微波辐射对大鼠大脑皮层和海马突触素Ⅰ及相关信号通路的影响

Influence of microwave radiation on synapsin Ⅰ and its mechanism in cerebral cortex and hippocampus in Wistar rats

目的探讨微波辐射对大鼠大脑皮层和海马突触素Ⅰ及其相关影响因子BDNF和受体TrkB表达的影响。方法采用30mW／cm^2微波辐射Wistar雄性大鼠40只，于辐射后6h、1d、3d和7d取材，通过免疫组织化学和RT-PCR检测大脑皮层和海马突触素Ⅰ，BDNF和TrkB表达的改变。结果30mW／cm^2辐射后，突触素ⅠmRNA在大脑皮层于辐射后6h和1d增加（P〈0．01），而3d和7d减少（P〈0．01）；海马突触素ⅠmRNA于辐射后6h和1d增加（P〈0．01）。BDNF蛋白在大脑皮层于辐射后6h表达增强（P〈0．05），1～3d达高峰（P〈0．01）；在海马于辐射后1d表达增强（P〈0．05），3d～7d达高峰（P〈0．01）。大脑皮层BDNF RNA辐射后6h增加（P〈0．01），1d减少（P〈0．01），3d和7d又见增加（P〈0．01或P〈0．05）；海马BDNF RNA于辐射后1d增加（P〈0．01）。TrkB蛋白在大脑皮层于辐射后1～3d表达增强（P〈0．01）；在海马于辐射后3～7d表达增强（P〈0．01）。TrkB mRNA在大脑皮层于辐射后6h和7d增加（P〈0．01）；海马TrkB mRNA于辐射后6h、3d和7d减少（P〈0．01或P〈0．05）。结论微波辐射可引起大脑皮层和海马突触素Ⅰ、BDNF及其受体TrkB表达异常，参与了微波辐射所致的突触传递障碍及其修复过程。

Objective To investigate the effect of microwave irradiation on expressions of synapsin Ⅰ , BDNF and TrkB. Methods 40 Wistar rats were exposed to microwave with the average power density of 30 mW/cm^2 . RT-PCR and immunohistochemistry were used to study the change of the expressions of synapsin Ⅰ , BDNF and TrkB. Results Synapsin Ⅰ mRNA were increased at 6 h and 1 d （ P 〈 0. 01 ）, but decreased at 3 d and 7 d （ P 〈 0.01） in cerebral cortex. It was increased at 6 h and 1 d （ P 〈 0.01） in hippocampus after radiation. The expression of BDNF was increased progressively in 6 h-3 d （P 〈 0.01 or P 〈 0.05） in cerebral cortex and in 1-7 d （P 〈 0.01 or P 〈 0.05） in hippocampus. BDNF mRNA was increased at 6 h （P 〈 0.01）, decreased at 1 d （ P 〈 0.01 ）, then increased at 3 d and 7 d （ P 〈 0.01 or P 〈 0.05） after radiation in cerebral cortex. It was increased at 1 d （P 〈 0.01 ） in hippocampus. The expression of TrkB was increased in 1-3 d （P 〈 0.01） in cerebral cortex and in 3-7 d （P 〈 0.01 ） in hippoeampus after radiation. TrkB mRNA was increased at 6 h and 7 d （ P 〈 0.01 ） in cerebral cortex, decreased at 6 h, 3 d and 7 d （ P 〈 0.01 or P 〈 0.05） in hippoeampus after radiation. Conclusions Microwave radiation can induce the abnormity of expressions of synapsin Ⅰ , BDNF and TrkB in cerebral cortex and hippocampus, which might play a role in the injury and repair of synaptie transmission.