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

EL[S]小鼠翻腾刺激致痫后脑内Fos表达在2 h达高峰，48h恢复至发作间期水平；美解脲诱导EL[S]和EL[ns]小鼠惊厥后1h Fos表达达高峰，至24 h才开始下降；美解脲诱导的非惊厥敏感ddy小鼠Fos表达在30min达高峰，1和4h后消失，与对照组比较差异有统计学意义(P<0.05在ddy和EL[ns]小鼠中。EL[S]小鼠抛起刺激惊厥后Jun的诱导时间比Fos诱导的短。Fos和Jun是由转录因子AP-1组成的异源二聚体，从含有目的基因启动子区域的AP-1DNA元件中出现。在EL和ddy小鼠中，EL[S]小鼠抛起刺激惊厥后的AP-1DNA活性持续长于bmggide诱导的惊厥发作。EL[EL]和ddy小鼠出生后3~4周的活性高于ddy小鼠。EL小鼠在发育期的表达水平高于Ddy小鼠，提示EL小鼠反复刺激致痫后，可能产生AP-1调节基因，参与神经可塑性异常而形成的癫痫易感性。

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.