Regulated mechanism of genetic expression in the brain of El mice as a model of incurable epilepsy.

在癫痫发作的El[s]小鼠中，颠起刺激引起的癫痫发作后脑内Fos表达在2h达到峰值，48h恢复到间期水平。大鼠栅格诱导的El[s]和未经历癫痫发作的El[ns]小鼠的Fos诱导在1h达到峰值，并在24h下降。在癫痫不敏感的ddY小鼠中，bemegride诱导的Fos表达在30 min达到峰值，在ddY和El[ns]小鼠中分别在1和4h消失。El[5]小鼠癫痫发作后的Jun诱导比Fos诱导短。Fos和Jun是由异源二聚体组成的，转录因子AP-1似乎来自AP-1与靶基因启动子区域有关的DNA元件。在El和ddY两组小鼠中，翻腾诱导的El[s]小鼠癫痫发作AP-1 DNA活性持续比贝美吉得诱导的癫痫发作时间更长。El小鼠出生后第3 ~ 4周活性高于ddY，此后逐渐下降，至第25周降至较低水平。El小鼠在生长过程中表达水平高于ddY小鼠。结果提示，倒立刺激诱发的El小鼠癫痫发作可能产生AP-1调节基因，该基因通过异常神经可塑性形成癫痫易感性。

The induction of Fos expression in the brain after seizures caused by tossed-up stimulation in seizure-experienced El[s]mice attained a peak at 2h and returned to the interictal level by 48h.The Fos induction after bemegride-induced seizures of El[s]and seizure-nonexperienced El[ns]mice reached a peak at 1h and decreased until 24h.Bemegride-induced Fos expression in seizure-nonsusceptible ddY mice attained a peak at 30 min, and disappeared at 1 and 4h, respectively, in ddY and El[ns]mice.The Jun induction after seizures of tossed-up stimulation was shorter in El[s]mice than Fos induction.Fos and Jun were composed heterodimers, transcriptional factor AP-1, whith is appeared to frome AP-1 DNA elements concerning promotor regions with in target genes.The AP-1 DNA activities of tossed-up induced seizures in El[s]mice continued to be longer than those of bemegide-induced seizures in two groups of El and ddY mice.The activites of 3rd to 4th week after birth of El mice were higher than those of ddY,decreased thereafter and reached to low level on 25th week.The El mice showed to be higher level of expression during the growth than ddY did.The results suggest that seizures induced by tossed-up stimulation of El mice may produce AP-1 regulating genes bening responsible for seizure susceptbility forming by abnormal neural plasticity.