大鼠尾核内一氧化氮在痛觉调制中作用机制的研究

THE INVOLVEMENT OF NITRIC OXIDE IN PAIN MODULATION IN RAT CAUDATE NUCLEUS

摘要:

目的：研究尾核中一氧化氮（NO）在痛觉调制中的作用及其作用机制.方法：以钾离子透入引起大鼠甩尾的电流强度（mA）作为痛反应指标,尾核内微量注射L-精氨酸（L-Arg）、NG-硝基-L-精氨酸甲酯（L-NAME）、亚甲基蓝（MB）等,观察0～30 min内大鼠痛阈的变化.放射免疫方法测定血液和脑组织中cGMP含量的变化,以免疫组织化学结合计算机图像分析的方法观察给药后6～72 h内nNOS表达的变化.结果：大鼠尾核内微量注射NO前体L-Arg引起明显的痛敏效应,血和脑中cGMP的含量明显升高,nNOS阳性神经元L-Arg组较正常表达增强;微量注射L-NAME和MB后大鼠痛阈显著升高,MB组大鼠血和脑中cGMP含量显著降低,L-NAME,MB组nNOS阳性神经元表达较正常减弱.结论：尾核内NO参与痛觉信息的传递,其作用机制可能是通过NO-cGMP途径实现的.

Abstract:

Objective:To investigate the involvement of nitric oxide (NO) in pain modulation in the rat caudate nucleus. Methods:The potassium iontophoresis induced tail-flick was used to measure the pain threshold (PT). The changes of PT were oberved after micro injection of L-arginine (L-Arg), N (omega)-nitro-L-arginine methyl ester (L-NAME) and methylene blue (MB) into caudate nucleus. cGMP level in blood and brain was measured by radio-immunity. The changes of nNOS expression was examined by immunohistochemistry and computer graphic analysis. Results:The significant hyperalgesic effects were observed by microinjection L-Arg into caudate nucleus. The PT of rats was increased significantly by L-NAME and MB. The cGMP in blood and brain was increased significantly by L-Arg but decreased significantly by MB. The expression of nNOS was increased by L-Arg but decreased by L-NAME and MB.Conclusion: NO in the caudate nucleus could be involved in the transmission of nociceptive injormation. The mechanism may be partially mediated by NO-cGMP pathway.