[脑缺血再灌注小鼠海马齿状回神经兴奋性分析]。

Q4 Medicine
Yucan Zhu, Hongli Yu, Xiuzhi Zhao, Chunfang Wang
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引用次数: 0

摘要

缺血性脑卒中通常会导致认知功能障碍,从而延缓患者的康复进程。然而,其发病机制尚不明确。本研究以脑缺血再灌注模型为实验对象,以海马齿状回(DG)为目标脑区。通过TTC染色评估脑梗死程度,收集神经细胞膜电位和局部场电位(LFPs)信号,探讨缺血再灌注小鼠认知功能障碍的机制。结果显示,模型组小鼠右侧脑梗死区呈白色。模型组小鼠海马DG神经细胞的静息膜电位、动作电位放电次数、超极化后电位和最大上升斜率显著低于对照组(P<0.01);动作电位的峰值时间、半波宽度、阈值和最大下降斜率显著高于对照组(P<0.01)。缺血组和再灌注组小鼠LFPs信号θ和γ波段的时频能量值明显降低(P<0.01),再灌注组的时频能量值较缺血组升高(P<0.01)。缺血组和再灌注组的LFP信号复杂度明显降低(P<0.05),再灌注组的信号复杂度比缺血组增加(P<0.05)。综上所述,脑缺血再灌注降低了小鼠海马DG区神经细胞的兴奋性;脑缺血降低了神经细胞的放电活性和信号复杂性,再灌注后电生理指标有所恢复,但在实验期间未能达到健康状态。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[Analysis of nerve excitability in the dentate gyrus of the hippocampus in cerebral ischaemia-reperfusion mice].

Ischemic stroke often leads to cognitive dysfunction, which delays the recovery process of patients. However, its pathogenesis is not yet clear. In this study, the cerebral ischemia-reperfusion model was built as the experimental object, and the hippocampal dentate gyrus (DG) was the target brain area. TTC staining was used to evaluate the degree of cerebral infarction, and nerve cell membrane potentials and local field potentials (LFPs) signals were collected to explore the mechanism of cognitive impairment in ischemia-reperfusion mice. The results showed that the infarcted area on the right side of the brain of the mice in the model group was white. The resting membrane potential, the number of action potential discharges, the post-hyperpolarization potential and the maximum ascending slope of the hippocampal DG nerve cells in the model mice were significantly lower than those in the control group ( P < 0.01); the peak time, half-wave width, threshold and maximum descending slope of the action potential were significantly higher than those in the control group ( P < 0.01). The time-frequency energy values of LFPs signals in the θ and γ bands of mice in the ischemia and reperfusion groups were significantly reduced ( P < 0.01), and the time-frequency energy values in the reperfusion group were increased compared with the ischemia group ( P < 0.01). The signal complexity of LFPs in the ischemia and reperfusion group was significantly reduced ( P < 0.05), and the signal complexity in the reperfusion group was increased compared with the ischemia group ( P < 0.05). In summary, cerebral ischemia-reperfusion reduced the excitability of nerve cells in the DG area of the mouse hippocampus; cerebral ischemia reduced the discharge activity and signal complexity of nerve cells, and the electrophysiological indicators recovered after reperfusion, but it failed to reach the healthy state during the experiment period.

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来源期刊
生物医学工程学杂志
生物医学工程学杂志 Medicine-Medicine (all)
CiteScore
0.80
自引率
0.00%
发文量
4868
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