RDF/XMLNTriplesTurtleShow queryShare
SubjectPredicateObject
http://purl.uniprot.org/citations/11161481http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/11161481http://www.w3.org/2000/01/rdf-schema#comment"The role of the extracellular matrix molecule tenascin-R (TN-R) in regulation of synaptic transmission and plasticity in the CA1 region of the hippocampus was studied using mice deficient in expression of this molecule. The mutant mice showed normal NMDA-receptor-mediated currents but an impaired NMDA-receptor-dependent form of long-term potentiation (LTP) as compared to wild-type littermates. Reduced LTP in mutants was accompanied by increased basal excitatory synaptic transmission in synapses formed on CA1 pyramidal neurons. A possible mechanism for increased excitatory synaptic transmission in mutants could involve modulation of inhibition, since TN-R and its associated carbohydrate HNK-1 decorate perisomatic interneurons. Indeed, the amplitudes of unitary perisomatic inhibitory currents were smaller in mutants compared to wild-type mice. Thus, our data show that a deficit in TN-R results in reduction of perisomatic inhibition and, as a consequence, in an increase of excitatory synaptic transmission in CA1 to the levels close to saturation, impeding further expression of LTP."xsd:string
http://purl.uniprot.org/citations/11161481http://purl.org/dc/terms/identifier"doi:10.1006/mcne.2000.0922"xsd:string
http://purl.uniprot.org/citations/11161481http://purl.uniprot.org/core/author"Schmidt S."xsd:string
http://purl.uniprot.org/citations/11161481http://purl.uniprot.org/core/author"Schuster T."xsd:string
http://purl.uniprot.org/citations/11161481http://purl.uniprot.org/core/author"Bartsch U."xsd:string
http://purl.uniprot.org/citations/11161481http://purl.uniprot.org/core/author"Schachner M."xsd:string
http://purl.uniprot.org/citations/11161481http://purl.uniprot.org/core/author"Dityatev A."xsd:string
http://purl.uniprot.org/citations/11161481http://purl.uniprot.org/core/author"Saghatelyan A.K."xsd:string
http://purl.uniprot.org/citations/11161481http://purl.uniprot.org/core/date"2001"xsd:gYear
http://purl.uniprot.org/citations/11161481http://purl.uniprot.org/core/name"Mol Cell Neurosci"xsd:string
http://purl.uniprot.org/citations/11161481http://purl.uniprot.org/core/pages"226-240"xsd:string
http://purl.uniprot.org/citations/11161481http://purl.uniprot.org/core/title"Reduced perisomatic inhibition, increased excitatory transmission, and impaired long-term potentiation in mice deficient for the extracellular matrix glycoprotein tenascin-R."xsd:string
http://purl.uniprot.org/citations/11161481http://purl.uniprot.org/core/volume"17"xsd:string
http://purl.uniprot.org/citations/11161481http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/11161481
http://purl.uniprot.org/citations/11161481http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/11161481
http://purl.uniprot.org/uniprot/Q8BYI9#attribution-9D09C2C33F3AA8A9AD80FA5B793D8891http://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/11161481
http://purl.uniprot.org/uniprot/#_A0A0A6YWD9-mappedCitation-11161481http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/11161481
http://purl.uniprot.org/uniprot/#_A0A0A6YWY3-mappedCitation-11161481http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/11161481
http://purl.uniprot.org/uniprot/#_Q8BYI9-mappedCitation-11161481http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/11161481
http://purl.uniprot.org/uniprot/Q8BYI9http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/11161481
http://purl.uniprot.org/uniprot/A0A0A6YWD9http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/11161481
http://purl.uniprot.org/uniprot/A0A0A6YWY3http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/11161481