神经科学通报(英文版)
神經科學通報(英文版)
신경과학통보(영문판)
NEUROSCIENCE BULLETIN
2007年
2期
92-100
,共9页
裴磊%林传友%戴甲培%殷光甫
裴磊%林傳友%戴甲培%慇光甫
배뢰%림전우%대갑배%은광보
辣椒素受体%面部痛%痛觉过敏%三叉神经节
辣椒素受體%麵部痛%痛覺過敏%三扠神經節
랄초소수체%면부통%통각과민%삼차신경절
vanilloid receptors%facial pain%hyperalgesia%trigeminal ganglion
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.
目的 探討辣椒素受體(transient receptor potential vanilloid receptor 1,TRPV1)參與和麵部炎癥痛相關的熱痛覺過敏與冷痛覺感受的可能機製.方法 于大鼠麵部皮下註射鬆節油造成麵部炎癥痛模型,分彆應用熱測痛和冷測痛裝置測量熱縮頭潛伏期(head withdrawal thermal latency,HWTL)和冷縮頭潛伏期(head withdrawal cold lentency,HWCL)的變化,每天測量一次,連續21天.應用免疫組織化學染色,細胞大小頻率分析和平均光密度值分析來研究麵部炎癥痛後第3、5、7、14、21天支配大鼠麵部錶皮區三扠神經節(trigeminal ganglion,TG)初級感覺神經元、觸鬚部皮膚末梢神經纖維和投射至三扠神經感覺尾側亞覈(trigeminal sensory nuclei caudalis,Vc)中樞突TRPV1錶達的改變.結果 註射鬆節油後第1至14天,熱退縮反應潛伏期與冷退縮反應潛伏期均明顯下降,分彆于註射後第5天和第3天達到最低,第21天恢複到正常水平;註射鬆節油後第1至14天,TRPV1錶達的細胞數量增加,併于第7天達到最大,第21天恢複到正常水平.正常大鼠TRPV1主要錶達于TG的中小神經元,觸鬚部皮膚以及三扠神經尾側亞覈含豐富的TRPV1暘性末梢;麵部炎癥痛後2週內,TG的中小神經元,觸鬚部皮膚末梢以及Vc的Ⅰ和Ⅱ外層均可見明顯的TRPV1錶達增加.結論 麵部炎癥痛可以引起大鼠對傷害性熱刺激和冷刺激的痛覺過敏,併導緻三扠神經節中TRPV1暘性神經元和外週與中樞暘性神經纖維末梢數目增加,錶明TRPV1在三扠神經節的中小神經元和末梢軸突錶型的改變可能對鬆節油引起麵部炎癥痛時熱痛覺過敏和冷痛覺感受的形成與維持起重要作用.
목적 탐토랄초소수체(transient receptor potential vanilloid receptor 1,TRPV1)삼여화면부염증통상관적열통각과민여랭통각감수적가능궤제.방법 우대서면부피하주사송절유조성면부염증통모형,분별응용열측통화랭측통장치측량열축두잠복기(head withdrawal thermal latency,HWTL)화랭축두잠복기(head withdrawal cold lentency,HWCL)적변화,매천측량일차,련속21천.응용면역조직화학염색,세포대소빈솔분석화평균광밀도치분석래연구면부염증통후제3、5、7、14、21천지배대서면부표피구삼차신경절(trigeminal ganglion,TG)초급감각신경원、촉수부피부말소신경섬유화투사지삼차신경감각미측아핵(trigeminal sensory nuclei caudalis,Vc)중추돌TRPV1표체적개변.결과 주사송절유후제1지14천,열퇴축반응잠복기여랭퇴축반응잠복기균명현하강,분별우주사후제5천화제3천체도최저,제21천회복도정상수평;주사송절유후제1지14천,TRPV1표체적세포수량증가,병우제7천체도최대,제21천회복도정상수평.정상대서TRPV1주요표체우TG적중소신경원,촉수부피부이급삼차신경미측아핵함봉부적TRPV1양성말소;면부염증통후2주내,TG적중소신경원,촉수부피부말소이급Vc적Ⅰ화Ⅱ외층균가견명현적TRPV1표체증가.결론 면부염증통가이인기대서대상해성열자격화랭자격적통각과민,병도치삼차신경절중TRPV1양성신경원화외주여중추양성신경섬유말소수목증가,표명TRPV1재삼차신경절적중소신경원화말소축돌표형적개변가능대송절유인기면부염증통시열통각과민화랭통각감수적형성여유지기중요작용.
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 TRPVl-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 TRPV 1 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.