Abstract
Activation of group 1 metabotropic glutamate receptors (mGluRs) stimulates dendritic protein synthesis and long-term synaptic depression (LTD), but it remains unclear how these effects are related. Here we provide evidence that a consequence of mGluR activation in the hippocampus is the rapid loss of both AMPA and NMDA receptors from synapses. Like mGluR-LTD, the stable expression of this change requires protein synthesis. These data suggest that expression of mGluR-LTD is at least partly postsynaptic, and that a functional consequence of dendritic protein synthesis is the regulation of glutamate receptor trafficking.
Publication types
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Amino Acids / pharmacology
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Animals
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Cells, Cultured
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Cycloheximide / pharmacology
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Dendrites / metabolism
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Electrophysiology
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Endocytosis / physiology*
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Excitatory Amino Acid Antagonists / pharmacology
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Excitatory Postsynaptic Potentials / physiology
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Glycine / analogs & derivatives
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Glycine / pharmacology
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Hippocampus / cytology
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Immunohistochemistry
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In Vitro Techniques
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Methoxyhydroxyphenylglycol / analogs & derivatives*
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Neurons / drug effects
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Neurons / metabolism*
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Protein Synthesis Inhibitors / pharmacology
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Rats
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Rats, Long-Evans
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Receptors, AMPA / metabolism*
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Receptors, Metabotropic Glutamate / metabolism*
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Receptors, N-Methyl-D-Aspartate / metabolism*
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Resorcinols / pharmacology
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Synapses / metabolism
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Synapsins / metabolism
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Synaptic Transmission / drug effects
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Xanthenes / pharmacology
Substances
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Amino Acids
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Excitatory Amino Acid Antagonists
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LY 341495
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Protein Synthesis Inhibitors
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Receptors, AMPA
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Receptors, Metabotropic Glutamate
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Receptors, N-Methyl-D-Aspartate
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Resorcinols
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Synapsins
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Xanthenes
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Methoxyhydroxyphenylglycol
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3,5-dihydroxyphenylglycine
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Cycloheximide
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Glycine
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3,4-dihydroxyphenylglycol