一氧化氮在大鼠海马脑片长时程增强效应中的作用  

Study of NO effects on long-term potentiation in hippocampal slices in rats

作　　者：胡志安[1] 罗东明[1] 刘祚周 

机构地区：[1]第三军医大学基础部生理学教研室

出　　处：《第三军医大学学报》1995年第4期296-300,共5页Journal of Third Military Medical University

基　　金：全军"八五"攻关项目

摘　　要：在大鼠海马脑片上，观察了一氧化氮（ＮＯ）对不同的条件刺激（ＣＳ）诱出的海马Ｓｃｈａｆｆｅｒ侧支一ＣＡ１区锥体细胞通路上的长时程突触传递长时程增强（ＬＴＰ）效应的影响。两种条件刺激方式（Ａ方式：二轮１００Ｈｚ、１００个脉冲、最大刺激强度、两轮间隔６０ｓ；Ｂ方式：一轮１００Ｈｚ、１００个脉冲，６０％的最大刺激强度）诱出的ＬＴＰ无显著差别；一氧化氮合成酶抑制剂ＮＧ－硝基－精氨酸（Ｌ－Ｎｏ－Ａｒｇ１００μｍｏｌ／Ｌ）显著地抑制两种方式的条件刺激诱出ＬＴＰ，该抑制作用能被ＮＯ的前体Ｌ－精氨酸翻转；通过耗竭胞外的ＮＯ，血红蛋白使ＬＴＰ发生受到阻滞；ＮＯ产生剂硝普钠灌流后，在测试刺激条件下，突触传递出现压抑。上述结果表明：内源性ＮＯ为海马ＬＴＰ所必需。The effects of nitric oxide(NO)on the long-term potentiation(LTP)of CA1 area evoked with 2 differently conditioning stimulations (CS) were investigated on the hippocampal slices of rats. Pattern ACS was composed of 2 times of l00 Hz 100 pulses were given with a minute interval at maximal intensity and pattern B CS was composed of one time of 100 Hz l00 pulses at 60% of maximal intensity. LTP evoked with 2 patterns of CS showed no significant difference. Administration of L-No-Arg (100 nmol/L),a NO synthase inhibitor,blocked the production of LTP when pattern A or pattern B CS was used.This blockage was abolished by L-arginine( 1 mmol/L ),a NO precursor,or hemoglobin(100 nmol/L),a NO scanvenger. Meanwhile,the LTP evoked was remarkably attenuated. After exposure of the hippocamplal slices to nitroprusside(1 mmol/L), field EPSP was suppressed.These findings suggest that NO is responsible for the production of LTP and acts as an important messenger. However,exogenous NO can suppress the efficiency of snaptic transmission in certain conditions.

关 键 词：一氧化氮 血红蛋白 记忆 海马 大鼠 

分 类 号：R338.64[医药卫生—人体生理学]