摘要
目的探讨双(7)-他克林(B7T)对持续性低血流灌注脑缺血老年大鼠学习记忆损害及海马胶质细胞可塑性的干预作用。方法雄性SD大鼠30只,随机分为缺血组、对照组和干预组,每组10只。Morris水迷宫实验评估大鼠学习记忆功能,免疫组织化学染色及图像分析技术检测海马CA1区胶质细胞的数量、胞质突起长度等可塑性变化。结果缺血组海马CA1区锥体细胞排列稀疏紊乱,凋亡多见;对照组和干预组锥体细胞排列整齐而密集,凋亡细胞少见。缺血组海马CA1区胶质细胞酸性蛋白(GFAP)阳性细胞和胞质突起长度明显少于对照组和干预组。缺血组逃逸时间明显多于对照组和干预组;缺血组在平台象限停留时间和跨越平台区域的次数明显少于对照组和干预组(P<0.05.P<0.01)。缺血组、对照组及干预组海马CA1区GFAP阳性细胞的数量、胞质突起长度与空间记忆改善呈正相关。结论 B7T可通过促进海马胶质细胞的可塑性改变,改善慢性脑缺血所致的学习记忆认知障碍。胶质细胞的可塑性变化是学习记忆功能改善的重要病理修复机制。
Objective To explore the treatment effects of bis(7)-tactrine(B7T) on hippocampal gliacyte plasticity and cognitive handicap in aged rats with chronic cerebral hypoperfusion. Methods Thirty male SD rats were randomly divided into ischemic model, control and B7T-treated groups,each group had 10 rats. Spatial learning and memory were assessed by Morris water maze test,immunohistochemistry and image analysis were employed to detect the number and cytoplas- mic process length of GFAP positive cells in hippocampal CA1 region. Results The pyramidal cells in hippocampal CA1 region of ischemic model group arranged sparser and more indiscrimi- nate, compared with control group and B7T-treated group. More apoptotic cells were observed in the rats of ischemic model group. GFAP positive cells were significantly less and their cytoplasmic process length was shorter in ischemic model group than in control group and B7T-treated group. Escape latency of rats in ischemic model group was longer than that in control group and BTT- treated group. Ischemic model group spent less time in the platform quadrant than control group and B7T-treated group. The number of crossing the platform area in rats of ischemic model group was less than that in control group and B7T-treated group(P〈0.05, P(0.01). Number and the cytoplasmic process length of glia ceils were positively correlated to spatial learning in ischemic model group,control group and B7T-treated group. Conclusion Chronic cerebral hypoperfusion impaired the spatial learning and memory in aged rats, B7T can enhance the congnitive function by promoting g|iacyte plasticity.
出处
《中华老年心脑血管病杂志》
CAS
北大核心
2012年第1期80-82,共3页
Chinese Journal of Geriatric Heart,Brain and Vessel Diseases
基金
武汉市科技计划项目(201051099415-14)
关键词
脑缺血
海马
记忆
受体
N-甲基-D天冬氨酸
认知障碍
神经胶质
干预性研究
brain ischemia
hippocampus
memory
receptors, N-methyl-D-aspartate
cognition dis-orders
neuroglia
intervention studies