摘要
目的建立外伤性癫痫模型,观察症状、脑电图(EEG)和病理改变,探讨病理及致痫机制。方法立体定向注射不同剂量氯化亚铁(FeCl2)于大鼠右侧运动皮层或杏仁体致痫,设立正常对照组、生理盐水对照组。连续30 d行为学评分、EEG记录,HE染色、普鲁士蓝和腾氏蓝反应及Nissl染色行病理学观察。结果 1 000 nmol氯化亚铁皮层注射后平均经过(60±18)s的潜伏期,大鼠EEG表现出多种形式的癫痫样放电波形,大鼠症状及EEG呈典型癫痫变化,该组模型成功率87．5％,其行为学评分与对照组及其他各组之间比较有显著性差异(P<0．01)。氯化亚铁皮层注射组大体外观见右额叶萎缩,明显棕黄色,为含铁血黄素沉着。氯化亚铁右杏仁体注射组亦可见边缘系统含铁血黄素沉着。普鲁士蓝和腾氏蓝反应证实含铁化合物的沉积。皮层及杏仁体氯化亚铁注射部位、实验侧海马CA3区神经元减少,核固缩,胶质增生明显。结论含铁化合物在大鼠的皮层和边缘结构的沉积可以导致慢性的、自发性发作的癫痫灶形成。皮层注射1 000 nmol氯化亚铁建立的外伤性癫痫动物模型比杏仁体注射铁离子建立的模型更接近人类的外伤性癫痫临床与病理改变。
Objective To establish the model ofposttraumatic epilepsy （PTE） in rats, observe the changes of symptoms, EEG and pathology during the course of the model development, and discuss the mechanisms of pathologic changes and epileptogenesis in this model. Methods Male SD rats were divided into 5 groups. To make an epileptic focus, different doses of FeCl2 were injected into the motor cortex or amygdaloid body with stereotactic technique. Behavior was observed in the 30 d following injection. EEG signals were recorded by an EEG polygraph. The pathologic examination was performed by means of HE, Prussian blue, Tumbull blue and Nissl stainings. Results Severe seizure activity was observed in a latency of（60±18） s in average after intracortical injection of 1000 nmol FeCl2 Most of the rats developed isolated epileptiform discharges. The achievement ratio of PTE model was 87.5% in this group. Slight seizure activity was observed in other groups, no seizure activity in the normal control group and the saline control group. The Racine＇ s behavior scores were significantly different from those in control group or other groups （P〈0.01）. There was the deposited haemosiderin into the right frontal cortex in the group of iron injection into cortex morphologically. Deposition of iron-containing compounds into cortex and amygdaloid body were observed by Prussian blue and Turnbull blue stainings. By cell counting, the neuronal cell loss, karyopyknosis and gliosis mainly occurred in the injured cortex, the injured amygdaloid body and CA3. Conclusion Epileptogenesis followed by chronic, spontaneous seizures could be initiated by deposition of iron-containing compounds into cortex and limbic structures of the rat. The rat model induced by intracortical injection of 1 000 nmol FeCl2 is an ideal animal model simulating human PTE clinically and pathologically.
出处
《中华神经医学杂志》
CAS
CSCD
2006年第4期372-377,共6页
Chinese Journal of Neuromedicine
关键词
外伤性癫痫
脑电图
模型
动物
氯化亚铁
Posttraumatic epilepsy
EEG
Models, animal
Ferrous chloride
