http://purl.uniprot.org/citations/24695230 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/24695230 | http://www.w3.org/2000/01/rdf-schema#comment | "The formation of precise connections between retina and lateral geniculate nucleus (LGN) involves the activity-dependent elimination of some synapses, with strengthening and retention of others. Here we show that the major histocompatibility complex (MHC) class I molecule H2-D(b) is necessary and sufficient for synapse elimination in the retinogeniculate system. In mice lacking both H2-K(b) and H2-D(b) (K(b)D(b)(-/-)), despite intact retinal activity and basal synaptic transmission, the developmentally regulated decrease in functional convergence of retinal ganglion cell synaptic inputs to LGN neurons fails and eye-specific layers do not form. Neuronal expression of just H2-D(b) in K(b)D(b)(-/-) mice rescues both synapse elimination and eye-specific segregation despite a compromised immune system. When patterns of stimulation mimicking endogenous retinal waves are used to probe synaptic learning rules at retinogeniculate synapses, long-term potentiation (LTP) is intact but long-term depression (LTD) is impaired in K(b)D(b)(-/-) mice. This change is due to an increase in Ca(2+)-permeable AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid) receptors. Restoring H2-D(b) to K(b)D(b)(-/-) neurons renders AMPA receptors Ca(2+) impermeable and rescues LTD. These observations reveal an MHC-class-I-mediated link between developmental synapse pruning and balanced synaptic learning rules enabling both LTD and LTP, and demonstrate a direct requirement for H2-D(b) in functional and structural synapse pruning in CNS neurons."xsd:string |
http://purl.uniprot.org/citations/24695230 | http://purl.org/dc/terms/identifier | "doi:10.1038/nature13154"xsd:string |
http://purl.uniprot.org/citations/24695230 | http://purl.uniprot.org/core/author | "Lee H."xsd:string |
http://purl.uniprot.org/citations/24695230 | http://purl.uniprot.org/core/author | "Cheng S."xsd:string |
http://purl.uniprot.org/citations/24695230 | http://purl.uniprot.org/core/author | "Shatz C.J."xsd:string |
http://purl.uniprot.org/citations/24695230 | http://purl.uniprot.org/core/author | "Brott B.K."xsd:string |
http://purl.uniprot.org/citations/24695230 | http://purl.uniprot.org/core/author | "Feller M.B."xsd:string |
http://purl.uniprot.org/citations/24695230 | http://purl.uniprot.org/core/author | "Adelson J.D."xsd:string |
http://purl.uniprot.org/citations/24695230 | http://purl.uniprot.org/core/author | "Datwani A."xsd:string |
http://purl.uniprot.org/citations/24695230 | http://purl.uniprot.org/core/author | "Kirkby L.A."xsd:string |
http://purl.uniprot.org/citations/24695230 | http://purl.uniprot.org/core/date | "2014"xsd:gYear |
http://purl.uniprot.org/citations/24695230 | http://purl.uniprot.org/core/name | "Nature"xsd:string |
http://purl.uniprot.org/citations/24695230 | http://purl.uniprot.org/core/pages | "195-200"xsd:string |
http://purl.uniprot.org/citations/24695230 | http://purl.uniprot.org/core/title | "Synapse elimination and learning rules co-regulated by MHC class I H2-Db."xsd:string |
http://purl.uniprot.org/citations/24695230 | http://purl.uniprot.org/core/volume | "509"xsd:string |
http://purl.uniprot.org/citations/24695230 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/24695230 |
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