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丝裂原活化蛋白激酶信号传导对于活性依赖的树突状蛋白合成至关重要。

Mitogen-activated protein kinase signaling is essential for activity-dependent dendritic protein synthesis.

作者信息

Gong Ruomu, Tang Shao-Jun

机构信息

Department of Neurobiology and Behavior, Center for Neurobiology of Learning and Memory, University of California, Irvine, California 92697-3800, USA.

出版信息

Neuroreport. 2006 Oct 23;17(15):1575-8. doi: 10.1097/01.wnr.0000234742.42818.ff.

Abstract

The expression of long-lasting synaptic plasticity requires synthesis of new proteins. A critical locus for protein synthesis to support synaptic plasticity is the dendrites. Previous studies demonstrate that synaptic activity activates dendritic protein synthesis. The mechanism by which synaptic activity stimulates protein synthesis in dendrites is, however, poorly understood. This study is to determine the role of the mitogen-activated protein kinase signaling pathway in activity-dependent dendritic protein synthesis. Using a green fluorescent protein reporter with CaMKII 5' and 3'untranslated regions, we show that dendritic synthesis of the green fluorescent protein induced by N-methyl-D-aspartate stimulation is abolished by U0126, a specific inhibitor of mitogen-activated protein kinase signaling. Our results suggest an important role of the mitogen-activated protein kinase signaling in dendritic protein synthesis induced by N-methyl-D-aspartate receptor activation.

摘要

持久的突触可塑性的表达需要新蛋白质的合成。支持突触可塑性的蛋白质合成的一个关键位点是树突。先前的研究表明,突触活动会激活树突中的蛋白质合成。然而,突触活动刺激树突中蛋白质合成的机制却知之甚少。本研究旨在确定丝裂原活化蛋白激酶信号通路在活动依赖性树突蛋白合成中的作用。使用带有CaMKII 5'和3'非翻译区的绿色荧光蛋白报告基因,我们发现N-甲基-D-天冬氨酸刺激诱导的绿色荧光蛋白的树突合成被U0126(丝裂原活化蛋白激酶信号的特异性抑制剂)所消除。我们的结果表明丝裂原活化蛋白激酶信号在由N-甲基-D-天冬氨酸受体激活诱导的树突蛋白合成中起重要作用。

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