Extracellular signal-regulated kinases are not involved in activity-dependent survival or apoptosis in cerebellar granule neurons

被引:8
|
作者
Song, Bin
Ma, Chi
Gong, Shoufang
Yuan, Zhongmin
Li, Dan
Liu, Wei
Li, Wenming
Chen, Ruzhu
Zhu, Xiaonan
Zeng, Jinsheng
Han, Yifan
Li, Mingtao
机构
[1] Sun Yat Sen Univ, Dept Pharmacol, Zhongshan Med Coll, Guangzhou 510089, Peoples R China
[2] Sun Yat Sen Univ, Proteom Lab, Zhongshan Med Coll, Guangzhou 510089, Peoples R China
[3] Sun Yat Sen Univ, Stroke Ctr, Affiliate Hosp 1, Guangzhou 510080, Peoples R China
[4] Sun Yat Sen Univ, Dept Neurol, Affiliate Hosp 1, Guangzhou 510080, Peoples R China
[5] Hong Kong Univ Sci & Technol, Dept Biochem, Kowloon, Hong Kong, Peoples R China
基金
中国国家自然科学基金;
关键词
ERK; 1/2; survival; apoptosis; cerebellar granule neurons;
D O I
10.1016/j.neulet.2006.08.040
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Cerebellar granule neurons (CGNs) depend on potassium depolarization for survival and undergo apoptosis when deprived of depolarizing concentration of potassium. Extracellular signal-regulated kinases (ERK1/2) are thought to be activated in response to potassium depolarization and responsible for the activity-dependent survival in CGNs, but one recent study has revealed that ERK1/2 is activated by potassium deprivation and is required for apoptosis of CGNs. In this study we showed that ERK1/2 was inactivated, rather than activated, by potassium deprivation, indicating a lack of ERK1/2 involvement in potassium deprivation-induced apoptosis. Furthermore, suppression of potassium depolarization-induced activation of ERK1/2 with chemical inhibitor U0126 or PD98059 had no influence on the pro-survival effect of potassium depolarisation. Thus, ERK1/2 was not required for potassium depolarization-dependent survival of CGNs. Taken together, our findings suggest that ERK1/2 is not involved in activity-dependent survival or apoptosis of CGNs. (c) 2006 Published by Elsevier Ireland Ltd.
引用
收藏
页码:214 / 218
页数:5
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