Activation of NK1 receptor of trigeminal root ganglion via substance P paracrine mechanism contributes to the mechanical allodynia in the temporomandibular joint inflammation in rats
Activation of NK1 receptor of trigeminal root ganglion via substance P paracrine mechanism contributes to the mechanical allodynia in the temporomandibular joint inflammation in rats
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DOI：
10.1016/j.pain.2005.05.007
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发表时间：
2005-08-01
期刊：
影响因子：
7.4
通讯作者：
Matsumoto, S
中科院分区：
文献类型：
--
作者：
Takeda, M;Tanimoto, T;Matsumoto, S
本研究的目的是通过使用多管电极进行细胞外电生理记录，研究在体内条件下，颞下颌关节 (TMJ) 炎症是否会改变支配面部皮肤的 A β-虹膜根神经节 (TRG) 神经元活动的兴奋性。将完全弗氏佐剂（CFA）注射到大鼠颞下颌关节中。发炎大鼠胡须垫区域逃避机械刺激的阈值（2 天）显着低于对照大鼠。在戊巴比妥麻醉的大鼠中，总共记录了 36 个 A beta-TRG 神经元对胡须垫电刺激的反应。颞下颌关节炎症大鼠中自发放电的 A beta-TRG 神经元数量及其放电率显着高于对照大鼠。在发炎大鼠而非非发炎大鼠中，通过局部离子电渗疗法应用 NK1 受体拮抗剂 (L-703,606)，A beta-TRG 神经元中自发活动的放电率呈电流依赖性降低。在对照和发炎大鼠中，通过局部离子电渗疗法应用 P 物质（SP），它们的自发活动呈电流依赖性增加。发炎大鼠Aβ-TRG神经元的机械反应阈值显着低于对照大鼠。使用L-703,606离子电渗疗法后，发炎大鼠的机械反应阈值与对照大鼠没有差异。这些结果表明，由于 TRG 神经元细胞体释放 SP，TMJ 炎症通过旁分泌机制调节支配面部皮肤的 A beta-TRG 神经元的兴奋性。这种 SP 释放可能在确定与颞下颌疾病有关的三叉神经炎性异常性疼痛中发挥重要作用。 (c) 2005 年国际疼痛研究协会。由 Elsevier B.V. 出版。保留所有权利。
The aim of this study was to investigate whether under in vivo conditions, temporomandibular joint (TMJ) inflammation alters the excitability of A beta-Irigeminal root ganglion (TRG) neuronal activity innervating the facial skin by using extracellular electrophysiological recording with multibarrel-electrodes. Complete Freund's adjuvant (CFA) was injected into the rat TMJ. Threshold for escape from mechanical stimulation applied to the whisker pad area in inflamed rats (2 days) was significantly lower than that in control rats. A total of 36 A beta-TRG neurons responding to electrical stimulation of the whisker pad was recorded in pentobarbital-anesthetized rats. The number of A beta-TRG neurons with spontaneous firings and their firing rate in TMJ inflamed rats were significantly larger than those in control rats. The firing rates of their spontaneous activity in the A beta-TRG neurons were current-dependently decreased by local iontophoretic application of an NK1 receptor antagonist (L-703,606) in inflamed, but not non-inflamed rats. Their spontaneous activities were current-dependently increased by local iontophoretic application of substance P (SP) in control and inflamed rats. The mechanical response threshold of A beta-TRG neurons in inflamed rats was significantly lower than that in control rats. The mechanical response threshold in inflamed rats after iontophoretic application of L-703,606 was not different from that in control rats. These results suggest that TMJ inflammation modulate the excitability of A beta-TRG neurons innervating the facial skin via paracrine mechanism due to SP released from TRG neuronal cell body. Such a SP release may play an important role in determining the trigeminal inflammatory allodynia concerning the temporomandibular disorder. (c) 2005 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.