海马长时程增强中一氧化氮变化与L型钙通道和神经细胞黏附分子的关系  

Correlation of the changes of nitric oxide production during hippocampal long term potentiation with L-calcium channel and neural cell adhesion molecule

作　　者：陈伯成[1] 胡志安[2] 罗峻[2] 

机构地区：[1]解放军第三军医大学2002级硕士课程班,重庆市400038 [2]解放军第三军医大学基础医学部生理教研室,重庆市400038

出　　处：《中国临床康复》2004年第16期3046-3048,共3页Chinese Journal of Clinical Rehabilitation

基　　金：国家自然科学基金资助项目(39600048;30270443)~~

摘　　要：目的:了解离体海马脑片CA1区突触传递长时程增强(longtermpoten-tiation,LTP)中调控一氧化氮变化的膜信号途径。方法:采用胞外记录方法检测LTP产生和维持。用生化反应方法检测一氧化氮含量和一氧化氮合酶(nitricoxidesynthase,NOS)活性变化。结果:LTP产生后,NOS活性为(2.11±0.21)nkat/g,一氧化氮含量为(10.24±3.1)nmol/g。NMDA受体抑制剂AP-5在抑制LTP产生的同时,也显著阻滞一氧化氮含量和NOS活性升高。同样,L型钙通道阻断剂Diltiazem(30μmol/L)作用下,NOS活性降为(0.41±0.10)nkat/g一氧化氮含量降为(2.0±0.8)nmol/g;神经细胞黏附分子抗体存在条件下,NOS活性降为(0.43±0.09)nkat/g,一氧化氮含量降为(2.0±1.2)nmol/g。结论:膜上NMDA受体、L型钙通道和神经细胞黏附分子共同参与了对LTP中一氧化氮活动的调控。AIM:To explore the membrane signal pathway involved in regulation of nitric o xide(NO) production during hippocampal CA1 long term potentiation(LTP) in vitro. METHODS:LTP production and maintenance were tested with extracelluar electrop hysiological recording.NO content and nitric oxide synthase activity were analys ed with biochemical reaction. RESULTS:After LTP production, the activity of NOS was(2.11±0.21)nkat/g and the content of NO was(102.4±3.1)nmol/g.LTP was blocked and the increase in NO content and NOS activity were prevented by the NMDA receptor inhibitor AP-5,an d similarly,under the influence of L-calcium channel inhibitor diltiazem(30 μm ol/L),the activity of NOS decreased to(0.41±0.10)nkat/g and the content of NO decreased to(2.0±0.8)nmol/g.In the presence of anti-neural cell adhesion mo lecule (NCAM) antibody ,NOS activity and NO content were decreased to(0.43±0.0 9)nkat/g and(2.0±1.2)nmol/g respectively. CONCLUSION:The membrane NMDA receptors,L-type calcium channels and NCAMs con tribute to the regulation of NO activity during LTP.

关 键 词：长时程增强 一氧化氮 神经细胞粘附分子 L型钙通道 

分 类 号：R338[医药卫生—人体生理学]