目的　研究一叶碱对麻醉大鼠突触可塑性形成中一氧化氮 (nitricoxide ,NO)的作用。方法　以在体记录突触传递长时程增强 (long termpotentiation ,LTP)的电生理学方法 ,记录大鼠海马齿状回颗粒细胞层群峰电位(populationspike,PS) ;以硝酸还原酶法测定NO含量。结果　在侧脑室给予 0 2nmol·L- 1 一叶碱 (securinine ,5 μL)前给予 1μmol·L- 1 7 硝基吲唑可抑制LTP的诱导。给药前ipL 精氨酸 2 5 0mg·kg- 1 可逆转这种抑制作用。取脑进行NO含量测定 ,与一叶碱对照组相比 ,7 硝基吲唑 +一叶碱给药组的NO含量明显下降。结论　选择性一氧化氮合酶 (nNOS)抑制剂 7 硝基吲唑抑制一叶碱对LTP的诱导 ;由nNOS催化产生的NO参与了一叶碱诱导LTP的过程。 Objective To investigate the effect of aescine on nitric oxide (NO) in the synaptic plasticity of anesthetized rats. Methods Electrophysiological methods were used to record synaptic transmission of long termpotentiation (LTP) in the hippocampus of rat hippocampal dentate gyrus granule cell layer population potential (postspike, PS); nitric acid reductase method for the determination of NO content . Results The intracerebroventricular administration of 0.2 μmol·L-1 securinine (5 μL) before administration of 1 μmol·L-1 7-nitroindazole suppressed the induction of LTP. Pretreatment ipL arginine 250mg · kg-1 reverses this inhibitory effect. The content of NO in brain was determined. Compared with the control group, the content of NO in the 7-nitroindazole + monocrotaline administration group decreased significantly. Conclusion NOS inhibitor 7 nitro-indazole inhibits the induction of LTP by monosodium hydroxide. NO catalyzed by nNOS is involved in the process of LTP induced by folic acid.