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目的探讨缺氧缺血性脑病新生大鼠发育期间海马神经元的变化与康复之间的关系。方法采用7日龄Wistar仔鼠,实验组制作缺氧缺血性脑病模型。采用形态学和形态计量学、突触体素免疫组织化学及学习记忆能力测试的方法,对生后7d到2个月,分8个时段对海马CA1区细胞形态及免疫反应阳性物质进行动态观察,对4周和2个月仔鼠进行学习记忆能力测试。结果随增龄对照组大鼠CA1区神经元数量有所减少,但突触体素阳性反应物吸光度值相对升高。实验组CA1区细胞质量明显降低,伴学习记忆能力降低,但与上一实验组比较,随增龄突触体素阳性反应物吸光度值升高(7d与72h比较t=2.012,P<0.05;2周与7d比较t=2.014,P<0.05;3周与2周比较,t=2.716,P<0.01;4周与3周比较,t=2.011,P<0.05)。结论海马区细胞减少、轴突溃变、突触损失是神经功能障碍的病理基础。早期干预可提高神经元的质量,促进神经系统功能发育。
Objective To investigate the relationship between the changes of hippocampal neurons and rehabilitation during the development of neonatal rats with hypoxic-ischemic encephalopathy. Methods 7-day-old Wistar rats were used in the experimental group to make a model of hypoxic-ischemic encephalopathy. Morphological and morphometric methods, synaptophysin immunohistochemistry and learning and memory ability test methods, 7d to 2 months after birth, 8 sub-periods of hippocampal CA1 cell morphology and immunoreactive substances were observed dynamically , 4 weeks and 2 months pupil learning and memory test. Results Compared with the control group, the number of neurons in CA1 area decreased, but the absorbance of synaptophysin-positive reaction increased. Compared with the previous experimental group, the absorbance value of neurons in CA1 region of experimental group decreased significantly (P <0.05) at 7d and 72h, T = 2.014, P <0.05 for 2 weeks and 7 days; t = 2.716 for 3 weeks vs 2 weeks, P <0.01; t = 2.011 for 4 weeks and 3 weeks; Conclusions Decreased cells, axon degeneration and synaptic loss in the hippocampus are the pathological basis of neurological dysfunction. Early intervention can improve the quality of neurons and promote the development of nervous system function.