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用免疫组化方法检测一次给予惊厥剂量海人酸（Ｋａｎｉｃａｃｉｄ， ＫＡ） 诱发ＳＤ大鼠出现急性癫痫发作后， 癫痫发作敏感性形成过程中（ＫＡ 后１～７ ｄ） ，海马内内源性强啡肽Ａ（１－ ８） 免疫反应活性（ＤＹＮＡ （１－ ８） － ＬＩ） 动态变化过程。结果表明， ＫＡ后１～７ ｄ， 背、腹侧海马苔状纤维（ＭＦ） ＤＹＮＡ（１－８） 明显增强， ＫＡ后２～４ ｄ， 在腹侧海马齿状回颗粒细胞（ＤＧＣｓ） 层部位出现ＤＹＮＡ（１－８） －ＬＩ免疫反应阳性神经元，５～７ ｄ 后上述改变逐渐消失。研究中另一组动物被秋水仙素（Ｃｏｌｃｈｉｃｉｎｅ， 简称ｃｏｌ－） １－５ μｇ／０－６ μｌ 选择性分别或同时破坏双侧背侧和腹侧海马ＤＧＣｓ， 用以删除海马内源性强啡肽的作用，７ｄ 后， 用８ ｍｇ／ｋｇ ＫＡ检测其对癫痫刺激的敏感性， 结果显示， ｃｏｌ－ 损伤双侧腹侧海马ＤＧＣｓ 组动物， 可使ＫＡ诱发的癫痫活动明显加重。表明一次ＫＡ后，腹侧海马ＤＧＣｓ 部位ＤＹＮＡ（１－８） － ＬＩ一过性高表达很可能与５ ～７ ｄ 前癫痫发作敏感性不能形成有关。
Immunohistochemical method was used to detect the sensitivity of epileptic seizures (1 ~ 7 days after KA), the strong endogenous in the hippocampus after acute epileptic seizures induced by a convulsant dose of kainic acid (Kanacacid, KA) (DYNA (1- 8) - LI), a dynamic change process of enkephalin A (1- 8) immunoreactivity. The results showed that the DYNA (1-8) in the dorsal and ventral hippocampal moss fibers (MF) increased significantly from 1 to 7 days after KA, and in the ventral hippocampal dentate gyrus granule cells (DGCs) layer from 2 to 4 days after KA DYNA (1-8) -LI immunoreactive neurons appeared on the site, and the above changes gradually disappeared after 5-7 days. Another group of animals in the study were treated with Colchicine (1-5μg / 0-6 μl colchicine) selectively or simultaneously disrupt both DG dorsal and ventral hippocampal DGCs to delete the endogenous strong After 7 days, 8 mg / kg KA was used to test its sensitivity to epilepsy stimulation. The results showed that Col-injured animals of bilateral ventral hippocampal DGCs group could significantly aggravate KA-induced seizure activity. After a KA, the transient high expression of DYNA (1-8) - LI in ventral hippocampal DGCs may be related to the inability of pre-seizure sensitivity to develop 5-7 days.