论文部分内容阅读
应用细胞外记录单位放电技术，在大鼠海马脑片上观察了左旋精氨酸（L－arg）、N-硝基左旋精氨酸（L－NNA）、SIN-1、及亚甲基蓝（methyleneblue，MB）对CAI区神经元自发放电的影响，旨在了解在旋精氨酸：NO通路在海马放电中的作用及其可能的机制。实验结果如下：（1）用L－arg（1mmol／L）灌流海马脑片2min，在54个放电单位中有42个单位（77．8％）放电频率降低，12个单位（22．2％）无明显反应。用L－NNA（0．15mmol／L）薄流海马脑片2min，在29个放电单位中有25个单位（86.2％）放电频率增加，4个单位（13．8％）无明显变化。L－NNA的作用可被预先灌流L－Arg而逆转。（2）给予一氧化氮（NO）供体SIN－1（5mmol／L）；25个单位（100％）放电频率均明显减少，是明显的剂量依赖性。（3）给脑片灌流鸟苷酸环化酶抑制剂亚甲基蓝（3μmol／L）30min后，10个单位的平均放电频率较对照时明显增加，但亚甲基蓝不能消除L－arg对海马神经元的作用。综合上述结果，似可以认为，静息的海马有基础性NO释放，NO可抑制海马的放电活动，其作用似不通过鸟着酸环化酶介导。
L-arginine, L-NNA, SIN-1 and methyleneblue (MB) were observed in rat hippocampal slices using extracellular recording unit discharge technique. ) On spontaneous firing of neurons in the CAI region to understand the role of the arginine-NO pathway in hippocampal discharge and its possible mechanism. The experimental results are as follows: (1) The perfusion of hippocampal slices by L-arginine (1 mmol / L) for 2 min reduced the discharge frequency of 42 units (77.8%) in 54 discharge units and 12 units (22.2% No significant reaction. The discharge frequency of 25 units (86.2%) of 29 discharge units increased at 4 min (13.8%) with 2 min of thin-flow hippocampal slices of L-NNA (0.15 mmol / L) The effect of L-NNA can be reversed by pre-perfusing L-Arg. (2) Nitric oxide (NO) donor SIN-1 (5 mmol / L) was given at 25 units (100%). The frequency of discharge was significantly reduced, which was obviously dose-dependent. (3) The average discharge frequency of 10 units increased obviously after perfusing the guanosine cyclase inhibitor methylene blue (3μmol / L) for 30min, but methylene blue could not eliminate the effect of L-arg on hippocampal neurons . Based on the above results, we can think that resting hippocampal NO release, NO can inhibit the discharge activity of the hippocampus, its role is not mediated by avian acid cyclase.