强啡肽对脊髓反射抑制作用的受体机制研究  

Study of the receptor mechanism of dynorphin-induced loss of spinal reflex

作　　者：陈语[1] 李明[1] 侯铁胜[1] 鲁凯伍[1] 倪春鸿[1] 傅强[1] 

机构地区：[1]第二军医大学长海医院骨科,上海200433

出　　处：《中华实验外科杂志》2001年第4期357-358,共2页Chinese Journal of Experimental Surgery

基　　金：上海市科技启明星计划资助项目 (98Q1 4 0 0 6)

摘　　要：目的　研究鞘内注射强啡肽 (Dyn)A( 1～ 13)对脊髓反射抑制作用的受体机制。方法通过大鼠蛛网膜下腔置管后鞘内注射 30nmolDynA( 1～ 13)导致热辐射刺激甩尾反射消失的模型 ,检测在应用DynA( 1～ 13)之前之后鞘内分别注射 5、30、15 0nmolMK 80 1(NMDA受体非竞争性拮抗剂 )对甩尾反射消失的影响。结果　MK 80 1在预先给药时对DynA( 1～ 13)所致大鼠甩尾反射消失有剂量相关的保护作用 ,其中 15 0nmolMK 80 1的保护率达 90 %。在迟后给药时则会产生时间相关的保护作用 ,30、15 0nmolMK 80 1的作用峰值分别在 15、30min。结论　Dyn致大鼠甩尾反射消失作用至少部分是由NMDA受体介导的。Objective To study the receptor mechani sm of loss of spinal reflex induced by intrathecal injection of dynorphinA(1～13 ).Methods A model of loss of tail-flick reflex induced by intrathecal administration of DynA(1～13) was established. The effects on th e loss of tail-flick reflex of 5 nmol, 30 nmol, 150 nmol MK-801 used before or after the administration of Dyn were detected. Results MK-801 administration before Dyn provided dose -dependent protection against loss of the tail-flick reflex. The protection ra te of 150 nmol MK-801 was 90%. While administration after Dyn had a time-depe ndent protection. The peak value of 30 nmol, 150 nmol MK-801 was manifested at 15 min and 30 min, respectively.Conclusion Loss of tail-flick reflex induced by Dyn was mediated, in part, by NMDA receptor.

关 键 词：强啡肽 NMDA受体 甩尾反射 脊髓反射抑制作用 受体机制 

分 类 号：R651.2[医药卫生—外科学]