Ischemic preconditioning-induced activation of ERK1/2 in the rat hippocampus
Ischemic preconditioning-induced activation of ERK1/2 in the rat hippocampus
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DOI：
10.1016/j.neulet.2006.09.053
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发表时间：
2006-12-06
影响因子：
2.5
通讯作者：
Lee, Mun-Yong
中科院分区：
文献类型：
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作者：
Choi, Jeong-Sun;Kim, Ha-Young;Lee, Mun-Yong
我们研究了大鼠缺血耐受诱导模型中细胞外信号调节激酶ERK1/2的激活和细胞定位。成年雄性Sprague-Dawley大鼠进行3 min的亚致死缺血预处理。ERK1/2的激活表现出典型的时间和细胞依赖模式。脑缺血3 min后，在海马齿状颗粒细胞和苔藓纤维中立即发现ERK的快速和短暂激活，然后在10 min时在CA3和CA1神经元以及齿状门神经元中依次发生。海马神经元ERK1/2的磷酸化有序地恢复到基础水平。在30分钟时，CA1神经元首先实现了基础水平的磷酸化，然后在CA3和颗粒细胞中观察到1小时，在一些齿状门区神经元中观察到12小时。相比之下，苔藓纤维和CA1树突状区ERK1/2的磷酸化持续了至少3天。刺激后1 d，齿状门区星形细胞也诱导了ERK1/2的短暂激活。这些数据表明，短时间脑缺血预处理诱导耐受获得性CA1神经元以及缺血抵抗性CA3和齿状颗粒细胞中ERK1/2的快速和短暂激活，并且短时间预处理在苔藓纤维和神经区持续激活，提示ERK1/2的激活可能参与大鼠海马缺血耐受的机制。2006爱思唯尔爱尔兰有限公司版权所有。
We investigated the activation and cellular localization of the extracellular signal-regulated kinases ERK1/2 in a rat model of ischemic tolerance induction. Adult male Sprague-Dawley rats were subjected to 3 min of sublethal ischemic preconditioning. Activation of ERK1/2 showed the characteristic time- and cell-dependent patterns. Rapid and short-lasting activation of ERK after 3 min of cerebral ischemia was noted immediately in the dentate granule cells and mossy fibers of the hippocampus, and then occurred sequentially in CA3 and CA1 neurons and dentate hilar neurons at 10 min. Phosphorylation of ERK1/2 in hippocampal neurons returned to the basal level in an ordered manner. Basal level phosphorylation was attained first, at 30 min, by the CA1 neurons, and was then observed in CA3 and granule cells by 1 h and noted in some dentate hilar neurons at 12 h. By contrast, phosphorylation of ERK1/2 in mossy fibers and the CA1 dendritic field was sustained for at least 3 d. Transient activation of ERK1/2 was induced also in astrocytes of the dentate hilar region at I d post-stimulation. These data demonstrate that the short cerebral-ischemic preconditioning induced rapid and transient activation of ERK 1/2 in tolerance-acquired CA1 neurons as well as in ischemia-resistant CA3 and dentate granule cells, and that the short preconditioning sustained activation in mossy fibers and neuropil areas, suggesting that ERK1/2 activation may be involved in the mechanism of ischemic tolerance in the rat hippocampus. (c) 2006 Elsevier Ireland Ltd. All rights reserved.