红藻氨酸快速点燃大鼠癫痫模型的建立及其海马神经发生

Establishment of kainic acid induced temporal lobe epilepsy in rat and study of its neurogenesis

目的建立红藻氨酸(kainite acid,KA)快速点燃癫痫模型,观察行为学、脑电图(electroencephalogrom,EEG)、海马病理改变及其神经发生。方法立体定向连续注射KA于侧脑室致痫。视频监测、深部EEG、Nissl染色、BrdU免疫组化染色。结果大鼠行为学及深部EEG呈急性期、静止期和慢性期3个阶段性变化。根据Racine行为学分级法,Ⅴ级8只,Ⅳ级12只,Ⅲ级2只,Ⅱ级2只;深部电极描记出起始于海马并向杏仁核、额叶皮质等传导癫痫样波;病理变化提示长期癫痫发作会导致海马锥体细胞逐渐变性、坏死、丢失。BrdU标记细胞主要分布于海马齿状回,并在癫痫发作后显著增多(P<0.01)。结论KA快速点燃大鼠模型为模拟颞叶癫痫的理想动模型,癫痫发作后神经发生显著增高。

Objective To establish kainite quickly induced emporal epilepsy rat model. Methods Kainic acid was continuously injected into right lateral ventricle of rat via stereotactic technique to make an epileptic focus. The behavior of the rats was recorded by a video camera. EEG signal was recorded by an EEG polygraph. The pathologic changes were observed with Nissl and BrdU staining. Results The changes in behavior and EEG experienced three phases, which were acute, silent and chronic. According to Racine＇ s scale, 8 rats were classified as type Ⅴ, 12 as type Ⅳ, 2 as type m and the other 2 as type Ⅱ The spike waves originated from hippocampus and spread to amygdala and frontal lobe. Pathologic changes showed that prolonged seizures induced pyramid cell loss in the hippocampus. BrdU labeled cells mainly localized in dentate gyrus（P 〈 0. 01 ）. Conclusion The kainic acid induced rat model is an ideal animal model to simulate human temporal lobe epilepsy. Development of epilepsy is accompanied by enhanced neurogenesis in the hippocampus.