中文摘要：

目的探讨岛叶在杏仁核点燃大鼠癫痫发作中的作用。方法健康雄性SD大鼠48只，按照随机数字表法分为空白组（n=8）、假手术组（n=8）和点燃组（n=32），点燃组以最后一次刺激为零点，再分为点燃后1h、3h、6h、12h4个亚组，每亚组8只。空白组不做任何处理；假手术组植入电极后不予刺激；点燃组植入电极后予以电刺激，制作杏仁核点燃模型。采用荧光原位杂交和免疫组化检测大鼠海马、岛叶脑区活性调节细胞骨架蛋白（ArclmRNA和蛋白表达的变化。结果点燃大鼠海马、岛叶的ArcmRNA在点燃后1h开始增高，3h达到高峰，与空白组、假手术组比较，差异均有统计学意义（P〈0．05）；6h时回到正常水平。Arc蛋白在点燃后3h开始增高，6h达到高峰，与空白组、假手术组比较，差异均有统计学意义（P〈0．05）；12h时回到正常水平。假手术组与空白组之间ArcmRNA和蛋白差异没有统计学意义（P〉0．05）。结论岛叶与杏仁核、海马构成了一个灶性复合体．共同参与了颞叶癫痫的发生。

英文摘要：

Objective To investigate the role of insular cortex in amygdala-kindled seizures in rats. Methods Forty-eight healthy male SD rats were randomly divided into blank control group （n=8）, sham-operated group （n=8） and amygdala-kindled group （n=32）; no treatment was performed in the blank control group, and only implantation of electrodes was performed in the sham-operated group; implantation of electrodes and electrophotoluminescence were performed in the amygdala-kindled group to induce amygdala-kindled seizure models. Rats in the amygdala-kindled group was divided into 4 sub-groups （n=8） at different times after the kindling （1, 3, 6 and 12 h）. Fluorescence in situ hybridization and immunohistochemistry staining were employed to investigate the altered mRNA and protein expressions of activity-regulated cytoskeleton-associated protein （Arc） in the hippocampus and insula of the rat brain. Results As compared with that in the blank control group and sham-operated group, Arc mRNA expression in the amygdala-kindled sub-groups increased at 1 h after the kindling （P〈0.05）, peaked at 3 h after the kindling （P〈0.05）, and returned to basic level at 6 h after the kindling （P〉0.05）. As compared with that in the blank control group and sham-operated group, Arc protein expression in the amygdala-kindled sub-groups increased at 3 h after the kindling, （P〈0.05）, peaked at 6 h after the kindling （P〈0.05）, and returned to basic level at 12 h after the kindling （P〉0.05）. No significant difference on mRNA and protein expressions of Arc was noted between the sham-operated group and blank control group （P〉0.05）. Conclusion Insular cortex, the amygdala and the hippocampus form a focus complex, which participates in the occurrence of temporal lobe epilepsy.