Takeda Mamoru, Tanimoto Takeshi, Nasu Masanori, Ikeda Mizuho, Kadoi Jun, Matsumoto Shigeji
Department of Physiology, School of Dentistry at Tokyo, Nippon Dental University, 1-9-20, Fujimi-cho, Chiyoda-ku, Tokyo,102-8159, Japan Rerseach Center for Odontology, School of Dentistry at Tokyo, Nippon Dental University, 1-9-20, Fujimi-cho, Chiyoda-ku, Tokyo,102-8159, Japan.
Pain. 2005 Aug;116(3):375-385. doi: 10.1016/j.pain.2005.05.007.
The aim of this study was to investigate whether under in vivo conditions, temporomandibular joint (TMJ) inflammation alters the excitability of Abeta-trigeminal 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 Abeta-TRG neurons responding to electrical stimulation of the whisker pad was recorded in pentobarbital-anesthetized rats. The number of Abeta-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 Abeta-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 Abeta-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 Abeta-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.
本研究旨在通过使用多管电极进行细胞外电生理记录，调查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三叉神经节（TRG）Aβ神经元活动的兴奋性。将完全弗氏佐剂（CFA）注射到大鼠TMJ中。对发炎大鼠（2天）的须垫区域施加机械刺激的逃避阈值显著低于对照大鼠。在戊巴比妥麻醉的大鼠中，共记录到36个对须垫电刺激有反应的Aβ-TRG神经元。TMJ发炎大鼠中具有自发放电的Aβ-TRG神经元数量及其放电频率显著高于对照大鼠。在发炎但非未发炎的大鼠中，通过局部离子电渗法应用NK1受体拮抗剂（L-703,606），Aβ-TRG神经元自发放电活动的放电频率呈电流依赖性降低。在对照和发炎大鼠中，通过局部离子电渗法应用P物质（SP），其自发放电活动呈电流依赖性增加。发炎大鼠中Aβ-TRG神经元的机械反应阈值显著低于对照大鼠。离子电渗法应用L-703,606后，发炎大鼠的机械反应阈值与对照大鼠无异。这些结果表明，TMJ炎症通过TRG神经元胞体释放的SP，经由旁分泌机制调节支配面部皮肤的Aβ-TRG神经元的兴奋性。这种SP释放可能在确定与颞下颌关节紊乱相关的三叉神经炎性痛觉过敏中起重要作用。
