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本实验给大鼠皮下注射红藻氨酸（ＫＡ，１０ｍｇ／ｋｇ）诱发癫痫活动，７２ｄ后进行深部前梨状皮层（ｄｅｅｐＰｒｅｐｙｒｉｆｏｒｍｃｏｒｔｅｘ，ＤＰＣ）电点燃刺激（ｋｉｎｄｌｉｎｓ），该组动物点燃形成加速，或再给予同样剂量ＫＡ，其再次诱发的癫痈活动明显加重。ｃ－Ｆｏｓ免疫反应活性（ｃ－Ｆｏｓ－ｉｒ）作为神经元兴奋的标志，标绘再次诱发癫痫活动时大鼠脑内细胞信息传递通路，并与对照组，即７２ｄ前给予生理盐水（Ｎ．Ｓ，１ｍｌ／ｋｇ）动物比较。结果表明，两组动物脑内细胞信息传递通路相同，实验组动物海马（ＨｉＰｐｏｃａｍｐｕｓ）内ｃ－ｆｏｓ，ｃ－ｊｕｎ基因表达呈非同步加速；海马邻近脑区内嗅皮层（ｅｎｔｏｒｈｉｎａｌｃｏｒｔｅｘ，Ｅｎｔ）激活加速，海马及Ｅｎｔ等部位前脑啡肽原（ｐｒｏｅｎｋｅｐｈａｌｉｎ，ＰＥＮＫ）ｍＲＮＡ合成明显增加，提示一次给予ＫＡ诱发动物出现短暂癫痫活动后，可使该动物对癫痫刺激敏感性增强长期存在，这可能与脑内ｃ－ｆｏｓ，ｃ－ｊｎｎ表达非同步加速及快速启动前脑啡肽原基因表达有关。
In this experiment, rats were injected with kainic acid (KA, 10 mg / kg) to induce epilepsy activity. After 72 days, deep prepyridium cortex (DPC) kindling was initiated, And then given the same dose of KA, its again induced epilepsy activity was significantly worse. c-Fos immunoreactivity (c-Fos-ir) was used as a marker of neuronal excitability, and the intracellular signal transduction pathway in the rat brain was re-induced by epilepsy. S, 1 ml / kg) animals. The results showed that the pathways of intracerebral cell information transmission were the same in both groups. The expression of c-fos and c-jun genes in hippocampus of rats in experimental group accelerated unsynchronously. The activation of entorhinalcortex (Ent) in hippocampus was accelerated , Hippocampus and Ent and other parts of the proenkephalin (proenkephalin, PENK) mRNA synthesis significantly increased, suggesting that once KA-induced epileptic animal epileptic activity, the animals can make the sensitivity of epilepsy stimulation long-term existence, which may be related to the brain C-fos, c-jnn expression of non-synchronous acceleration and rapid activation of proenkephalin gene expression before.