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作 者:罗其中[1] 张佳梦[1] 郭辉[1] 邱永明[1]
机构地区:[1]上海第二医科大学附属仁济医院神经外科,200001
出 处:《上海交通大学学报(医学版)》1999年第S1期22-25,共4页Journal of Shanghai Jiao tong University:Medical Science
基 金:卫生部科研基金!962287
摘 要:目的探讨脑缺血引起组织学改变以前,海马神经元功能的变化及其机制。方法通过胸部挤压造成窒息建立全脑缺血大鼠模型,Cr6SylViolet染色观察不同时相神经元的病理形态变化,电生理记录海马CA1区突触传导的兴奋性和抑制性功能变化,以及NO合酶抑制剂L-NNA对它们的影响。结并脑缺血24h,海马CAI神经元形态病理变化少于20%,3d后>90%;群峰电位和兴奋性突触后电位的幅度明显降低(P<0.05);小剂量(0.12mg/kg)多次应用L-NNA可改善海马CAI区神经元和突触的电活动,但不能完全逆转。结论海马神经元在缺血后出现形态病理变化之前,电生理功能已经降低;NO参与缺血后损伤过程,但并非唯一机制;L-NNA能改善突触的电活动,可能是部分阻断了NMDA受体介导的谷氨酸的细胞毒性,影响了NO合酶依赖性钙调节蛋白的活动。Objecti We We examined the altered function and electrophysiologic featureof the rat hippocapal CA1 neurons after early cerebral ischemia, and discussed theunderlying mechanism. Methods Cerebral ischemia was induced by cardiac arrest;pathomorphologic changes were observed by cresyl violet stain at 6h, 24h, 3d afterreperfusion; for assessing the excitory of inhibitory abilities of synaptic transmission andeffect of NO inhibitor L- NNA on them, electrophysiologic recording was taken. ResuItsWithin 24h after the insult, the number of hippocampal CA1 neurons showing pathomorpho-logic damage were smaller than 6%, and more than 90% after 3d. Amplitudes of somaticpopulation spike(PS) and dendritic field EPSP showed substantial changes (P<0.05).Administration of L - NNA at a low dose (0.12mg/kg) could promote PS and EPSP recoverypartly, but not completely. ConcI'sio' Decrease in electrophysiologic activities precededmorphoIogic deterioration in the postischemic CAl neurons; NO was involved in the processof injuring neurons, but was not the only mechanism; L- NNA could improve synaptictransmission recovery partly, probably from blocking NMDA receptor - mediated activationof calmodulin - dependent nitric oxide(NO) synthese to f0rm NO from L- arginine, andreduced neuronal injury induced by Ca2+ over influx.
分 类 号:R743[医药卫生—神经病学与精神病学]
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