大鼠岛叶电点燃模型海马GAP43、P38 mRNA和蛋白的表达

目的 探讨神经生长相关蛋白(GAP43)和突触素(P38)基因及蛋白在岛叶电点燃致癫大鼠海马的表达及其意义.方法 健康雄性SD大鼠72只,随机分为点燃组和假手术组,每组均36只大鼠.点燃组和假手术组各随机分为1、3、7、15、30及60 d 6个亚组,每亚组大鼠6只.点然后,标本应用免疫组化、原位杂交组织化学方法研究岛叶电点燃致癫大鼠海马GAP-43及P38表达的变化.结果 致癫1 d,海马齿状同颗粒细胞、门区、CA3区锥体细胞层GAP-43mRNA及蛋白表达高于对照组(P＜0.05);致癫3 d,表达减少(P＞0.05),致癫7 d后,表达呈现第2次增高;15 d、30 d显著高于对照组(P＜0.01);致癫60 d,仍高于对照组,但差异无统计学意义(P＞0.05).P38 mRNA及蛋白表达:致癫7 d,齿状回颗粒细胞层、门区、CA3区椎体细胞杂交信号及免疫染色开始增;15 d时差异达高峰(P＜0.01),这些变化一直持续到4周开始下降.结论 岛叶癫痫和颞叶海马密切相关;GAP43及P38可能是岛叶癫痫的病理基础--突触可塑性的重要分子机制.

Expressions of GAP43, P38 mRNA and protein in insular electrical kindled rats and its significance

Objective To investigate the expression of neural growth-associated protein (GAP-43)and synaptophysin(P38)gene and protein in insular electrical kindled epileptic rats and its significance. Methods Seventy-two male adult rats were divided into kindled group ( n = 36) and sham group (n =36) randomly. Each group was further divided into 1,3, 7, 15, 30 and 60 d sub-groups (n =6) respectively.After kindling with immunohistochemical staining and hybridization in situ, the altered expressions of GAP-43 and P38 were detected in hippocampus of insular electrical kindled epilepsy rats. Results Epilepsy day 1 : GAP-43 mRNA and protein expression at hippocampus dentate gyrus granular cell layer, hilus and CA:3 pyramidal layer in the kindled group were higher than the sham group ( P ＜ 0. 05). The expressions declined at Day 3 ( P ＞ 0. 05 ). Expressions became elevated again at Day 7 and they were significantly higher than those in the sham group at Days 15 and 30 ( P ＜ 0. 05 ). There was no statistical difference between two groups at Day 60 ( P ＞ 0. 05 ). Expressions of P38 mRNA and protein:hybridization signal and immunostaining at hippocampus dentate gyrus granular cell layer, hilus and CA3 pyramidal layer began to rise at Day 7 and peaked at Day 15 ( P ＜ 0. 01 ). They lasted 4 weeks and then began to decline. Conclusion Insular epilepsy is closely related with temporal hippocampus. GAP-43 and P38 may be the pathological basis of insular epilepsy and the key molecular mechanism of synaptie plasticity.