丰富环境对缺氧缺血性脑损伤大鼠海马突触超微结构及突触素表达的影响

目的探讨早期丰富环境干预对缺氧缺血性脑损伤(HIBD)新生大鼠海马CA1区神经元突触超微结构和突触素(p38)表达的影响.方法按Rcie法制作HIBD新生动物模型,共计20只,随机分为干预组和非干预组.同时设假手术对照组10只.干预组大鼠于术后第2天开始给予丰富环境刺激,持续20 d.干预结束后用透射电镜观察各组海马CA1区锥体神经元超微结构,免疫组化和图像分析技术检测p38的表达.结果与对照组比较,非干预组海马CA1区锥体细胞见部分核膜消失、线粒体嵴模糊、神经元突触数量减少,突触间隙增宽,突触囊泡减少,突触后致密物变薄;干预组神经元和突触无明显异常.非干预组海马CA1区突出素光密度值明显低于干预组和对照组(P<0.01),而干预组和对照组之间无显著差异(P>0.05).结论阻止或减轻HI后突触超微结构的损伤、促进突触的重建可能是丰富环境发挥作用的物质基础.

Effects of enriched environmental intervention on synaptic ultrastructure and synaptophysin expression in hippocampus of neonatal rats

Objective To observe the effect of early enriched environmental intervention on synaptic ultrastructure and the synaptophysin expression (p38) in hippocampal CA1 area after hypoxia-ischemic brain damage(HIBD) in neonatal rats. Methods The rat model of HIBD was made by the method of Rice in 20 Sprague-Dawley rats, and divided randomly into 2 groups: the intervention group, non-intervention group. Another 10 rats underwent sham-operation as control. From the second day after HIBD, the rats of the intervention group were kept in an enriched environment for 20 d, the rats of non-intervention group and sham-operation group were raised in standard enviroment instead. The hippocampal ultrastructure was observed with electron microscope and the p38 expression was detected immunohistochemically in all rats. Results The ultrastructure of hippocampus CA1 pyramidal neuron in the non-intervention group were distorted as compared with that in the intervention group and control group. The corrected optical densities (COD) of immunoreactive products of the hippocampal p38 were significantly decreased in non-intervention group as compared with intervention group and control group (P<0.01). There were no marked difference of either ultrastructure or immunohistochemically reactived COD of p38 between intervention group and control group (P>0.05). Conclusion Early enriched environment intervention could improve the synaptic reconstruction and reduce the ultrastructural damage induced by hypoxic-ischemia.