海人酸致痫大鼠海马CA3区神经元线粒体超微结构损伤的观察

目的 观察海人酸（KA）诱导的癫痫持续状态（SE）大鼠海马CA3区线粒体超微结构的损伤。方法 选用成年雄性Wistar大鼠40只，随机分为KA组和生理盐水对照组（NS组）。用KA诱导大鼠SE持续2h，分别于SE终止后第1、3小时制作脑切片，采用光镜观察神经元的大体变化，并用电镜进一步观察线粒体的超微结构。结果 SE终止后3h，大鼠海马线粒体出现了不同程度的损伤：从嵴的肿胀到膜的崩解。结论 KA诱导的SE在早期即可导致海马神经元线粒体的损伤，这可能是SE后神经元损伤的关键环节。

MITOCHONDRIAL ULTRASTRUCTURAL DAMAGE IN THE NEURONS IN HIPPOCAMPAL CA3 AREA OF KAINIC-ACID-INDUCED RATS

Objective To observe the mitochondrial ultrastructure damage in the neurons of hippocampal CA3 area during kainic-acid (KA)-induced status epilepticus(SE) in rats. Methods Forty adult male Wistar rats were divided into two groups in random: KA group and control group.SE was induced for two hours.At the first and the third hour after termination of SE,rats were killed and the brain sections made.The gross changes of neuron were observed with light microscope,and the mitochondrial ultrastructure with electron microscope. Results Three hours after the end of SE,various damages of mitochondria,from swelling of cristae to rupture of membrane,were noted. Conclusion Kainic-acid-induced status epilepticus,in its early stage,may result in mitochondrial damage in the neurons of hippocampus,which might be the key link of neuronal lesion after status epilepticus.