Yu -M X, Sessle J B, Haas A D, Izzo A, Vernon H, Hu W J
Faculty of Dentistry, University of Toronto,Toronto, Ont. M5G 1G6,Canada Canadian Memorial Chiropractic College,Toronto, Ont. M4G 3E6,Canada.
Pain. 1996 Nov;68(1):169-178. doi: 10.1016/S0304-3959(96)03181-8.
The aim of this study was to examine the possible role of N-methyl-D-aspartate (NMDA) receptor mechanisms in responses induced by the small-fibre excitant and inflammatory irritant mustard oil injected into the temporomandibular joint (TMJ) region of rats. The effects of the non-competitive NMDA antagonist MK-801 were tested on the mustard oil-evoked increases in electromyographic (EMG) activity of the masseter and digastric muscles and Evans Blue plasma extravasation. Five minutes before the mustard oil injection, MK-801 or its vehicle was administered systemically (i.v.), into the third ventricle (i.c.v.), or locally into the TMJ region. Compared with control animals receiving vehicle, the rats receiving MK-801 at an i.v. dose of 0.5 mg/kg (n = 5) showed a significant reduction in the incidence and magnitude of EMG responses as well as in the plasma extravasation evoked by mustard oil; MK-801 at an i.v. dose of 0.1 mg/kg (n = 5) had no significant effect on plasma extravasation or on the incidence and magnitude of EMG responses but did significantly increase the latency of EMG responses. An i.c.v. dose of 0.1 mg/kg (n = 5) or 0.01 mg/kg (n = 5) had no significant effect on plasma extravasation or incidence of EMG responses but did significantly reduce the magnitudes of the masseter EMG response; the 0.01 mg/kg dose also significantly increased the latency of the digastric EMG response. The magnitudes of both the masseter and digastric EMG responses were also significantly reduced by MK-801 administered into the TMJ region at a dose of 0.1 mg/kg (n = 5) but not by 0.01 mg/kg (n = 5); neither dose significantly affected the incidence of EMG responses or the plasma extravasation. These data suggest that both central and peripheral NMDA receptor mechanisms may play an important role in EMG responses evoked by the small-fibre excitant and inflammatory irritant mustard oil, but that different neurochemical mechanisms may be involved in the plasma extravasation induced by mustard oil.
本研究的目的是探讨N-甲基-D-天冬氨酸(NMDA)受体机制在注射到大鼠颞下颌关节(TMJ)区域的小纤维兴奋剂和炎性刺激物芥子油所诱发反应中的可能作用。测试了非竞争性NMDA拮抗剂MK-801对芥子油诱发的咬肌和二腹肌肌电图(EMG)活动增加以及伊文思蓝血浆外渗的影响。在注射芥子油前5分钟,将MK-801或其溶媒全身给药(静脉注射)、注入第三脑室(脑室内注射)或局部注入TMJ区域。与接受溶媒的对照动物相比,静脉注射剂量为0.5 mg/kg(n = 5)的MK-801大鼠,芥子油诱发的EMG反应的发生率和幅度以及血浆外渗均显著降低;静脉注射剂量为0.1 mg/kg(n = 5)的MK-801对血浆外渗或EMG反应的发生率和幅度无显著影响,但显著增加了EMG反应的潜伏期。脑室内注射剂量为0.1 mg/kg(n = 5)或0.01 mg/kg(n = 5)对血浆外渗或EMG反应的发生率无显著影响,但显著降低了咬肌EMG反应的幅度;0.01 mg/kg剂量也显著增加了二腹肌EMG反应的潜伏期。剂量为0.1 mg/kg(n = 5)的MK-801注入TMJ区域也显著降低了咬肌和二腹肌EMG反应的幅度,但0.01 mg/kg(n = 5)则无此作用;两种剂量均未显著影响EMG反应的发生率或血浆外渗。这些数据表明,中枢和外周NMDA受体机制可能在小纤维兴奋剂和炎性刺激物芥子油诱发的EMG反应中起重要作用,但芥子油诱导的血浆外渗可能涉及不同的神经化学机制。