P2X and NMDA receptor involvement in temporomandibular joint-evoked reflex activity in rat jaw muscles.

P2X and NMDA receptor involvement in temporomandibular joint-evoked reflex activity in rat jaw muscles.
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DOI:
10.1016/j.brainres.2010.05.055
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发表时间:
2010-07-30
期刊:
影响因子:
2.9
通讯作者:
Hu, J. W.
Hu, J. W.
中科院分区:
医学3区
文献类型:
--
作者:
Watanabe, T.;Tsuboi, Y.;Sessle, B. J.;Iwata, K.;Hu, J. W.

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我们以前已经表明,兴奋性氨基谷氨酸注射到大鼠颞下颌关节(TMJ)引起的反射活动,在前二腹肌(DIG)和咬肌(MASS)肌肉,可以通过预先TMJ注射N-甲基-D-天冬氨酸(NMDA)受体拮抗剂衰减。本研究的目的是测试是否也可以通过向大鼠TMJ区域注射P2 X受体激动剂来诱发下颌肌活动,以及是否可以通过TMJ注射P2 X受体拮抗剂或NMDA受体拮抗剂来调节反射活动。将选择性P2 X亚型激动剂α,β-亚甲基腺苷5′-三磷酸(α,β-meATP)和载体(磷酸盐缓冲液)或选择性P2 X亚型拮抗剂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)注入大鼠颞下颌关节区。记录DIG和MASS肌肉的肌电图(EMG)反射活动。与基线EMG活动相比,在预先注射溶剂后向TMJ中注射α,β-me-ATP(但不是全身给药)以剂量依赖性方式显著增加同侧DIG和MASS EMG活动的幅度和持续时间。在同一颞下颌关节部位预先注射TNP-ATP可拮抗α,β-me-ATP诱发的反应,而对侧颞下颌关节注射TNP-ATP无效。此外,APV也能拮抗α,β-me-ATP诱发的反应,而全身注射APV则无此作用。这些结果表明,外周嘌呤能以及naphthamatergic受体机制在颞下颌关节伤害性传入的输入,引起反射活动的下颌肌肉的处理的相互作用。
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 a 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 α,β-methylene adenosine 5′-triphosphate (α,β-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 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, α,β-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 α,β-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 α,β-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.
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