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我们以往的研究表明,脑缺血再灌流后细胞膜兴奋性降低可能是海马CA1区锥体细胞迟发性死亡的机制之一,而膜兴奋性降低与钾通道活动增强密切相关.因此,本实验研究了钾通道阻断剂TEA对短暂性前脑缺血后海马CA1区锥体细胞死亡的影响,以期探讨钾通道在神经元迟发性死亡中的作用.成年雄性Wistar大鼠(200～250g)随机分为6组:(1)正常对照组,(2)缺血组,(3)1.25mM TEA组,(4)2.5mM TEA组,(5)5mM TEA组,(6)生理盐水对照组.实验采用改良的四血管闭塞法制作15分钟前脑缺血模型.再灌注30分钟后,经侧脑室分别给子5ul生理盐水或TEA溶液(终浓度分别为1.25mM、2.5mM、5mM),每日1次,连续7天.常规病理石蜡切片(片厚5um),光镜下计数CA1区存活的锥体细胞密度(个/mm).结果:正常对照组:192±12(n=10);缺血组:7±2(n=10);生理盐水对照组:21±7(n=8);1.25mM TEA组:20±3(n=10);2.5mM TEA组:69±13(n=8);5mM TEA组:61±14(n=4).经统计,2.5mM TEA组、5mM TEA组与缺血组及生理盐水对照
Our previous studies showed that the decrease of cell membrane excitability after cerebral ischemia and reperfusion may be one of the mechanisms of delayed apoptosis of pyramidal cells in hippocampal CA1 region and the decrease of membrane excitability is closely related to the increase of potassium channel activity.Therefore, To investigate the effect of potassium channel blocker TEA on pyramidal cell death in hippocampal CA1 region after transient forebrain ischemia in order to explore the role of potassium channel in neuronal delayed death.Animal male Wistar rats (200 ~ 250g ) Were randomly divided into 6 groups: (1) normal control group, (2) ischemic group, (3) 1.25mM TEA group, (4) 2.5mM TEA group, (5) 5mM TEA group, Group.The model of 15-minute forebrain ischemia was made by modified four-vessel occlusion method.After 30 minutes of reperfusion, sub-5ul normal saline or TEA solution (1.25mM, 2.5mM, 5mM, respectively) , Once a day for 7 consecutive days.The routine pathological paraffin section (thickness 5um) was counted under the light microscope for the number of pyramidal cells that survived in CA1 area.Results: The normal control group was 192 ± 12 (n = 10); ischemic group: 7 ± 2 (n = 10); saline control group: 21 ± 7 (n = 8); 1.25 mM TEA group: 20 ± 3 ± 13 (n = 8); 5mM TEA group: 61 ± 14 (n = 4) .According to statistics , 2.5mM TEA group, 5mM TEA group and ischemic group and saline control