摘要
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。
Using extracellular recording technique, the effects of L-arginine (L-arg), N-ni-tro-L-arginine (L-NNA), SIN-1 and methylene blue (MB) on spontaneous dischargesof neurons in CA1 area of hippocampal slices were examined to determine the role of Larg: NO pathway and the possible underlying mechanism. The results were as follows:(1) In response to the application of L-arg (1 mmol/L) into the superfusate for 2 min,spontaneous discharge rate (SDR ) of 42/54 (77. 8 % ) neurons was decreased significantly, while that of 12/54 (22. 2 % ) neurons showed no change. Following the application of L-NNA (0. 15 mmol/L) into the superfusate for 2 min, SDR of 25/ 29(86. 2 % ) neurons was increased markedly and that of 4/29 (13. 8 % ) neurons wasn0t affected. The effect of L-NNA might be reversed by pretreatment with L-arg.(2) With application of NO donor SIN-1 (5 mmol/L), SDR of 25 (100% ) neuronswas decreased in a dose-dependent manner. (3) After superfusing the brain slice withguanylate cyc1ase inhibitor, MB (3 Umol/L) for 30 min, SDR of 10 units showed significant increase as compared with control, However, MB failed to abolish the effect ofL-arg on hippocampal neurons. Taken together, it is likely that NO is released duringthe resting state of hippocampal neurons and may inhibit the activity of hippocampus,an effect not mediated by the action of guanylate cyclase.
出处
《生理学报》
CAS
CSCD
北大核心
1997年第4期375-381,共7页
Acta Physiologica Sinica
关键词
一氧化氮
海马脑片
神经元
nitric oxide
hippocampal slices
methylene blue
