Department of Neurosurgery, Tongji Hospital, Tongji University, Shanghai 200065, China.
Acta Neurol Belg. 2010 Jun;110(2):180-5.
A new rat model associated with cerebral arteriovenous malformations (AVMs) was developed to study the effect of chronic cerebral hypoperfusion on cognitive function and neuronal plasticity in rats. Aged-matched animals comprised a control group. Three months after surgery, Morris water waze test was performed to evaluate the cognitive function in rats. Neuronal plasticity was assessed by measuring the protein expression of MAP-2, GAP-43 and synaptophysin in the hippocampal regions of rats with immunohistochemistry and western blotting. The average time of escape latency was significantly longer in the model rats than that in the control rats, and both the time spent in the platform quadrant and the frequency of original platform crossing during space probe trials were less than those in the control animals. The expression levels of MAP-2 and synaptophysin protein in hippocampal areas in the model rats were less than those in the control rats. However there was no difference on the GAP-43 expression between the two groups. These data suggest that chronic cerebral hypoperfusion associated with AVMs could lead to cognitive impairment in rats, which may be partially explained by reduced expression of MAP-2 and synaptophysin at the protein level in the hippocampal area.
一种与脑动静脉畸形（AVM）相关的新的大鼠模型被开发出来，用于研究慢性脑灌注不足对大鼠认知功能和神经元可塑性的影响。年龄匹配的动物构成对照组。手术后 3 个月，进行 Morris 水迷宫测试以评估大鼠的认知功能。通过免疫组织化学和 Western blot 测量大鼠海马区 MAP-2、GAP-43 和突触素蛋白的表达来评估神经元可塑性。模型大鼠的逃避潜伏期平均时间明显长于对照组大鼠，空间探测试验中平台象限停留时间和原始平台穿越次数均少于对照组动物。模型大鼠海马区 MAP-2 和突触素蛋白的表达水平低于对照组大鼠。然而，两组之间 GAP-43 表达没有差异。这些数据表明，与 AVM 相关的慢性脑灌注不足可导致大鼠认知障碍，这可能部分解释为海马区 MAP-2 和突触素蛋白表达降低。
