缺氧缺血性脑损伤对大鼠学习记忆的慢性进行性影响及可能机制

目的 探讨缺氧缺血性脑损伤（HIBD）对新生大鼠学习记忆行为功能的长期持续性影响及其可能机制。方法 按Rcie法制作HIBD新生动物模型，共计24只，同时设假手术对照组24只，分别在日龄4周、8周、12周各取8只，用Morris水迷宫检测学习记忆能力，免疫组化和图像分析技术观察海马CA1区突触素（p38）表达的变化。结果 缺氧缺血后4周、8周、12周学习记忆能力呈进行性下降趋势。海马CA1区神经元数目进行性减少，突触素免疫活性逐渐降低，模型组与同龄对照组比较以及模型组各时间点比较均有显著统计学意义（P〈0．05）。结论 新生鼠缺氧缺血可导致学习记忆功能长期慢性进行性的损害。海马神经元进行性减少、突触素表达进行性下降是其可能机制之一。

Slowly progressive effects of hypoxic-ischemic brain damage in neonatal rats on learning and memory and its possible mechanism

Objective To investigate the slowly progressive effects of hypoxic ischemic brain damage in neonatal rats on learning and memory and and its possible mechanism.Methods The animal model of HIBD was made by the method of Rice with 24 Sprague-Dawley rats.The sham-operation rats were served as normal control group.We observated changes after 4,8 and 12 weeks of recovery following the HI insult.The learning and memory abilities were measured by test of morris water maze.The expression of synaptophysins was estimated immunohistochemically in paraffin sections of hippocampal formation.Results The spatial learning and memory impairments in the morris water maze and the loss of neuron in hippocampal CA1 districts of rats progressed from 4 up to 12 weeks of recovery.The corrected optical densities of immunoreactive products of the hippocampus CA1 district were significantly decreased and severely progressed from 4 up to 12 weeks of recovery(P<0.05).Conclusion Hypoxia-ischemic insult in neonatal rats induced slowly progressive brain damage related to learning and memory imparment,which maybe associated with the reduction of synaptophysin and neuron in hippocampal formation.