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rdf:type |
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lifeskim:mentions |
umls-concept:C0010453,
umls-concept:C0019564,
umls-concept:C0027882,
umls-concept:C0044602,
umls-concept:C0072899,
umls-concept:C0206249,
umls-concept:C0441587,
umls-concept:C1514873,
umls-concept:C1546857,
umls-concept:C1556066,
umls-concept:C1619636,
umls-concept:C1879547
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pubmed:issue |
4
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pubmed:dateCreated |
2003-5-26
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pubmed:abstractText |
Hippocampal CA1 homosynaptic long-term potentiation (LTP) is expressed specifically at activated synapses. Increased insertion of postsynaptic alpha-amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid receptors (AMPARs) appears to be crucial for CA1 LTP. However, the mechanism underlying AMPAR insertion during LTP remains largely unknown. We now report that phosphatidylinositol 3-kinase (PI3K) is complexed with AMPARs at synapses and activated by selective stimulation of synaptic N-methyl-D-aspartate (NMDA) receptors. Activation of the AMPAR-associated PI3K is required for the increased cell surface expression of AMPARs and LTP. Thus, our results strongly suggest that the AMPAR-PI3K complex may constitute a critical molecular signal responsible for AMPAR insertion at activated CA1 synapses during LTP, and consequently, this lipid kinase may serve to determine the polarity of NMDA receptor-dependent synaptic plasticity.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0896-6273
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pubmed:author |
pubmed-author:AhmadianGholamrezaG,
pubmed-author:BeckerLarry ELE,
pubmed-author:D'SouzaSandraS,
pubmed-author:DadoDD,
pubmed-author:DayJ OJO,
pubmed-author:JuWilliamW,
pubmed-author:LiuLidongL,
pubmed-author:LuJieJ,
pubmed-author:LuWei-YangWY,
pubmed-author:MacDonaldJohn FJF,
pubmed-author:ManHeng-YeHY,
pubmed-author:TaghibiglouCC,
pubmed-author:WangQinhuaQ,
pubmed-author:WangYu TianYT,
pubmed-author:WontT WTW,
pubmed-author:WymannMatthias PMP
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pubmed:issnType |
Print
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pubmed:day |
22
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pubmed:volume |
38
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
611-24
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pubmed:dateRevised |
2010-11-18
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pubmed:meshHeading |
pubmed-meshheading:12765612-Androstadienes,
pubmed-meshheading:12765612-Animals,
pubmed-meshheading:12765612-Cells, Cultured,
pubmed-meshheading:12765612-Chromones,
pubmed-meshheading:12765612-Enzyme Inhibitors,
pubmed-meshheading:12765612-Excitatory Postsynaptic Potentials,
pubmed-meshheading:12765612-Hippocampus,
pubmed-meshheading:12765612-Long-Term Potentiation,
pubmed-meshheading:12765612-Mice,
pubmed-meshheading:12765612-Morpholines,
pubmed-meshheading:12765612-Neuronal Plasticity,
pubmed-meshheading:12765612-Neurons,
pubmed-meshheading:12765612-Phosphatidylinositol 3-Kinases,
pubmed-meshheading:12765612-Protein Transport,
pubmed-meshheading:12765612-Rats,
pubmed-meshheading:12765612-Rats, Sprague-Dawley,
pubmed-meshheading:12765612-Receptors, AMPA,
pubmed-meshheading:12765612-Signal Transduction
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pubmed:year |
2003
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pubmed:articleTitle |
Activation of PI3-kinase is required for AMPA receptor insertion during LTP of mEPSCs in cultured hippocampal neurons.
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pubmed:affiliation |
Brain and Behavior Program and Department of Pathology, Research Institute of the Hospital for Sick Children, University of Toronto, Toronto, Ontario, Canada M5S 1A8.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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