脑缺血再灌注小鼠海马齿状回神经兴奋性分析

Analysis of nerve excitability in the dentate gyrus of the hippocampus in cerebral ischaemia-reperfusion mice

缺血性卒中常会引起认知功能障碍,从而延缓了患者的康复进程,然而,其发病机制尚未明确。本文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,TTC染色评估脑梗死程度,采集神经元膜电位和局部场电位(LFPs)信号,旨在探究脑缺血再灌注小鼠认知功能的损伤机制。结果发现,模型组小鼠大脑右侧梗死区呈白色;该模型小鼠海马DG神经元静息膜电位、动作电位放电个数、后超极化电位和最大上升斜率显著低于对照组(P<0.01),动作电位达峰时间、半波宽、阈值和最大下降斜率均显著高于对照组(P<0.01)。缺血和缺血再灌注组小鼠在θ和γ频段的LFPs信号时频能量值显著降低(P<0.01),但缺血再灌注组比缺血组明显提高(P<0.01);缺血及缺血再灌注组的LFPs信号复杂度显著降低(P<0.05),但缺血再灌注组与缺血组相比信号复杂度明显增加(P<0.05)。综上所述,脑缺血再灌注使小鼠海马DG区神经元兴奋性降低;脑缺血使神经元放电活动和信号复杂度降低,经再灌注后电生理指标有所恢复,但实验周期内没能恢复到正常水平。

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 theθandγbands 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.