在神经病理、电生理及分子水平，不同惊厥模型观察发育期大鼠惊厥后不同时间大脑皮层及海马神经元数目、突触重构、脑片放电、NMDA受体各亚基基因表达及功能的改变，并用反义技术从反面加以印证；同时观察发育期惊厥对远期惊厥易感性及学习记忆的影响，分析这些影响与上述改变的关系。以期认识发育中脑惊厥性损伤特点，为早期干预提供理论依据。

We used the in vivo and in vitro models to study the seizure-induced brain injury. We found that brief Mg2+-free treatment could make a cultured developing cortical neuron "seizure" model, this recurrent epileptiform discharge could induce transient mitochondrial dysfunction without obvious cell loss; in this model, relatively more immature neurons had less severe injury, but their injury occurred earlier. Although we had not found the obvious long term neuropathologic changes in the brain of rats after the seizures in early childhood, the susceptibility to seizure-induced brain injury, such as apoptosis, mossy fiber sprouting, and learning and memory defect after the second seizure in adulthood, increased in rats that had seizure experience during development, either febrile convulsion or the kainate convulsion. NMDA receptor (NR) expression up-regulated, NR function enhanced, and the intracellular calcium concentration ([Ca2+]i) increase played a role in this functional neuronal injury. NR antagonist, calcium channel blocker and IL-1 receptor antagonist can protect the neurons to some different extent from the [Ca2+]i increase and the mitochondrial functional change (MTT conversion rates decrease) after the recurrent epileptiform induced by transient Mg2+-free culture. These results had great significance to clarify the mechanism and long-term prognosis of the seizure-induced developmental brain injury, and to find the new therapeutic strategy for this injury.