成年大鼠弥漫性脑损伤后海马齿状回神经前体细胞增殖的Glu - iGlURs通路机制研究

 目的观察选择性iGluRs拮抗剂MK-801对弥漫性脑损伤后齿状回神经发生的调控作用,探讨Glu-iGluRs通路在神经发生中的角色.方法选用成年弥漫性脑损伤大鼠模型,采用BrdU标记分裂细胞及免疫组织化学方法,比较弥漫性脑损伤后2、4、6、8、12 d时MK-801干预弥漫性脑损伤组大鼠与相应对照组大鼠之间海马齿状回神经前体细胞的增殖速度.结果MK-801 1 mg/kg腹腔注射后,明显抑制了成年大鼠弥漫性脑损伤后4、6、8、12 d时齿状回神经前体细胞增殖,BrdU免疫阳性细胞数目较相应对照组明显减少(P＜0.01).结论弥漫性脑损伤后脑组织Glu-iGluRs通路的激活促进了海马齿状回神经发生,在这一过程中,NMDA受体介导的级联生物学事件可能发挥了重要作用.

Effects of Glu- iGluRs pathway on dentate gyrus granule cell neurogenesis after diffuse brain injury in adult rat

Objective To investigate the effects of selective iGluRs antagonist MK - 801 on dentate gyrus granule cell neurogenesis after the injury in the adult rat, and to explore the role of Glu - iGluRs pathway in neurogenesis after diffuse brain injury. Methods Adult male SD rats were subjected to diffuse brain injury. By using bromodeoxyuridine ( BrdU ) labelling and immuno histochemistry to observe dividing cells, we compared the proliferation rates of neural precursor cells in the dentate gyrus between the intervention group and the control group at 2,4,6,8, and 12 d after diffuse brain injury. Results MK - 801 (1 mg/kg i. p.) significantly reduced the number of BrdU labeled cells in the dentate gyrus 4,6,8 and 12 d after diffuse brain injury ( P < 0.01) , and inhibited the proliferation rate of neural precursor cells in the dentate gyrus. Conclusions The activation of Glu - iGluRs pathway after diffuse brain injury promotes the neurogenesis in the dentate gyrus. A series of cascade biological events mediated by NMDA receptor after diffuse brain injury probably play an important role in neurogenesis after diffuse brain injury.