Watanabe T, Tsuboi Y, Sessle B J, Iwata K, Hu J W
Faculty of Dentistry, University of Toronto, Toronto, ON, Canada.
Brain Res. 2010 Jul 30;1346:83-91. doi: 10.1016/j.brainres.2010.05.055. Epub 2010 May 23.
We have previously shown that injection of the excitatory amino glutamate into the rat temporomandibular joint (TMJ) evokes reflex activity in both anterior digastric (DIG) and masseter (MASS) muscles that can be attenuated by prior TMJ injection of an N-methyl-d-aspartate (NMDA) receptor antagonist. The aim of the present study was to test if jaw muscle activity could also be evoked by P2X receptor agonist injection into the rat TMJ region and if the reflex activity could be modulated by TMJ injection of P2X receptor antagonist or NMDA receptor antagonist. The selective P2X subtype agonist alpha,beta-methylene adenosine 5'-triphosphate (alpha,beta-me ATP) and vehicle (phosphate-buffered saline) or the selective P2X antagonist, 2'-(or-3')-O-(2,4,6-trinitrophenyl) adenosine 5'-triphosphate (TNP-ATP) or the selective NMDA antagonist (+/-)-d-2-amino-5-phosphonovalerate(APV) were injected into the rat TMJ region. Electromyographic (EMG) reflex activity was recorded in both DIG and MASS muscles. Compared with the baseline EMG activity, alpha,beta-me-ATP injection into the TMJ (but not its systemic administration) following pre-injection of the vehicle significantly increased the magnitude and the duration of ipsilateral DIG and MASS EMG activity in a dose-dependent manner. The alpha,beta-me-ATP-evoked responses could be antagonized by pre-injection of TNP-ATP into the same TMJ site but contralateral TMJ injection of TNP-ATP proved ineffective. Furthermore, the alpha,beta-me-ATP-evoked responses could also be antagonized by APV injected into the same TMJ site but not by its systemic injection. These results indicate the interaction of peripheral purinergic as well as glutamatergic receptor mechanisms in the processing of TMJ nociceptive afferent inputs that evoke reflex activity in jaw muscles.
我们之前已经表明，向大鼠颞下颌关节（TMJ）注射兴奋性氨基酸谷氨酸会在前腹二腹肌（DIG）和咬肌（MASS）中诱发反射活动，而在TMJ预先注射N-甲基-D-天冬氨酸（NMDA）受体拮抗剂可减弱这种活动。本研究的目的是测试向大鼠TMJ区域注射P2X受体激动剂是否也能诱发颌骨肌肉活动，以及反射活动是否能通过向TMJ注射P2X受体拮抗剂或NMDA受体拮抗剂来调节。将选择性P2X亚型激动剂α,β-亚甲基腺苷5'-三磷酸（α,β-me ATP）和赋形剂（磷酸盐缓冲盐水）或选择性P2X拮抗剂2'-(或-3')-O-(2,4,6-三硝基苯基)腺苷5'-三磷酸（TNP-ATP）或选择性NMDA拮抗剂(+/-)-D-2-氨基-5-磷酸戊酸（APV）注射到大鼠TMJ区域。记录DIG和MASS肌肉中的肌电图（EMG）反射活动。与基线EMG活动相比，在预先注射赋形剂后向TMJ注射α,β-me-ATP（而非全身给药）以剂量依赖的方式显著增加了同侧DIG和MASS EMG活动的幅度和持续时间。预先向同一TMJ部位注射TNP-ATP可拮抗α,β-me-ATP诱发的反应，但向对侧TMJ注射TNP-ATP则无效。此外，向同一TMJ部位注射APV也可拮抗α,β-me-ATP诱发的反应，但全身注射则无效。这些结果表明，在处理诱发颌骨肌肉反射活动的TMJ伤害性传入输入时，外周嘌呤能和谷氨酸能受体机制之间存在相互作用。
