面部炎症痛诱发大鼠三叉神经节神经元中辣椒素受体表达的改变

目的探讨辣椒素受体（transient receptor potential vanilloid receptor 1,TRPV1）参与和面部炎症痛相关的热痛觉过敏与冷痛觉感受的可能机制。方法于大鼠面部皮下注射松节油造成面部炎症痛模型,分别应用热测痛和冷测痛装置测量热缩头潜伏期（head withdrawal thermal latency,HWTL）和冷缩头潜伏期（head withdrawal cold lentency,HWCL）的变化,每天测量一次,连续21天。应用免疫组织化学染色,细胞大小频率分析和平均光密度值分析来研究面部炎症痛后第3、5、7、14、21天支配大鼠面部表皮区三叉神经节（trigeminal ganglion,TG）初级感觉神经元、触须部皮肤末梢神经纤维和投射至三叉神经感觉尾侧亚核（trigeminal sensory nuclei caudalis,Vc）中枢突TRPV1表达的改变。结果注射松节油后第1至14天,热退缩反应潜伏期与冷退缩反应潜伏期均明显下降,分别于注射后第5天和第3天达到最低,第21天恢复到正常水平;注射松节油后第1至14天,TRPV1表达的细胞数量增加,并于第7天达到最大,第21天恢复到正常水平。正常大鼠TRPV1主要表达于TG的中小神经元,触须部皮肤以及三叉神经尾侧亚核含丰富的TRPV1阳性末梢;面部炎症痛后2周内,TG的中小神经元,触须部皮肤末梢以及Vc的Ⅰ和Ⅱ外层均可见明显的TRPV1表达增加。结论面部炎症痛可以引起大鼠对伤害性热刺激和冷刺激的痛觉过敏,并导致三叉神经节中TRPV1阳性神经元和外周与中枢阳性神经纤维末梢数目增加,表明TRPV1在三叉神经节的中小神经元和末梢轴突表型的改变可能对松节油引起面部炎症痛时热痛觉过敏和冷痛觉感受的形成与维持起重要作用。

Facial pain induces the alteration of transient receptor potential vanilloid receptor 1 expression in rat trigeminal ganglion

OBJECTIVE: To investigate the involvement of transient receptor potential vanilloid receptor 1 (TRPV1) in the facial inflammatory pain in relation to thermal hyperalgesia and cold pain sensation. METHODS: Facial inflammatory pain model was developed by subcutaneous injection of turpentine oil (TO) into rat facial area. Head withdrawal thermal latency (HWTL) and head withdrawal cold latency (HWCL) were measured once a day for 21 d after TO treatment using thermal and cold measurement apparatus. The immunohistochemical staining, cell-size frequency analysis and the survey of average optical density (OD) value were used to observe the changes of TRPV1 expression in the neurons of the trigeminal ganglion (TG), peripheral nerve fibers in the vibrissal pad, and central projection processes in the trigeminal sensory nuclei caudalis (Vc) on day 3, 5, 7, 14, and 21 after TO injection. RESULTS: HWTL and HWCL decreased significantly from day 1 to day 14 after TO injection with the lowest value on day 5 and day 3, respectively, and both recovered on day 21. The number of TRPV1-labeled neurons increased remarkably from day 1 to day 14 with a peak on day 7, and returned back to the normal level on day 21. In control rats, only small and medium-sized TG neurons were immunoreactive (IR) to TRPV1, and the TRPV1-IR terminals were abundant in both the vibrissal pad and the Vc. Within 2 weeks of inflammation, the expression of TRPV1 in small and medium-sized TG neurons increased obviously. Also the TRPV1 stained terminals and fibers appeared more frequent and denser in both the vibrissal pad skin and throughout laminae I and the outer zone of laminae II (IIo) of Vc. CONCLUSION: Facial inflammatory pain could induce hyperalgesia to noxious heat and cold stimuli, and result in increase of the numbers of TRPV1 positive TG neurons and the peripheral and central terminals of TG. These results suggest that the phenotypic changes of TRPV1 expression in small and medium-sized TG neurons and terminals might play an important role in the development and maintenance of TO-induced inflammatory thermal hyperalgesia and cold pain sensation.