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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 coldlentency, 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。
Objective To investigate the possible mechanism of TRPV1 involved in thermal hyperalgesia and cold pain perception associated with facial inflammatory pain. Methods The facial inflammatory pain model was induced by subcutaneous injection of turpentine on the face of rats, and the head withdrawal thermal latency (HWTL) and headache cold latency (HWCL) Change, measured once a day for 21 consecutive days. Immunohistochemical staining, frequency of cell size analysis and mean optical density were used to investigate the primary sensory effects of trigeminal ganglion (TG) on the facial epidermis of rats on the 3rd, 5th, 7th, 14th and 21st day after the facial inflammatory pain Neurons, the peripheral nerve fibers of the tentorium, and the TRPV1 expression in the central nervous system of the trigeminal sensory nuclei caudalis (Vc). Results On the 1st to 14th day after injection of turpentine, the latency of incubation and the latency of cold withdrawal decreased significantly, reaching the lowest on the 5th and the 3rd day after injection and returned to the normal level on the 21st day. By 14 days, the number of TRPV1-expressing cells increased and reached its maximum on day 7 and returned to normal on day 21. Normal rats TRPV1 mainly expressed in small and medium-sized neurons of TG, the skin of the tentacles and the trigeminal nucleus caudal sub-nucleus rich TRPV1-positive; facial inflammatory pain within 2 weeks after the TG small and medium-sized neurons, tentorial skin tip and Vc The obvious increase of TRPV1 expression was observed in the outer layers Ⅰ and Ⅱ. Conclusions Facial inflammatory pain can cause hyperalgesia in both nociceptive and cold stimuli in rats and lead to an increase in the number of TRPV1 positive neurons and peripheral and central nerve fibers in the trigeminal ganglion. Changes in the phenotypes of the meta- and distal axons may play an important role in the formation and maintenance of thermal hyperalgesia and cold pain sensation when turpentine causes facial inflammatory pain.