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本实验试图进一步探讨经长期存活后，脑缺血及不全脑缺血大鼠海马的可塑性变化，并验证它们之间的关系。脑缺血模型采用pulsinelli四血管结扎及其改变法，苔藓纤维显示采用Timm染色法．结果显示，大鼠脑缺血20muin、再存活90d后，海马CAI区细胞几乎全部丧失，CA2／CA3也出现严重的细胞消亡，CAI区明显萎缩，多数伴有苔藓纤维的侧枝抽芽，同期不全脑缺血大鼠海马未见或仅见局限于CAI的部分细胞丢失，齿状回或CA3区也伴有苔藓纤维抽芽．提示脑缺血经长期存活后引起的苔藓纤维的侧枝抽芽并不依赖于CAI区的细胞死亡．
This experiment attempts to further explore the changes of hippocampal plasticity after long-term survival in rats with cerebral ischemia and incomplete ischemia, and to verify the relationship between them. Cerebral ischemia model was pulsinelli four-vessel ligation and its change method, moss fiber showed Timm staining method. The results showed that after the cerebral ischemia of 20muin and the survival of 90d, almost all of the cells were lost in CA1 area of hippocampus, and the cells died of CA2 / CA3. The area of CAI was obviously atrophied. Most of the cells were accompanied by mossy fiber collateral buds, No or only part of the cells confined to CAI were lost in the hippocampus of ischemic rats. Mossy fiber buds were also found in the dentate gyrus or CA3 area. Suggesting that long-term survival of cerebral ischemia caused mossy fiber collateral sprouting does not depend on cell death in the CAI area.