Research article summary (published 12 May 2009):

Converging signal on ERK1/2 activity regulates group I mGluR-mediated Arc transcription.

Full Abstract

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 (R,S)-3,5-dihydroxyphenylglycine (DHPG) in cultured cortical neurons. The increase in Arc mRNA did not require de novo 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.

Author information

Author/s: Wang, Yan (Y); Zheng, Fei (F); Zhou, Xianju (X); Sun, Zhongsheng (Z); Wang, Hongbing (H);

Affiliation: Behavioral Genetics Center, Institute of Psychology, Chinese Academy of Science, Beijing 100101, PR China.

Grants: MH076906 (Agency:NIMH NIH HHS)

Journal and publication information

Publication Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

Journal: Neuroscience letters (Neurosci Lett), published in Ireland. (Language: eng)

Reference: 2009-Aug; vol 460 (issue 1) : pp 36-40

Dates: Created 2009/06/10; Completed 2009/09/01;

PMID: 19446601, status: MEDLINE (last retrieval date: 9/1/2009, IMS Date: )

Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.

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MeSH headings (categories)

This article was linked to the MESH Headings shown below.

Animals CREB-Binding Protein - metabolism Cells, Cultured Cerebral Cortex - cytology Cytoskeletal Proteins - genetics; metabolism Enzyme Inhibitors - pharmacology Excitatory Amino Acid Antagonists - pharmacology Extracellular Signal-Regulated MAP Kinases - metabolism Methoxyhydroxyphenylglycol - analogs & derivatives; pharmacology Mice

Mice, Inbred C57BL Nerve Tissue Proteins - genetics; metabolism Neurons - drug effects Proto-Oncogene Proteins c-fos - genetics Pyridines - pharmacology RNA, Messenger - metabolism Receptors, Metabotropic Glutamate - antagonists & inhibitors; physiology Signal Transduction - drug effects; physiology Time Factors Up-Regulation - drug effects; physiology

Associated Chemicals: 6-methyl-2-(phenylethynyl)pyridine (0) ; Cytoskeletal Proteins (0) ; Enzyme Inhibitors (0) ; Excitatory Amino Acid Antagonists (0) ; Nerve Tissue Proteins (0) ; Proto-Oncogene Proteins c-fos (0) ; Pyridines (0) ; RNA, Messenger (0) ; Receptors, Metabotropic Glutamate (0) ; activity regulated cytoskeletal-associated protein (0) ; metabotropic glutamate receptor type 1 (0) ; dihydroxyphenylethylene glycol (3343-19-9) ; Methoxyhydroxyphenylglycol (534-82-7) ; CREB-Binding Protein (EC 2.3.1.48) ; Extracellular Signal-Regulated MAP Kinases (EC 2.7.1.37)

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