原发传入伤害感受器的间接作用介导。 H1受体拮抗剂吡咯胺的局部给药以剂量依赖的方式阻止了福尔马林引起的TMJ伤害感受。在TMJ中局部施用组胺（250微克）会引起伤害感受行为，利多卡因N-乙基溴化季铵盐QX-314（2％）或选择性的H1受体拮抗剂吡咯胺（400微克）可以共同抑制。组胺诱导的伤害感受也可以通过色甘酸钠（800微克）的预处理和5-HT（3）受体拮抗剂tropisetron（400杯）的共同给药来抑制，而吡拉明（400杯）则不能抑制诱导的伤害由TMJ中的5-羟色胺（5-HT，250微克）制成。此外，组胺以自身不诱导伤害感受的剂量强烈增强了5-HT诱导的伤害感受。最后，亚阈值剂量的5-HT（100微克）而不是组胺（100微克）的施用引起了先前用炎性角叉菜胶（100微克）攻击的TMJ的伤害感受。总之，这些数据表明，组胺通过一种间接机制诱导TMJ伤害感受，该机制涉及5-HT（3）受体的内源性释放和感官传入的激活。建议组胺激活H1受体，以诱导5-HT的释放，通过激活5-HT（3）受体使伤害感受器去极化。

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