Linked Life Data

12151550

Source:http://linkedlifedata.com/resource/pubmed/id/12151550

Statements in which the resource exists.
SubjectPredicateObjectContext
pubmed-article:12151550rdf:typepubmed:Citationlld:pubmed
pubmed-article:12151550lifeskim:mentionsumls-concept:C0684336lld:lifeskim
pubmed-article:12151550lifeskim:mentionsumls-concept:C0026809lld:lifeskim
pubmed-article:12151550lifeskim:mentionsumls-concept:C0424295lld:lifeskim
pubmed-article:12151550lifeskim:mentionsumls-concept:C0080093lld:lifeskim
pubmed-article:12151550lifeskim:mentionsumls-concept:C1274040lld:lifeskim
pubmed-article:12151550lifeskim:mentionsumls-concept:C0205082lld:lifeskim
pubmed-article:12151550lifeskim:mentionsumls-concept:C0162735lld:lifeskim
pubmed-article:12151550lifeskim:mentionsumls-concept:C0005456lld:lifeskim
pubmed-article:12151550lifeskim:mentionsumls-concept:C1148574lld:lifeskim
pubmed-article:12151550lifeskim:mentionsumls-concept:C1152805lld:lifeskim
pubmed-article:12151550lifeskim:mentionsumls-concept:C0599894lld:lifeskim
pubmed-article:12151550lifeskim:mentionsumls-concept:C0206243lld:lifeskim
pubmed-article:12151550lifeskim:mentionsumls-concept:C1521840lld:lifeskim
pubmed-article:12151550lifeskim:mentionsumls-concept:C0920644lld:lifeskim
pubmed-article:12151550pubmed:issue15lld:pubmed
pubmed-article:12151550pubmed:dateCreated2002-8-1lld:pubmed
pubmed-article:12151550pubmed:abstractTextNMDA receptor hypofunction has been implicated in the pathophysiology of schizophrenia, and pharmacological and genetic approaches have been used to model such dysfunction. We previously have described two mouse lines carrying point mutations in the NMDA receptor glycine binding site, Grin1(D481N) and Grin1(K483Q), which exhibit 5- and 86-fold reductions in receptor glycine affinity, respectively. Grin1(D481N) animals exhibit a relatively mild phenotype compatible with a moderate reduction in NMDA receptor function, whereas Grin1(K483Q) animals die shortly after birth. In this study we have characterized compound heterozygote Grin1(D481N/K483Q) mice, which are viable and exhibited biphasic NMDA receptor glycine affinities compatible with the presence of each of the two mutated alleles. Grin1(D481N/K483Q) mice exhibited a marked NMDA receptor hypofunction revealed by deficits in hippocampal long-term potentiation, which were rescued by the glycine site agonist d-serine, which also facilitated NMDA synaptic currents in mutant, but not in wild-type, mice. Analysis of striatal monoamine levels revealed an apparent dopaminergic and serotonergic hyperfunction. Behaviorally, Grin1(D481N/K483Q) mice were insensitive to acute dizocilpine pretreatment and exhibited increased startle response but normal prepulse inhibition. Most strikingly, mutant mice exhibited a sustained, nonhabituating hyperactivity and increased stereotyped behavior that were resistant to suppression by antipsychotics and the benzodiazepine site agonist Zolpidem. They also displayed a disruption of nest building behavior and were unable to perform a cued learning paradigm in the Morris water maze. We speculate that the severity of NMDA receptor hypofunction in these mice may account for their profound behavioral phenotype and insensitivity to antipsychotics.lld:pubmed
pubmed-article:12151550pubmed:languageenglld:pubmed
pubmed-article:12151550pubmed:journalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:12151550pubmed:citationSubsetIMlld:pubmed
pubmed-article:12151550pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:12151550pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:12151550pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:12151550pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:12151550pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:12151550pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:12151550pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:12151550pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:12151550pubmed:statusMEDLINElld:pubmed
pubmed-article:12151550pubmed:monthAuglld:pubmed
pubmed-article:12151550pubmed:issn1529-2401lld:pubmed
pubmed-article:12151550pubmed:authorpubmed-author:HigginsGuy...lld:pubmed
pubmed-article:12151550pubmed:authorpubmed-author:BallardTheres...lld:pubmed
pubmed-article:12151550pubmed:authorpubmed-author:KempJohn AJAlld:pubmed
pubmed-article:12151550pubmed:authorpubmed-author:MutelVincentVlld:pubmed
pubmed-article:12151550pubmed:authorpubmed-author:Pauly-EversMe...lld:pubmed
pubmed-article:12151550pubmed:authorpubmed-author:OuagazzalAbde...lld:pubmed
pubmed-article:12151550pubmed:authorpubmed-author:BorroniEdilio...lld:pubmed
pubmed-article:12151550pubmed:authorpubmed-author:BluethmannHor...lld:pubmed
pubmed-article:12151550pubmed:authorpubmed-author:KewJames N...lld:pubmed
pubmed-article:12151550pubmed:issnTypeElectroniclld:pubmed
pubmed-article:12151550pubmed:day1lld:pubmed
pubmed-article:12151550pubmed:volume22lld:pubmed
pubmed-article:12151550pubmed:ownerNLMlld:pubmed
pubmed-article:12151550pubmed:authorsCompleteYlld:pubmed
pubmed-article:12151550pubmed:pagination6713-23lld:pubmed
pubmed-article:12151550pubmed:dateRevised2006-11-15lld:pubmed
pubmed-article:12151550pubmed:meshHeadingpubmed-meshheading:12151550...lld:pubmed
pubmed-article:12151550pubmed:meshHeadingpubmed-meshheading:12151550...lld:pubmed
pubmed-article:12151550pubmed:meshHeadingpubmed-meshheading:12151550...lld:pubmed
pubmed-article:12151550pubmed:meshHeadingpubmed-meshheading:12151550...lld:pubmed
pubmed-article:12151550pubmed:meshHeadingpubmed-meshheading:12151550...lld:pubmed
pubmed-article:12151550pubmed:meshHeadingpubmed-meshheading:12151550...lld:pubmed
pubmed-article:12151550pubmed:meshHeadingpubmed-meshheading:12151550...lld:pubmed
pubmed-article:12151550pubmed:meshHeadingpubmed-meshheading:12151550...lld:pubmed
pubmed-article:12151550pubmed:meshHeadingpubmed-meshheading:12151550...lld:pubmed
pubmed-article:12151550pubmed:meshHeadingpubmed-meshheading:12151550...lld:pubmed
pubmed-article:12151550pubmed:meshHeadingpubmed-meshheading:12151550...lld:pubmed
pubmed-article:12151550pubmed:meshHeadingpubmed-meshheading:12151550...lld:pubmed
pubmed-article:12151550pubmed:meshHeadingpubmed-meshheading:12151550...lld:pubmed
pubmed-article:12151550pubmed:meshHeadingpubmed-meshheading:12151550...lld:pubmed
pubmed-article:12151550pubmed:meshHeadingpubmed-meshheading:12151550...lld:pubmed
pubmed-article:12151550pubmed:meshHeadingpubmed-meshheading:12151550...lld:pubmed
pubmed-article:12151550pubmed:meshHeadingpubmed-meshheading:12151550...lld:pubmed
pubmed-article:12151550pubmed:meshHeadingpubmed-meshheading:12151550...lld:pubmed
pubmed-article:12151550pubmed:meshHeadingpubmed-meshheading:12151550...lld:pubmed
pubmed-article:12151550pubmed:meshHeadingpubmed-meshheading:12151550...lld:pubmed
pubmed-article:12151550pubmed:meshHeadingpubmed-meshheading:12151550...lld:pubmed
pubmed-article:12151550pubmed:meshHeadingpubmed-meshheading:12151550...lld:pubmed
pubmed-article:12151550pubmed:meshHeadingpubmed-meshheading:12151550...lld:pubmed
pubmed-article:12151550pubmed:meshHeadingpubmed-meshheading:12151550...lld:pubmed
pubmed-article:12151550pubmed:meshHeadingpubmed-meshheading:12151550...lld:pubmed
pubmed-article:12151550pubmed:meshHeadingpubmed-meshheading:12151550...lld:pubmed
pubmed-article:12151550pubmed:meshHeadingpubmed-meshheading:12151550...lld:pubmed
pubmed-article:12151550pubmed:meshHeadingpubmed-meshheading:12151550...lld:pubmed
pubmed-article:12151550pubmed:meshHeadingpubmed-meshheading:12151550...lld:pubmed
pubmed-article:12151550pubmed:year2002lld:pubmed
pubmed-article:12151550pubmed:articleTitleSevere impairment of NMDA receptor function in mice carrying targeted point mutations in the glycine binding site results in drug-resistant nonhabituating hyperactivity.lld:pubmed
pubmed-article:12151550pubmed:affiliationPreclinical CNS Research, F. Hoffmann-La Roche Limited, CH-4070 Basel, Switzerland.lld:pubmed
pubmed-article:12151550pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:12151550pubmed:publicationTypeIn Vitrolld:pubmed
entrez-gene:14810entrezgene:pubmedpubmed-article:12151550lld:entrezgene
http://linkedlifedata.com/r...entrezgene:pubmedpubmed-article:12151550lld:entrezgene
http://linkedlifedata.com/r...pubmed:referesTopubmed-article:12151550lld:pubmed
http://linkedlifedata.com/r...pubmed:referesTopubmed-article:12151550lld:pubmed
http://linkedlifedata.com/r...pubmed:referesTopubmed-article:12151550lld:pubmed
http://linkedlifedata.com/r...pubmed:referesTopubmed-article:12151550lld:pubmed
http://linkedlifedata.com/r...pubmed:referesTopubmed-article:12151550lld:pubmed
http://linkedlifedata.com/r...pubmed:referesTopubmed-article:12151550lld:pubmed
http://linkedlifedata.com/r...pubmed:referesTopubmed-article:12151550lld:pubmed
http://linkedlifedata.com/r...pubmed:referesTopubmed-article:12151550lld:pubmed
http://linkedlifedata.com/r...pubmed:referesTopubmed-article:12151550lld:pubmed