Central sensitization and MAPKs are involved in occlusal interference-induced facial pain in rats.
Central sensitization and MAPKs are involved in occlusal interference-induced facial pain in rats.
复制标题
DOI：
10.1016/j.jpain.2013.02.005
复制
发表时间：
2013-08
期刊：
影响因子：
4
通讯作者：
Sessle, Barry J.
中科院分区：
文献类型：
--
作者：
Cao, Ye;Li, Kai;Fu, Kai-Yuan;Xie, Qiu-Fei;Chiang, Chen-Yu;Sessle, Barry J.
关键词：
我们之前建立了一个大鼠牙齿咬合干扰面部疼痛模型，该模型是通过将牙冠粘接在右侧上颌第一磨牙上产生的，并反映在持续的面部过敏中，这表明中枢致敏机制的参与。本研究的目的是探讨潜在的中枢机制参与咬合干扰诱导的面部过敏。对98只雄性成年Sprague-Dawley大鼠进行了行为、免疫组织化学、Western blot和电生理记录，这些大鼠要么接受了咬合干扰，要么是假手术大鼠或幼稚大鼠。免疫组织化学标记的三叉神经尾侧亚核（Vc）星形胶质细胞和小胶质细胞在咬合干扰后表现出星形胶质细胞和小胶质细胞活化的形态学变化。在放置咬合干扰后，Vc中也记录了p38 MAPK和ERK的持续上调，并在大鼠表现出机械面部超敏反应峰值的时间点在神经元和神经胶质细胞中表达。将p38 MAPK抑制剂SB203580直接作用于髓质可显著抑制咬合干扰诱导的超敏反应，而ERK抑制剂PD98059的作用更强。细胞外电生理记录也记录了在咬合干扰放置后功能识别的Vc伤害性神经元的中枢敏化，并且给予PD98059可以逆转神经元的中枢敏化。这些新发现表明，包括三叉神经痛觉神经元的中枢致敏和涉及MAPKs的非神经元过程在内的中枢机制在咬合干扰诱导的面部疼痛的产生中发挥了重要作用。中枢机制包括三叉神经痛觉神经元致敏、涉及胶质细胞激活和MAPKs的非神经元过程在咬合干扰诱导的面部疼痛中发挥重要作用。这些机制可能涉及面部疼痛的临床表现，已报道的患者咬合干扰。
We previously developed a rat dental occlusal interference model of facial pain that was produced by bonding a crown onto the right maxillary first molar and was reflected in sustained facial hypersensitivity that was suggestive of the involvement of central sensitization mechanisms. The aim of the present study was to investigate potential central mechanisms involved in the occlusal interference-induced facial hypersensitivity. A combination of behavioral, immunohistochemical, Western blot and electrophysiological recording procedures was used in 98 male adult Sprague-Dawley rats that either received the occlusal interference or were sham-operated or naive rats. Immunohistochemically labeled astrocytes and microglia in trigeminal subnucleus caudalis (Vc) showed morphological changes indicative of astrocyte and microglial activation after the occlusal interference. Prolonged upregulation of p38 MAPK and ERK was also documented in Vc after placement of the occlusal interference, and was expressed in both neurons and glial cells at time points when rats showed peak mechanical facial hypersensitivity. The i.t. administration of the p38 MAPK inhibitor SB203580 to the medulla significantly inhibited the occlusal interference-induced hypersensitivity, and the ERK inhibitor PD98059 produced an even stronger effect. Central sensitization of functionally identified Vc nociceptive neurons following placement of the occlusal interference was also documented by extracellular electrophysiological recordings, and i.t. administration of PD98059 could reverse the neuronal central sensitization. These novel findings suggest that central mechanisms including central sensitization of trigeminal nociceptive neurons and non-neuronal processes involving MAPKs play significant roles in the production of occlusal interference-induced facial pain. Central mechanisms including trigeminal nociceptive neuronal sensitization, non-neuronal processes involving glial activation and MAPKs play significant roles in occlusal interference-induced facial pain. These mechanisms may be involved in clinical manifestations of facial pain that have been reported in patients with an occlusal interference.
登录
查看更多内容
影响因子：
25
作者：
Ji, RR;Baba, H;Woolf, CJ
通讯作者：
Woolf, CJ
影响因子：
3.3
作者：
Itoh, K.;Chiang, C. -Y.;Li, Z.;Lee, J. -C.;Dostrovsky, J. O.;Sessle, B. J.
通讯作者：
Sessle, B. J.
影响因子：
4.6
作者：
Clark, GT;Tsukiyama, Y;Watanabe, T
通讯作者：
Watanabe, T
影响因子：
2.5
作者：
BROTON, JG;HU, JW;SESSLE, BJ
通讯作者：
SESSLE, BJ
影响因子：
2.5
作者：
Iwata, K;Imai, T;Hu, J
通讯作者：
Hu, J