Zhu Yucan, Yu Hongli, Zhao Xiuzhi, Wang Chunfang
School of Health Sciences and Biomedical Engineering, Hebei University of Technology, Tianjin 300130, P. R. China.
Tianjin Key Laboratory of Bioelectromagnetic Technology and Intelligent Health, Hebei University of Technology, Tianjin 300130, P. R. China.
Sheng Wu Yi Xue Gong Cheng Xue Za Zhi. 2024 Oct 25;41(5):926-934. doi: 10.7507/1001-5515.202311055.
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 ( < 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 ( < 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 ( < 0.01), and the time-frequency energy values in the reperfusion group were increased compared with the ischemia group ( < 0.01). The signal complexity of LFPs in the ischemia and reperfusion group was significantly reduced ( < 0.05), and the signal complexity in the reperfusion group was increased compared with the ischemia group ( < 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.
缺血性中风常导致认知功能障碍，这会延迟患者的康复进程。然而，其发病机制尚不清楚。在本研究中，以脑缺血再灌注模型作为实验对象，海马齿状回（DG）作为目标脑区。采用TTC染色评估脑梗死程度，并收集神经细胞膜电位和局部场电位（LFP）信号，以探究缺血再灌注小鼠认知障碍的机制。结果显示，模型组小鼠脑右侧梗死区域呈白色。模型小鼠海马DG神经细胞的静息膜电位、动作电位发放次数、超极化后电位及最大上升斜率均显著低于对照组（<0.01）；动作电位的峰值时间、半波宽度、阈值及最大下降斜率均显著高于对照组（<0.01）。缺血再灌注组小鼠θ和γ频段LFP信号的时频能量值显著降低（<0.01），且再灌注组的时频能量值较缺血组有所增加（<0.01）。缺血再灌注组LFP的信号复杂度显著降低（<0.05），且再灌注组的信号复杂度较缺血组有所增加（<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动和信号复杂度，再灌注后电生理指标有所恢复，但在实验期间未恢复至健康状态。
