慢性激活MrgC受体上调CGRP表达的nNOS机制  

The Mechanism of Up-Regulation of CGRP on MrgC in Cultured Dorsal Root Ganglia of Rats

作　　者：王冬梅[1] 戴飞红[1] 洪炎国[1] 周小龙[1] 阮丽钦[1] 

机构地区：[1]福建师范大学生命科学学院,福建省发育与神经生物学重点实验室,福建福州350108

出　　处：《现代生物医学进展》2014年第2期214-216,222,共4页Progress in Modern Biomedicine

基　　金：国家自然科学基金项目(30970985)

摘　　要：目的:检查持续应用BAM8-22对体外组织培养感觉神经节合成钙调素基因相关肽(CGRP)的影响。方法:将体外培养的大鼠三叉神经节和背根神经节经BAM8-22和L-NAME处理后,用酶联免疫法测定CGRP的表达含量变化。结果:与对照组相比,连续4天给予SNSR的选择性激动剂BAM8-22,CGRP的合成会增加。联合给予BAM8-22和NOS的非选择性抑制剂L-NAME,CGRP的表达随不同剂量的L-NAME引起不同程度的上调。结论:持续激活SNSR能使感觉神经节合成CGRP增多,是在体动物慢性激活SNSR后吗啡镇痛作用降低的细胞学机制。Objective： To investigate the effect of chronic BAM8-22 treatment on the expression of calmodulin gene related with peptide （ CGRP ） in cultured sensory ganglion. Methods： DRG and TG tissue of rats were cultured in vitro after BAM8-22 and L-NAME treatment. The changes of CGRP content was detected by enzyme linked immunosorbent assay. Results： Compared with the control group, the expression of CGRP increased after the consecutive treatment of selective SNSR agonist （BAM8-22） for 4 days. Combined that treated with L-NAME （a non-selective nitricoxide synthesis inhibitor）, the expression of CGRP was up-regulated differently with different doses of L-NAME. Conclusion： Chronic activation of SNSR resulted in the enhanced expression of CGRP, it may be the cellular mechanism for reducing the analgesic effect of morphine after continuous activation of SNSR.

关 键 词：MrgC受体(SNSR) 背根神经节 降钙素基因相关肽 一氧化氮合酶 

分 类 号：Q95-3[生物学—动物学] Q42