液压打击诱导外伤后癫痫大鼠海马病理改变的初步探索

Primary study of the histopathological changes of hippocampus in the PTE rats induced by lateral fluid percussion

目的通过外侧液压打击损伤诱导大鼠外伤后癫痫,初步比较外伤后癫痫大鼠的海马与人类外伤后癫痫的海马之间的病理改变。方法通过随机数字表将32只雄性SD大鼠分为A、B两组,A组为开颅+打击+安电极组(16只)、B组为对照开颅+安电极组(16只)。对A组大鼠行重度外侧液压打击,所有存活大鼠通过视频脑电分别记录早期发作和晚期发作的表现、频率及持续时间。于第6个月,从A、B组大鼠中随机取4只,处死行硫素染色,光镜下观察海马的改变;于第11个月,对A、B组剩余大鼠处死行硫素染色,光镜下观察海马的改变。结果 A组共存活的9只大鼠,第6个月时癫痫发作共5只(55.56%),随机处死的4只大鼠均出现海马形态改变,视频脑电监测结果显示有2只癫痫发作大鼠并出现海马神经细胞缺失;第11个月时,A组剩下的5只大鼠视频脑电监测结果显示均有癫痫发作,病理表现海马形态改变、海马神经细胞缺失;而B组所有大鼠均存活,第6个月及第11个月时相应地均未见海马病理改变。结论外伤后癫痫大鼠出现损伤同侧海马神经细胞缺失,类似于人类外伤后癫痫的海马病理改变之一,为探究人类外伤后癫痫的发病机制提供了研究基础。

Objective To compare the histopathological changes of hippocampus between PTE humans and PTE rats induced by lateral fluid percussion injury. Methods Thirty--two a- dult male Sprague--Dawley rats were randomized into group A, and B. In group A, sixteen rats re- ceived craniotomy, LFPI and electrode implantation. In group B, sixteen rats received craniotomy and electrode implantation. Severe LFPI was performed in group A. Behavioral features, frequency and duration of early and late seizures were recorded in group A,and B. On the 6th month,4 rats in group A and 4 rats in group B were randomly selected, and then their rats were perfused for histology after finishing one week video--EEG monitoring. The sections were stained for Thi- onin. On the llth month, the remained rats in group A, and B were perfused for histology after finishing one week video--EEG monitoring. Results 9 rats were alive in group A, on the 6th month,5 rats （55.56%） were monitored seizure all the 4 killed rats were observed the morpho- logical changes of hippocampus,including two PTE rats with hippocampal cell loss. On the llth month,all the five rats were observed PTE with hippocampal cell loss. No morphological changes of hippocarnpus were observed in group B on the 6th and llth month. Conclusion Hippocampal cell loss was observed in the ipsilateral injury site in the PTE rats,which was similar with human PTE. This research provided the basis for the study of the pathogenesis of human PTE.