Bakke M, Hu J W, Sessle B J
Department of Oral Function and Physiology, School of Dentistry, Faculty of Health Sciences, University of Copenhagen, Denmark.
Pain. 1998 Apr;75(2-3):219-27. doi: 10.1016/s0304-3959(97)00223-6.
An electromyographic (EMG) study was carried out in 51 anesthetized rats to assess if neurokinin, NK-1 and NK-2, receptor mechanisms and tachykinins were involved in the increased jaw muscle activity which can be reflexly evoked by injection of the small-fiber excitant and inflammatory irritant mustard oil (MO) into the temporomandibular joint (TMJ) region. A baseline level of EMG activity was recorded bilaterally for 20 min from digastric (DIG) and masseter (MASS) muscles and then each animal was treated with NK-1 or NK-2 antagonist or vehicle. In one series of experiments either the NK-1 antagonist CP-99,994 (20 microg approximately 54 nmol), the NK-2 antagonist MEN-10,376 (10 microg approximately 9 nmol or 20 microg approximately 18 nmol) or vehicle (control) was administrated into the lateral ventricle (i.c.v.); in another series the NK-1 antagonist (4 mg/kg approximately 3-4 micromol/rat) or vehicle (control) was given intravenously (i.v.). After 10 min, MO (20 microl, 20%) was applied to one TMJ (first injection) and 45 min later, MO was applied to the opposite TMJ (second injection). Pretreatment with neurokinin antagonists had little effect on the incidence of the MO-evoked EMG responses but did significantly reduce the EMG magnitude and duration. In the animals pretreated with NK-1 antagonist only the responses to the second MO injection was significantly affected whereas NK-2 pretreatment reduced the EMG responses to both MO injections to the TMJ. The systematic depression of the MO-evoked EMG responses by the NK-2 antagonist suggests that neurokinin A may be involved in the EMG responses. Since the NK-1 antagonist produced no systematic changes in responses elicited by the first MO injection, substance P does not seem to be associated directly with the initiation or maintenance of the EMG responses but may be involved if a 'central sensitization' has been induced by the first MO injection to the TMJ.
在51只麻醉大鼠身上进行了一项肌电图（EMG）研究，以评估神经激肽、NK-1和NK-2受体机制以及速激肽是否参与了下颌肌肉活动的增加，这种增加可通过将小纤维刺激物和炎性刺激物芥子油（MO）注射到颞下颌关节（TMJ）区域而反射性诱发。从二腹肌（DIG）和咬肌（MASS）双侧记录20分钟的EMG活动基线水平，然后每只动物用NK-1或NK-2拮抗剂或赋形剂进行处理。在一系列实验中，将NK-1拮抗剂CP-99,994（20微克，约54纳摩尔）、NK-2拮抗剂MEN-10,376（10微克，约9纳摩尔或20微克，约18纳摩尔）或赋形剂（对照）注入侧脑室（脑室内）；在另一系列实验中，静脉注射NK-1拮抗剂（4毫克/千克，约3-4微摩尔/大鼠）或赋形剂（对照）。10分钟后，将MO（20微升，20%）应用于一个TMJ（首次注射），45分钟后，将MO应用于对侧TMJ（第二次注射）。用神经激肽拮抗剂预处理对MO诱发的EMG反应发生率影响不大，但确实显著降低了EMG幅度和持续时间。在仅用NK-1拮抗剂预处理的动物中，仅对第二次MO注射的反应受到显著影响，而NK-2预处理则降低了对TMJ两次MO注射诱发的EMG反应。NK-2拮抗剂对MO诱发的EMG反应的系统性抑制表明神经激肽A可能参与了EMG反应。由于NK-1拮抗剂对首次MO注射诱发的反应没有产生系统性变化，P物质似乎与EMG反应的起始或维持没有直接关联，但如果首次向TMJ注射MO诱导了“中枢敏化”，则可能参与其中。
