家族性肌萎缩侧索硬化模型SOD1^(G93A)转基因鼠学习、记忆功能研究

Learning and memory dysfunction in the SOD1^(G93A) transgenic mouse model of familial amyotrophic lateral sclerosis

目的了解SOD1G93A转基因鼠的学习、记忆功能。方法采用跳台试验及免疫组化方法,对30只SOD1G93A转基因鼠及30只同窝阴性对照小鼠进行研究比较。结果 60天、90天及120天SOD1G93A转基因鼠的记忆潜伏时间分别为68.00±47.16s、55.20±92.99s和110.10±116.52s,对照组分别为65.60±89.94s、158.00±88.31s和169.80±122.96s,5min内记忆错误次数分别为3.40±2.84次、5.20±3.08次和1.80±1.32次,对照组分别为3.30±2.16次、2.30±1.95次和2.00±2.75次,两者均有显著性差异。免疫组化可见SOD1G93A转基因鼠海马CA1、CA3及齿状回区泛素化蛋白的胞质内异常聚集,且阳性神经元比率较对照组有显著性差异(P<0.05)。结论 SOD1G93A转基因鼠存在空间辨别记忆功能受损,且可能与海马区泛素化蛋白异常聚集有关。

Objective To investigate the learning and memory function in the SOD1G93A transgenic mouse.Methods 30 transgenic mouse and 30 controls were tested with step down test and immunohistochemistry.Results The memory action time of the 60 days,90 days,and 120 days SOD1G93A transgenic mouse are 68.00±47.16s,55.20±92.99s and 110.10±116.52s,and respectively the memory errors frequency in 5 minutes are 3.40±2.84 times,5.20±3.08 times and 1.80±1.32 times,respectively.Both have statistical significance comparing to the negative controls（P0.05）.Immunohistochemistry finds ubiquitinpositive protein aggregated abnormally in neurons cytoplasmic in CA1,CA3 and dentate gyrus of hippocampus.Conclusions SOD1G93A transgenic mouse＇ identify memory was damaged at presymptomatic stage.And ubiquitinpositive protein aggregated in neuronal cytoplasm of hippocampus abnormally maybe correlated with the memory ability impairment.