Ahn Dong K, Kim Kwang H, Jung Chang Y, Choi Hyo S, Lim Eun J, Youn Dong H, Bae Yong C
Department of Oral Physiology and Neurobiology, School of Dentistry, Kyungpook National University, 188-1 Sam Deok 2 ga, Chung-gu, Daegu 700 412, South Korea.
Pain. 2005 Nov;118(1-2):53-60. doi: 10.1016/j.pain.2005.07.017. Epub 2005 Sep 9.
The present study investigated the role of peripheral group I and II metabotropic glutamate receptors (mGluRs) in interleukin-1beta (IL-1beta)-induced mechanical allodynia in the orofacial area. Experiments were carried out on Sprague-Dawley rats weighing between 230 and 280 g. After subcutaneous administration of 0.01, 0.1, 1, or 10 pg of IL-1beta, we examined withdrawal behavioral responses produced by 10 successive trials of a ramp of air-puffs pressure applied ipsilaterally or contralaterally to the IL-1beta injection site. The thresholds of air puffs were measured 10, 30, 60, 120, or 180 min after 25 microl of IL-1beta was administered through an implanted tube. Subcutaneous injection of IL-1beta produced bilateral mechanical allodynia. While the IL-1beta-induced mechanical allodynia was blocked by pretreatment with an IL-1 receptor antagonist, the IL-1beta-induced mirror-image mechanical allodynia was not blocked by an IL-1 receptor antagonist injected into the contralateral side. Subcutaneous administration of CPCCOEt or LY367385, an mGluR1 antagonist, or MPEP or SIB1893, an mGluR5 antagonist, 10 min prior to injection of IL-1beta abolished IL-1beta-induced mechanical allodynia. Pretreatment with APDC or DCG4, a group II mGluR agonist, blocked the IL-1beta-induced mechanical allodynia. The anti-allodynic effect induced by APDC was inhibited by pretreatment with LY341495, a group II mGluR antagonist. These results suggest that peripheral group I and II mGluRs participate in IL-1beta-induced mechanical allodynia in the orofacial area. Peripheral group I mGluR antagonists blocked the IL-1beta-induced mechanical allodynia, while peripheral group II mGluR agonists produced anti-allodynic effects on IL-1beta-induced mechanical allodynia in the orofacial area of rats.
本研究调查了外周I组和II组代谢型谷氨酸受体（mGluRs）在白细胞介素-1β（IL-1β）诱导的口面部机械性异常性疼痛中的作用。实验在体重230至280克的Sprague-Dawley大鼠身上进行。皮下注射0.01、0.1、1或10皮克的IL-1β后，我们检查了在IL-1β注射部位同侧或对侧连续10次施加递增气流压力试验所产生的退缩行为反应。在通过植入管给予25微升IL-1β后10、30、60、120或180分钟测量气流阈值。皮下注射IL-1β产生双侧机械性异常性疼痛。虽然IL-1β诱导的机械性异常性疼痛可被IL-1受体拮抗剂预处理阻断，但IL-1β诱导的镜像机械性异常性疼痛不能被注入对侧的IL-1受体拮抗剂阻断。在注射IL-1β前10分钟皮下给予CPCCOEt或LY367385（一种mGluR1拮抗剂）或MPEP或SIB1893（一种mGluR5拮抗剂）可消除IL-1β诱导的机械性异常性疼痛。用II组mGluR激动剂APDC或DCG4预处理可阻断IL-1β诱导的机械性异常性疼痛。LY341495（一种II组mGluR拮抗剂）预处理可抑制APDC诱导的抗异常性疼痛作用。这些结果表明，外周I组和II组mGluRs参与了IL-1β诱导的口面部机械性异常性疼痛。外周I组mGluR拮抗剂可阻断IL-1β诱导的机械性异常性疼痛，而外周II组mGluR激动剂对大鼠口面部区域IL-1β诱导的机械性异常性疼痛产生抗异常性疼痛作用。
