【摘要】 目的　探讨大鼠急性脑梗死后运动功能可塑性的物质基础及其发生机制。方法　用肾性高血压大鼠 (RHR)行大脑中动脉闭塞 (MACO) ,以横木行走试验 (BWT)评定运动功能 ,应用电镜、免疫组织化学观察突触、凋亡细胞、神经丝蛋白 (NF)、微管相关蛋白 2 (MAP2 )、生长相关蛋白 43(GAP43)、突触素 (SYP)等变化。结果　MCAO后大鼠全部偏瘫 ,3周起运动功能明显恢复并逐渐升高 ,TUNEL染色阳性细胞随时间的推移逐渐减少 ,第 9周恢复正常 (第 1周为 74.6个 / 2 0 0倍视野±8 8个 / 2 0 0倍视野 ,第 9周为 2 .6个 / 2 0 0倍视野± 2 .5个 / 2 0 0倍视野 ) ,突触的数目和结构 (突触间隙、活性区长度、突触后膜致密物质厚度等 )也逐渐恢复 (突触数目第 1周为 8.8个 / 80 0 0倍视野± 1.7个/ 80 0 0倍视野 ,第 9周为 15 .3个 / 80 0 0倍视野± 2 .4个 / 80 0 0倍视野 ,正常对照为 12 .3个 / 80 0 0倍视野± 2 .0个 / 80 0 0倍视野 ) ,NF、MAP2 ,以及SYP也有类似过程。GAP43仅在第 1周末增高。结论　急性脑梗死后随着神经细胞凋亡逐渐减少 ,突触数量、功能、结构的相应变化 ,构成了脑梗死后运动功能可塑性的物质基础。神经生长或再生不起主要作用。更多还原

【Abstract】 Objective To investigate the structure basis of motor skill plasticity and the recovery mechanism after acute cerebral infarction. Methods After MCAO, the motor skill of rats was examined via beam walking test; and the neuron, synapse and the distribution of neurofilament (NF), microtubule associated protein 2 (MAP2), growth associated protein 43 (GAP43) and synaptophysin (SYP) were observed by electron scope and immunohistology staining. Results All rats had paralysis after MCAO. The motor skill began to recover significantly at the end of 3 weeks, and kept to improve. The number of injured neuron decreased to normal level at week 9 after an increase resulted from MCAO(1st week: 74.6±8.8/200 field, 9th week: 2.6±2.5/200 field); the number and structure of synapse regained to normal level gradually, at last outstripped the control group (number of synapse, 1st week: 8.8±1.7/8 000 field, 9th week: 15.3±2.4/8 000 field; normal control: 12.3±2.0/8 000 field); So did SYP, NF and MAP2. The GAP43 increased only at week 1. Conclusion With the reduction of apoptosis cell, the relevant changes in the number, function and structure of synapse form the material basis of motor skill’s plasticity together after cerebral infarction. The regeneration of neuron dose not play important role in motor skill recovery.更多还原