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

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0～30min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6～72h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。

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.