浙江大学 生物医学工程与仪器科学学院 生物医学工程教育部重点实验室,浙江大学 生物医学工程与仪器科学学院 生物医学工程教育部重点实验室,浙江大学 生物医学工程与仪器科学学院 生物医学工程教育部重点实验室,浙江大学 生物医学工程与仪器科学学院 生物医学工程教育部重点实验室
国家重点基础研究发展规划资助项目(2011CB504400),国家自然科学基金资助项目(30970753)
Zhejiang University, College of Biomedical Engineering and Instrumentation Science, Key Lab of Biomedical Engineering of Ministry of Education,Zhejiang University, College of Biomedical Engineering and Instrumentation Science, Key Lab of Biomedical Engineering of Ministry of Education,Zhejiang University, College of Biomedical Engineering and Instrumentation Science, Key Lab of Biomedical Engineering of Ministry of Education,Zhejiang University, College of Biomedical Engineering and Instrumentation Science, Key Lab of Biomedical Engineering of Ministry of Education
This work was supported by grants from National Basic Research Program of China (2011CB504400) and The National Natural Science Foundation of China (30970753)
全身麻醉若操作不当可能造成致命的中枢神经系统损伤,因此其安全性受到广泛关注.为了揭示麻醉不断加深的过程中神经元活动的变化规律,本文研究了大鼠在乌拉坦(urethane)深度麻醉至脑死亡期间海马区神经元兴奋性和信号传导功能的变化.利用微电极阵列记录和电刺激技术,在海马CA1区胞体层分别记录Schaffer侧支上正向刺激和海马白质上反向刺激诱发的群峰电位(population spike,PS).以PS的幅值和潜伏期为指标,分析海马神经元活动的变化.结果表明,随着乌拉坦血药浓度的增加,PS幅值逐渐减小,潜伏期逐渐延长,意味着乌拉坦抑制了神经元的兴奋性以及轴突传导和突触传递.特别是这些变化存在明显的转折点(即突变),将整个衰减过程分成慢变和快变2个阶段.快变期的剧烈衰减迅速导致脑死亡.而且,引起突变的决定性因素可能是乌拉坦的血药浓度,而非麻醉时间的长短.但是,当乌拉坦注射速率较慢时,延长的慢变期仍然会使神经元功能的受损加重.这些研究结果为动物实验的麻醉操作和临床麻醉的安全应用提供了重要的信息.
Improper usage of general anesthesia may cause fatal damage to the central nervous system. Therefore, its safety becomes a major concern. In order to reveal the changing patterns of neuronal activity during the period of increasing anesthetic depth, the present paper investigated the changes of excitability and signal conduction of neurons in the rat hippocampus during deep anesthesia till brain death with urethane. By using the techniques of microelectrode array recording and electrical stimulation, we recorded population spikes (PS) in the pyramidal layer of hippocampal CA1 region that were evoked either by orthodromic stimulation of the Schaffer collateral or by antidromic stimulation of the alveus. The amplitude and latency of PS were used as indices to evaluate the changes of neuronal activity. The results showed that as the urethane concentration in the plasma increased, the amplitudes of PS decreased and the latencies of PS increased, indicating that the urethane suppressed the neuronal excitability as well as the synaptic transmission and axon conduction. Particularly, there was a turning point that divided the whole decline period of neuronal activity into two distinct stages: slow stage and fast stage. The catastrophic decline of fast stage resulted in brain death rapidly. In addition, the urethane concentration in plasma, rather than the duration of anesthesia, might cause the appearance of turning point. However, the prolonged duration of slow stage caused by slower injection rate of urethane could also induce more damage to neuronal functions. These results provide important information for the safe application of narcotics in both animal experiments and clinic usage.
曹嘉悦,封洲燕,郑晓静,陈白璐.深度麻醉至脑死亡期间大鼠海马神经元活动的突变[J].生物化学与生物物理进展,2014,41(4):379-387
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