Abstract
Recent work has demonstrated that specific patterns of synaptic stimulation can induce long-term depression (LTD) in area CA1 that depends on activation of metabotropic glutamate receptors (mGluRs) and rapid protein synthesis. Here we show that the same form of synaptic modification can be induced by brief application of the selective mGluR agonist (RS)-3,5-dihydroxyphenylglycine (DHPG). DHPG-LTD 1) is a saturable form of synaptic plasticity, 2) requires mGluR5, 3) is mechanistically distinct from N-methyl-D-aspartate receptor (NMDAR)--dependent LTD, and 4) shares a common expression mechanism with protein synthesis-dependent LTD evoked using synaptic stimulation. DHPG-LTD should be useful for biochemical analysis of mGluR5- and protein synthesis-dependent synaptic modification.
MeSH terms
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2-Amino-5-phosphonovalerate / pharmacology
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Animals
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Excitatory Amino Acid Antagonists / pharmacology
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Excitatory Postsynaptic Potentials / drug effects
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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 / physiology*
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Long-Term Potentiation / drug effects
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Long-Term Potentiation / physiology*
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Mice
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Mice, Knockout
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Neural Inhibition / drug effects
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Neural Inhibition / physiology*
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Organ Culture Techniques
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RNA, Messenger / metabolism
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Rats
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Rats, Long-Evans
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Receptor, Metabotropic Glutamate 5
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Receptors, Metabotropic Glutamate / genetics*
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Receptors, Metabotropic Glutamate / metabolism*
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Resorcinols / pharmacology
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Stimulation, Chemical
Substances
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Excitatory Amino Acid Antagonists
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Grm5 protein, mouse
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Grm5 protein, rat
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RNA, Messenger
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Receptor, Metabotropic Glutamate 5
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Receptors, Metabotropic Glutamate
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Resorcinols
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3,5-dihydroxyphenylglycine
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2-Amino-5-phosphonovalerate
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Glycine