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The Journal of Neuroscience, May 19, 2004, 24(20):4859-4864; doi:10.1523/JNEUROSCI.5407-03.2004
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Extracellular Signal-Regulated Protein Kinase Activation Is Required for Metabotropic Glutamate Receptor-Dependent Long-Term Depression in Hippocampal Area CA1
Sean M. Gallagher,1 Christine A. Daly,1 Mark F. Bear,2 andKimberly M. Huber1 1Center for Basic Neuroscience, Department of Physiology, University of Texas Southwestern Medical Center, Dallas, Texas 75390, and 2Howard Hughes Medical Institute and The Picower Center for Learning and Memory, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139
Activation of group 1 metabotropic glutamate receptors (mGluRs) induces long-term depression (LTD) of synaptic transmission that relies on dendritic protein synthesis. We investigated the signal transduction pathways required for mGluR-LTD to identify candidate mechanisms for mGluR regulation of synaptic protein synthesis. Our results demonstrate a role for extracellular signal-regulated protein kinase (ERK), a subclass of the mitogen-activated protein kinases (MAPKs), in mGluR-LTD in area CA1 of the rat hippocampus. Inhibitors of the upstream kinase of ERK, MAP/ERK kinase significantly reduce mGluR-LTD induced by the group 1 agonist dihydroxyphenylglycine (DHPG) and synaptic stimulation but do not affect NMDA receptor-dependent LTD. In contrast, inhibitors of p38 MAPK were ineffective against DHPG-induced LTD. Consistent with the role of ERK in mGluR-LTD, we observed that DHPG treatment of hippocampal slices (isolated CA1), at concentrations that induce LTD, results in a robust phosphorylation of ERK but not of p38 MAPK. These results point to ERK as an important regulator of mGluR-LTD and a potential mechanism for mGluR regulation of synaptic protein synthesis.
Key words: metabotropic glutamate receptor; long-term depression; ERK; hippocampus; CA1; p38 MAPK
Received Sep 30, 2003; revised March 17, 2004; accepted April 13, 2004.
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