Role of NMDA receptors in the trigeminal pathway, and the modulatory effect of magnesium in a model of rat temporomandibular joint arthritis
Role of NMDA receptors in the trigeminal pathway, and the modulatory effect of magnesium in a model of rat temporomandibular joint arthritis
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DOI：
10.1111/eos.12093
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发表时间：
2013-12-01
影响因子：
1.9
通讯作者：
Vale, Mariana L.
中科院分区：
文献类型：
--
作者：
Cavalcante, Andre L. C.;Siqueira, Rafaelly M. P.;Vale, Mariana L.
颞下颌关节（TMJ）关节炎是一种常见的原因口面疼痛。在本研究中，N-甲基-D-天冬氨酸受体（NMDA-Rs）和镁的调制作用TMJ关节炎高伤害性感受。雄性Wistar大鼠接受关节内注射角叉菜胶（Cg）的TMJ，和机械hypernociception进行了测量。在关节炎诱导前给予NMDA-R拮抗剂MK-801和氯化镁（MgCl 2）。通过在注射Cg之前给大鼠喂食合成的无镁饮食9 d来促进镁缺乏。Cg可诱导持续120 h的机械性高伤害性感受。MK-801可抑制这种痛觉超敏状态。MgCl 2预处理阻止Cg诱导的高伤害性感受，并在Cg不存在的情况下改变伤害性感受阈值。缺镁可增加痛觉过敏反应并诱导自发性痛觉过敏行为。TMJ关节炎增加了所有NMDA-R亚基的mRNA表达和磷酸化NR 1（磷酸化NR 1）的免疫染色。MgCl 2抑制NR 2B mRNA和磷酸化NR 1的表达，增加NR 3 mRNA的表达。缺镁增加了三叉神经尾侧亚核NR 1和NR 3 mRNA的表达和磷酸化NR 1免疫染色。我们发现，镁调节伤害性行为，并诱导尾侧亚核NMDA-R亚单位重排。目前的研究结果可能会导致更好地了解在三叉神经通路的伤害性中枢处理和新的方法来治疗颞下颌关节起源的口面疼痛的发展。
Temporomandibular joint (TMJ) arthritis is a common cause of orofacial pain. In the present study, the modulatory effects of N-methyl-D-aspartate receptors (NMDA-Rs) and magnesium were investigated in TMJ arthritis hypernociception. Male Wistar rats received an intra-articular injection of carrageenan (Cg) in the TMJ, and mechanical hypernociception was measured. The NMDA-R antagonist, MK-801, and magnesium chloride (MgCl2) were administered before arthritis induction. Magnesium deficiency was promoted by feeding rats a synthetic magnesium-free diet for 9 d before injection of Cg. The Cg induced mechanical hypernociception that lasted for 120 h. MK-801 inhibited this hypernociceptive state. MgCl2 pretreatment prevented Cg-induced hypernociception and altered the nociceptive threshold in the absence of Cg. Magnesium deficiency increased hypernociception and induced spontaneous hypernociceptive behavior. TMJ arthritis increased the expression of mRNA for all NMDA-R subunits and immunostaining of phosphorylated NR1 (phospho-NR1). MgCl2 inhibited expression of NR2B mRNA and phospho-NR1 immunostaining and increased expression of NR3 mRNA. Magnesium deficiency increased expression of both NR1 and NR3 mRNAs and phospho-NR1 immunostaining in the trigeminal subnucleus caudalis. We found that magnesium modulates nociceptive behavior and induces NMDA-R subunit rearrangement in the subnucleus caudalis. The present results may lead to a better understanding of central processing in the nociceptive trigeminal pathway and the development of new approaches to treat orofacial pain with a TMJ origin.