Abstract
The change in the number of post-synaptic alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA)-type glutamatergic receptors (AMPARs) by neuronal activity is recognized as a molecular basis of synaptic plasticity. Here, we show that Ca(2+) transients evoked by brain-derived neurotrophic factor (BDNF) induce translocation of a subunit of AMPAR, GluR1, but not NMDAR, to the post-synaptic membrane in cultured cortical pyramidal neurons. Among BDNF-induced Ca(2+) transients, that dependent on IP3R was fully required, while store-operated calcium influx through the non-selective cation channel TRPC (transient receptor potential canonical) was partially required for the GluR1 up-regulation, suggesting that spatial and temporal calcium signaling regulate translocation of GluR1 to the polarized membrane domain.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Brain-Derived Neurotrophic Factor / pharmacology*
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Calcium Channels / metabolism*
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Calcium Signaling / drug effects*
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Dendritic Spines / drug effects
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Disks Large Homolog 4 Protein
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Guanylate Kinases
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Humans
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Inositol 1,4,5-Trisphosphate Receptors
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Intracellular Signaling Peptides and Proteins / metabolism
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Membrane Glycoproteins / metabolism*
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Membrane Proteins / metabolism
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Mice
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Protein Transport / drug effects
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Pyramidal Cells / cytology
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Pyramidal Cells / drug effects
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Receptors, AMPA / metabolism*
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Receptors, Cytoplasmic and Nuclear / metabolism*
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Synaptic Membranes / drug effects*
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TRPC Cation Channels / metabolism*
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Time Factors
Substances
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Brain-Derived Neurotrophic Factor
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Calcium Channels
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Disks Large Homolog 4 Protein
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Dlg4 protein, mouse
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Inositol 1,4,5-Trisphosphate Receptors
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Intracellular Signaling Peptides and Proteins
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Itpr1 protein, mouse
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Membrane Glycoproteins
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Membrane Proteins
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Receptors, AMPA
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Receptors, Cytoplasmic and Nuclear
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TRPC Cation Channels
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Guanylate Kinases
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glutamate receptor ionotropic, AMPA 1