http://purl.uniprot.org/citations/18195348 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/18195348 | http://www.w3.org/2000/01/rdf-schema#comment | "Excitatory synapses in the mammalian brain contain two types of ligand-gated ion channels: AMPA receptors (AMPARs) and NMDA receptors (NMDARs). AMPARs are responsible for generating excitatory synaptic responses, whereas NMDAR activation triggers long-lasting changes in these responses by modulating the trafficking of AMPARs toward and away from synapses. AMPARs are tetramers composed of four subunits (GluR1-GluR4), which current models suggest govern distinct AMPAR trafficking behavior during synaptic plasticity. Here, we address the roles of GluR2 and GluR3 in controlling the recycling- and activity-dependent endocytosis of AMPARs by using cultured hippocampal neurons prepared from knockout (KO) mice lacking these subunits. We find that synapses and dendritic spines form normally in cells lacking GluR2/3 and that upon NMDAR activation, GluR2/3-lacking AMPARs are endocytosed in a manner indistinguishable from GluR2-containing AMPARs in wild-type (WT) neurons. AMPARs lacking GluR2/3 also recycle to the plasma membrane identically to WT AMPARs. However, because of their permeability to calcium, GluR2-lacking but not WT AMPARs exhibited robust internalization throughout the dendritic tree in response to AMPA application. Dendritic endocytosis of AMPARs also was observed in GABAergic neurons, which express a high proportion of GluR2-lacking AMPARs. These results demonstrate that GluR2 and GluR3 are not required for activity-dependent endocytosis of AMPARs and suggest that the most important property of GluR2 in the context of AMPAR trafficking may be its influence on calcium permeability."xsd:string |
http://purl.uniprot.org/citations/18195348 | http://purl.org/dc/terms/identifier | "doi:10.1073/pnas.0711412105"xsd:string |
http://purl.uniprot.org/citations/18195348 | http://purl.uniprot.org/core/author | "Bhattacharyya S."xsd:string |
http://purl.uniprot.org/citations/18195348 | http://purl.uniprot.org/core/author | "Biou V."xsd:string |
http://purl.uniprot.org/citations/18195348 | http://purl.uniprot.org/core/author | "Malenka R.C."xsd:string |
http://purl.uniprot.org/citations/18195348 | http://purl.uniprot.org/core/date | "2008"xsd:gYear |
http://purl.uniprot.org/citations/18195348 | http://purl.uniprot.org/core/name | "Proc Natl Acad Sci U S A"xsd:string |
http://purl.uniprot.org/citations/18195348 | http://purl.uniprot.org/core/pages | "1038-1043"xsd:string |
http://purl.uniprot.org/citations/18195348 | http://purl.uniprot.org/core/title | "Endocytosis and recycling of AMPA receptors lacking GluR2/3."xsd:string |
http://purl.uniprot.org/citations/18195348 | http://purl.uniprot.org/core/volume | "105"xsd:string |
http://purl.uniprot.org/citations/18195348 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/18195348 |
http://purl.uniprot.org/citations/18195348 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/18195348 |
http://purl.uniprot.org/uniprot/#_A0A0A6YW90-mappedCitation-18195348 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/18195348 |
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http://purl.uniprot.org/uniprot/#_B0QZW2-mappedCitation-18195348 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/18195348 |
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http://purl.uniprot.org/uniprot/#_C9K0Z1-mappedCitation-18195348 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/18195348 |
http://purl.uniprot.org/uniprot/#_E9QKC0-mappedCitation-18195348 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/18195348 |
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http://purl.uniprot.org/uniprot/#_P23819-mappedCitation-18195348 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/18195348 |