咬合创伤大鼠Vc内sP和NMDAR1的表达

目的；观察大鼠咬合创伤后Vc内SP和NMDA受体亚单位1型（NMDAR1）表达的变化，分析咬合创伤后Vc内初级感觉神经元中枢端末梢的敏感化和传导机制。方法：应用免疫组织化学方法，观察咬合创伤大鼠，双测Vc内SP、NMDAR1表达的变化。结果：空白对照大鼠Vc内SP和NMDAR1免疫阳性结构为终末和纤维，主要分布在VcⅠ、Ⅱ两层，呈新月形染色弧。两侧分布对称，咬合创伤7d组，实验侧Vc内SP、NMDAR1表达均上调，灰度值与对照侧相比有显差异。咬合创伤15d组，实验侧Vc内SP、NMDAR1表达比对照侧高，但无显差异。咬合创伤30d，实验侧Vc内SP、NMDAR1免疫阳性结构在同一切片中左右密度不对称，有的切片实验侧密度大于对照侧，有的切片实验侧密度低于对照侧。结论：咬合创伤后，Vc内SP、NMDAR1的表达发生变化，提示咬合创伤后初级中枢发生敏感化，是咬合创伤导致口面部慢性疼痛的机制之一。

Expression of SP, NMDAR1 in Vc during occlusal trauma in rat

Objective:To investigate the expression of SP and N-methyl-D-aspartate receptor 1 ( NMDAR1) intrigeminal subnucleus caudalis ( Vc ) during occlusal trauma in rat, and analyse the effect of occlusal trauma on sensitizationand conduction of primary sensory neurons in Vc. Methods: Adopting immunohistochemistry, expression of SP andNMDAR1 in Vc were tested in rat during occlusal trauma. Results: In control group, SP- and NMDAR1-immunoreactivestructures in Vc, which correspond to the nerve endings and fibres, mostly distribute I and II layers of Vc showing thecrescent staining, and the distribution is symmetric. At 7 days, expression of SP and NMDAR1 upregulate, and the grey-scale of staining between the experimental and control side has significant difference. At 15 days of occlusal trauma,expression of SP and NMDAR1 of experimental side was higher than control side, but no statistical significance. At 30days, the density of SP- and NMDAR1-immunoreactive structures in Vc are asymmetric on the same slice, the density ofexperimental side are either higher or lower than control side. Conclusions: Expression of SP and NMDAR1 in Vc variesas occlusal trauma. It suggests that sensitization of primary center is a mechanism of chronic orofacial pain followingocclusal trauma.