Hypothermia inhibits translocation of CaM kinase II and PKC-α, β, γ isoforms and fodrin proteolysis in rat brain synaptosome during ischemia-reperfusion

被引:27
|
作者
Harada, K
Maekawa, T
Tsuruta, R
Kaneko, T
Sadamitsu, D
Yamashima, T
Yoshida, K
机构
[1] Yamaguchi Univ, Sch Med, Dept Emergency & Crit Care Med, Ube, Yamaguchi 7558505, Japan
[2] Kanazawa Univ, Sch Med, Dept Neurosurg, Kanazawa, Ishikawa 920, Japan
[3] Univ Tokyo, Grad Sch Med, Dept Forens Med, Tokyo, Japan
关键词
mild hypothermia; protein kinase C (PKC); CaM kinase II; glutamate receptor; calpain;
D O I
10.1002/jnr.10159
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
To clarify the involvement of intracellular signaling pathway and calpain in the brain injury and its protection by mild hypothermia, immunoblotting analyses were performed in the rat brain after global forebrain ischemia and reperfusion. After 30 min of ischemia followed by 60 min of reperfusion, Ca2+/calmodulin-dependent kinase II (CaM kinase II) and protein kinase C (PKC)-alpha, beta, gamma isoforms translocated to the synaptosomal fraction, while mild hypothermia (32degreesC) inhibited the translocation. The hypothermia also inhibited fodrin proteolysis caused by ischemia-reperfusion, indicating the inhibition of calpain. These effects of hypothermia may explain the mechanism of the protection against brain ischemia-reperfusion injury through modulating synaptosomal function. (C) 2002 Wiley-Liss, Inc.
引用
收藏
页码:664 / 669
页数:6
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