论文部分内容阅读
用细胞外记录单位放电技术，在大鼠海马脑片上观察了L-精氨酸（L-arg）、N-硝基L-精氨酸（L-NNA）及SIN-1对谷氨酸（glutamate，Glu）诱发的CA1区神经元放电的影响。旨在了解L-精氨酸：NO通路在谷氨酸诱发的海马放电中的作用及其可能的机制。结果如下：（1）用Gln（0.5mmol／L）灌流海马脑片1min，12个放电单位放电频率明显增加，表现为癫痛样放电；（2）预先用含Glu（0．5mmol／L）的人工脑脊液（ACSF）灌流脑片，继而应用L-arg（10mmol／L）灌流海马脑片2min，10个放电单位放电频率均明显降低；（3）预先用含Gln（0．5mmol／L）的ACSF灌流脑片，再用一氧化氮供体SIN－1（5mmol／L）灌流海马脑片1min，12个放电单位放电频率明显减少；（4）在预先用含Glu（0．5mmol／L）的ACSF灌流脑片基础上，应用L-NNA（0．15mmol／L）灌流脑片2min，12个放电单位放电频率均明显增加，并有一些神经元最终突然停止放电。综合上述结果，似可以认为，Glu与海马神经元上的NMDA受体结合后，不仅引发神经元放电明显增加，而且激活L-arg：NO通路而生成NO，再通过负反馈机制对神经元起保护作用。
L-arginine (L-arginine), N-nitro L-arginine (L-NNA) and SIN-1 to glutamic acid glutamate, Glu) -induced neuronal discharge in the CA1 region. It aims to understand the role of L-arginine: NO pathway in glutamate-induced hippocampal discharge and its possible mechanism. The results were as follows: (1) The perfusion of hippocampal slices with Gln (0.5mmol / L) for 1min significantly increased the discharge frequency of 12 discharge units and showed epileptic discharge. (2) (10 mmol / L) perfusion of hippocampal slices for 2 min, the discharge frequency of 10 discharge units were significantly reduced; (3) pre-treated with Gln (0.5 mmol / L) (5mmol / L) for 1min, the discharge frequency of 12 discharge units was significantly reduced. (4) After preincubation with Glu (0.5mmol / L) On the basis of ACSF perfusion brain slices, the discharge frequency of 12 discharge units increased obviously with L-NNA (0.15 mmol / L) for 2 minutes, and some neurons finally stopped discharging suddenly. Based on the above results, it seems to be concluded that the combination of Glu and NMDA receptors on the hippocampal neurons not only induces a significant increase in neuronal discharge, but also activates the L-arg: NO pathway to produce NO, which then acts on the neurons via a negative feedback mechanism Protective effects.