ATP在Aβ_(1-42)导致的突触可塑性损害中的作用  

The effect of ATP on Aβ_(1-42) mediated disruption of synaptic plasticity

作　　者：周治平[1] 郑戈[2] 赖玉洁[1] 王年臻 杨国帅[1] 王爱岳[1] 余丹[1] 

机构地区：[1]海口市人民医院神经内科,海南海口570208 [2]吉林大学第二医院肝胆胰外科,吉林长春130041

出　　处：《中风与神经疾病杂志》2016年第8期724-726,共3页Journal of Apoplexy and Nervous Diseases

摘　　要：目的探讨ATP在调节神经元突触可塑性中的作用。方法培养大鼠原代神经元细胞,应用Aβ_(1-42)孵育原代培养的神经元细胞48 h,或者在Aβ_(1-42)孵育原代培养的神经元细胞前30 min预先给予ATP处理细胞。应用Alexa Fluor 488-phalloidin dye染色观察不同处理后神经元树突棘的变化。同时,应用Western blot检测Aβ_(1-42)及ATP处理后对PDS-95蛋白表达的影响。结果 ATP能减少Aβ_(1-42)所导致的神经元树突棘丢失,Aβ_(1-42)孵育原代培养的神经元细胞48 h后,PSD-95蛋白水平降低;而经过ATP预处理30 min后,神经元PSD-95蛋白表达无显著变化。结论 ATP能够调节神经元突触可塑性,从而发挥脑保护作用。Objective This study was conducted to investigate the effect of ATP in regulatory on synaptic plasticity.Methods Primary neurons were cultured successfully. Neurons were treated with Aβ1-42 or ATP. The neuronal spine lossand PSD-95 expression were studied by using immunohistochemistry and Western blotting, respectively. Results We foundthat exogenous ATP protected Aβ1-42 mediated reduction in synaptic molecules, such as PSD-95 and prevented Aβ1-42 inducedspine reduction in cultured primary hippocampal neurons. Conclusion Our findings suggested that ATP plays a protectiverole against Aβ1-42 mediated disruption of synaptic plasticity.

关 键 词：胶质递质 Β淀粉样蛋白 突触可塑性 

分 类 号：R749.1[医药卫生—神经病学与精神病学]