电针对缺血性脑损伤大鼠海马齿状回突触传递活动的影响

目的]观察电针对实验性脑缺血大鼠海马齿状回(DG)突触传递活动的影响。方法]Wistar大鼠60只,随机分为 基础组和高频刺激(HFS)组,每组又分为假手术组(手术暴露双侧颈总动脉,但不阻断血流)、脑缺血模型组(丝线牵拉 法阻断双侧颈总动脉)及针刺组(造模并加用电针治疗)。采用在体记录突触传递长时程增强(LTP)的电生理学方法,观 察电针对海马齿状回基础突触活动的影响;高频刺激组动物均在造模后给予HFS诱发LTP,然后观察电针对HFS诱导海马 齿状回LTP的影响。结果]假手术组120min内群峰电位(PS)幅值无明显变化;模型组10min时PS幅值开始下降,与同 时间点假手术组比较具有显著性差异(P<0.01),随后逐渐回升接近假手术组水平;针刺组在造模前、后分别给予电针刺 激,造模后10 min PS幅值未出现明显下降,随后逐渐上升,与同时间点模型组比较均有显著性差异(P<0.05或P< 0.01)。在给予HFS诱导出LTP后,假手术组PS幅值显著增大,并维持3 h无明显减弱;模型组在HFS 30 min后诱发LTP; 针刺组在HFS后30min给予电针刺激,HFS后60min的PS幅值逐渐增高,其中HFS120min和180min的PS幅值与同时间点 模型组比较均有显著性差异(P<0.05或P<0.01)。结论]电针可增强缺血性脑损伤大鼠海马齿状回的基础突触传递活 动和HFS所诱导的LTP。这可

Effect of Electroacupuncture on Synaptic Transmission in Hippocampal Dentate Gyrus of Rats with Cerebral Ischemic Damage

Objective ] To investigate the effect of electroacupuncture ( EA) on synaptic transmission in hippocampal dentate gyrus of rats with cerebral ischemic damage. Methods] Sixty Wistar rats were enrolled into this study. Among them, 30 were given high-frequency stimulation (HFS) and the other 30 were not. Then the HFS rats were randomized into sham-operation group (group A), model group (group B) and acupuncture group (group C); so did the non-HFS rats. Bilateral carotid arteries were exposed but not blocked in Group A, while were blocked by traction with silk thread for modeling in group B. Group C were treated with EA before and after modeling. Effects of EA on synaptic transmission in hippocampal dentate gyrus of non-HFS rats were evaluated with in-vivo long-term potential ( LTP) recorded by electrophysiological technique. Effects of EA on LTP in hippocampal dentate gyrus of HFS rats were observed after LTP was induced by HFS. Results] In non-HFS rats, no significant changes of magnitude of population spike (PS) occurred within 120 min in group A; magnitude of PS in group B decreased at 10th min after modeling ( P < 0.01 compared with group A) and then ascended to that of group A; magnitude of PS in group C showed no obvious decrease at 10th min after modeling but began to increase after 10 min ( P < 0.05 or P < 0.01 compared with group B). In HFS rats, magnitude of PS increased and maintained high level for 3 hours in group A after the occurrence of LTP induced by HFS; LTP occurred in group B 30 min after HFS; given EA 30 min after HFS, magnitude of PS in group C began to increase at 60 min after HFS, and it differed from that of group B at 120th min and 180th min after HFS ( P < 0.05 or P < 0.01) . Conclusion] EA promotes the synaptic transmission in hippocampal dentate gyrus of non-HFS rats and increases LTP after HFS, which may be one of the therapeutic mechanisms of EA for cerebral ischemia.