Temporomandibular joint inflammation activates glial and immune cells in both the trigeminal ganglia and in the spinal trigeminal nucleus.
Temporomandibular joint inflammation activates glial and immune cells in both the trigeminal ganglia and in the spinal trigeminal nucleus.
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DOI：
10.1186/1744-8069-6-89
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发表时间：
2010-12-10
期刊：
影响因子：
3.3
通讯作者：
Abbracchio MP
中科院分区：
文献类型：
--
作者：
Villa G;Ceruti S;Zanardelli M;Magni G;Jasmin L;Ohara PT;Abbracchio MP
神经胶质细胞已被证明直接参与感觉神经节和中枢神经系统（CNS）中慢性疼痛的发生和维持。事实上，已经报道了坐骨神经损伤或炎症后背根神经节和脊髓中的胶质细胞活化，但目前没有三叉神经致敏动物模型的数据。因此，在本研究中，我们评估了在颞下颌关节注射完全弗氏佐剂（CFA）后三叉神经脊髓系统中的胶质细胞活化，这会产生炎性疼痛和三叉神经过敏。CFA注射的动物表现出同侧的机械性异常性疼痛和颞下颌关节水肿，伴随着在三叉神经节的GFAP阳性的卫星胶质细胞环绕神经元的数量和居民巨噬细胞的激活的强烈增加。CFA注射后72小时，在同侧三叉神经尾侧亚核和颈后角中观察到活化的小胶质细胞，Iba1免疫反应性显著上调，但在相同区域未检测到反应性星形胶质细胞增生的迹象。由于嘌呤能系统已被牵连在神经病理性疼痛过程中的小胶质细胞的激活，我们还评估了小胶质细胞特异性P2Y12受体亚型的表达。在诱导TMJ炎症后未检测到该受体的上调，表明P2Y12在这种炎性疼痛范例中的任何可能作用不涉及受体表达的变化。我们的数据表明，特定的神经胶质细胞群成为激活后，在三叉神经节和中枢神经系统诱导颞下颌关节炎症，并建议他们可能代表创新的目标，在三叉神经敏化控制疼痛。
Glial cells have been shown to directly participate to the genesis and maintenance of chronic pain in both the sensory ganglia and the central nervous system (CNS). Indeed, glial cell activation has been reported in both the dorsal root ganglia and the spinal cord following injury or inflammation of the sciatic nerve, but no data are currently available in animal models of trigeminal sensitization. Therefore, in the present study, we evaluated glial cell activation in the trigeminal-spinal system following injection of the Complete Freund's Adjuvant (CFA) into the temporomandibular joint, which generates inflammatory pain and trigeminal hypersensitivity. CFA-injected animals showed ipsilateral mechanical allodynia and temporomandibular joint edema, accompanied in the trigeminal ganglion by a strong increase in the number of GFAP-positive satellite glial cells encircling neurons and by the activation of resident macrophages. Seventy-two hours after CFA injection, activated microglial cells were observed in the ipsilateral trigeminal subnucleus caudalis and in the cervical dorsal horn, with a significant up-regulation of Iba1 immunoreactivity, but no signs of reactive astrogliosis were detected in the same areas. Since the purinergic system has been implicated in the activation of microglial cells during neuropathic pain, we have also evaluated the expression of the microglial-specific P2Y12 receptor subtype. No upregulation of this receptor was detected following induction of TMJ inflammation, suggesting that any possible role of P2Y12 in this paradigm of inflammatory pain does not involve changes in receptor expression. Our data indicate that specific glial cell populations become activated in both the trigeminal ganglia and the CNS following induction of temporomandibular joint inflammation, and suggest that they might represent innovative targets for controlling pain during trigeminal nerve sensitization.
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