Converging signal on ERK1/2 activity regulates group I mGluR-mediated Arc transcription
Wang, Yan1,2,3,4; Zheng, Fei1,2; Zhou, Xianju1,2; Sun, Zhongsheng3; Wang, Hongbing1,2; Z. Sun; H.Wang
2009-08-21
发表期刊NEUROSCIENCE LETTERS
ISSN0304-3940
文章类型Article
卷号460期号:1页码:36-40
摘要The expression of Arc is tightly coupled to synaptic activities. Recent studies suggested the functional relevance of Arc translation in group I metabotropic glutamate receptor (mGluR)-mediated long-term depression. The present study investigated the transcription-dependent changes of Arc in response to the activation of group I mGluR by (RS)-3,5-dihydroxyphenylglycine (DHPG) in cultured cortical neurons. The increase in Arc mRNA did not require de nova protein synthesis, indicating that Arc is an immediate early gene upon DHPG stimulation. We further examined the major pathways involved in group I mGluR signaling, and found that DHPG-induced Arc up-regulation depended on CaMK, PLC, and ERK1/2 activity. Moreover, the activity of NMDA receptors, but not L-type voltage gated calcium channels (L-VGCC), was required for Arc transcription. Interestingly, blocking CaMK, PLC, and NMDAR, but not L-VGCC, suppressed DHPG-stimulated ERK1/2 activation. These data suggest the central role of ERK1/2 in group I mGluR-mediated Arc transcription.; The expression of Arc is tightly coupled to synaptic activities. Recent studies suggested the functional relevance of Arc translation in group I metabotropic glutamate receptor (mGluR)-mediated long-term depression. The present study investigated the transcription-dependent changes of Arc in response to the activation of group I mGluR by (RS)-3,5-dihydroxyphenylglycine (DHPG) in cultured cortical neurons. The increase in Arc mRNA did not require de nova protein synthesis, indicating that Arc is an immediate early gene upon DHPG stimulation. We further examined the major pathways involved in group I mGluR signaling, and found that DHPG-induced Arc up-regulation depended on CaMK, PLC, and ERK1/2 activity. Moreover, the activity of NMDA receptors, but not L-type voltage gated calcium channels (L-VGCC), was required for Arc transcription. Interestingly, blocking CaMK, PLC, and NMDAR, but not L-VGCC, suppressed DHPG-stimulated ERK1/2 activation. These data suggest the central role of ERK1/2 in group I mGluR-mediated Arc transcription. (C) 2009 Elsevier Ireland Ltd. All rights reserved.
关键词Arc NMDA receptor L-Type voltage-gated calcium channel Group1 metabotropic glutamate receptors Transcription ERK1/2
学科领域遗传学
收录类别SCI
语种英语
WOS记录号WOS:000267633400008
引用统计
文献类型期刊论文
条目标识符http://ir.psych.ac.cn/handle/311026/5275
专题中国科学院心理研究所回溯数据库(1956-2010)
通讯作者Z. Sun; H.Wang
作者单位1.Michigan State Univ, Dept Physiol, E Lansing, MI 48824 USA
2.Michigan State Univ, Neurosci Program, E Lansing, MI 48824 USA
3.Chinese Acad Sci, Inst Psychol, Behav Genet Ctr, Beijing 100101, Peoples R China
4.Chinese Acad Sci, Grad Sch, Beijing, Peoples R China
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Wang, Yan,Zheng, Fei,Zhou, Xianju,et al. Converging signal on ERK1/2 activity regulates group I mGluR-mediated Arc transcription[J]. NEUROSCIENCE LETTERS,2009,460(1):36-40.
APA Wang, Yan.,Zheng, Fei.,Zhou, Xianju.,Sun, Zhongsheng.,Wang, Hongbing.,...&H.Wang.(2009).Converging signal on ERK1/2 activity regulates group I mGluR-mediated Arc transcription.NEUROSCIENCE LETTERS,460(1),36-40.
MLA Wang, Yan,et al."Converging signal on ERK1/2 activity regulates group I mGluR-mediated Arc transcription".NEUROSCIENCE LETTERS 460.1(2009):36-40.
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