摘要
目的观察弥漫性脑损伤(Diffuse brain injury,DBI)大鼠延髓内脏带(Medullary visceral zone,MVZ)中迷走复合体(Dorsal vagalcomplex,DVC)的神经元和小胶质细胞上P2X4受体的表达变化,为临床防治DBI提供理论依据。方法在成功建立DBI大鼠模型基础上,应用免疫荧光组织化学和免疫电镜的方法,观察DBI发生后大鼠MVZ中迷走复合体神经元和小胶质细胞上P2X4受体的变化。结果 DBI发生后1小时,迷走复合体神经元和小胶质细胞上P2X4受体表达不明显。P2X4受体呈现第1次变化高峰是在DBI发生后的2小时。DBI发生后12小时,P2X4受体表达出现第2次变化高峰。免疫电镜上显示:正常状态下,P2X4受体在DVC的神经元以及小胶质细胞上几乎没有表达。而在DBI发生后2小时,在神经元和小胶质细胞上表达明显增加;在DBI发生后12小时,P2X4受体在DVC的神经元以及小胶质细胞上表达明显增加。而DBI发生后24小时,P2X4受体的表达下降。结论 DBI发生后,P2X4受体可能是神经元和小胶质细胞间"信息"交流的媒介,也可能是加重脑水肿发生的的启动因素。
Objective To observe the expression change of P2X4 receptor in glia cells and neurons in dorsal vagal complex(DVC) of medullary visceral zone(MVZ) after diffuse brain injury(DBI) in rats.To provide the data for clinical prevention of DBI.Methods Based on successful model of rat DBI,immuno-fluorescence staining and immune electron microscopy methods were used to observe the expression of P2X4 receptor in glia cells and neurons in DVC of MVZ after DBI.Results The expression of P2X4 receptor in glia cells and neurons in DVC of MVZ is not obviously 1 hour after DBI.And the first peak of P2X4 receptor expression happened in 2 hours after DBI.12 hours after DBI,another peak of P2X4 receptor expression took place.Immune electron microscopy showed that P2X4 receptor is almost not expressed on normal neurons of DVC and glia cells.The P2X4 receptor began to express 2 hours after DBI.The expression of P2X4 receptor increased obviously 12 hours after DBI and decreased 24 hours after DBI.Conclusion P2X4 receptor might be the information medium of neurons of DVC and glia cells after DBI.It also might be the initiating factor to aggravate cerebral edema.
出处
《浙江创伤外科》
2012年第1期1-4,共4页
Zhejiang Journal of Traumatic Surgery