Abstract
Corticosterone facilitates hippocampal glutamate transmission, but the cellular pathways by which AMPA receptor (AMPAR) signaling is adjusted remain elusive. Single quantum-dot imaging in live rat hippocampal neurons revealed that corticosterone triggers, via distinct corticosteroid receptors, time-dependent increases in GluR2-AMPAR surface mobility and synaptic surface GluR2 content. Furthermore, corticosterone potentiates the increase of synaptic surface GluR2 contents by a chemical long-term potentiation stimulus, revealing the influence that corticosterone has on AMPAR trafficking.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Cell Membrane / metabolism*
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Cells, Cultured
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Corticosterone / pharmacology
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Corticosterone / physiology*
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Drug Synergism
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GABA Antagonists / pharmacology
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Glycine / pharmacology
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Hippocampus / cytology
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Long-Term Potentiation / drug effects
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Long-Term Potentiation / physiology*
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Neurons / drug effects
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Neurons / physiology*
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Protein Transport / drug effects
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Protein Transport / physiology
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Quantum Dots
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Rats
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Receptors, AMPA / metabolism*
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Stimulation, Chemical
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Synaptic Transmission / drug effects
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Synaptic Transmission / physiology*
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Time Factors
Substances
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GABA Antagonists
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Receptors, AMPA
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glutamate receptor ionotropic, AMPA 2
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Glycine
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Corticosterone