http://purl.uniprot.org/citations/25662838 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/25662838 | http://www.w3.org/2000/01/rdf-schema#comment | "An increase in the ratio of cellular excitation to inhibition (E/I ratio) has been proposed to underlie the pathogenesis of neuropsychiatric disorders, such as autism spectrum disorders (ASD), obsessive-compulsive disorder (OCD), and Tourette's syndrome (TS). A proper E/I ratio is achieved via factors expressed in neuron and glia. In astrocytes, the glutamate transporter GLT1 is critical for regulating an E/I ratio. However, the role of GLT1 dysfunction in the pathogenesis of neuropsychiatric disorders remains unknown because mice with a complete deficiency of GLT1 exhibited seizures and premature death. Here, we show that astrocyte-specific GLT1 inducible knockout (GLAST(CreERT2/+)/GLT1(flox/flox), iKO) mice exhibit pathological repetitive behaviors including excessive and injurious levels of self-grooming and tic-like head shakes. Electrophysiological studies reveal that excitatory transmission at corticostriatal synapse is normal in a basal state but is increased after repetitive stimulation. Furthermore, treatment with an N-methyl-D-aspartate (NMDA) receptor antagonist memantine ameliorated the pathological repetitive behaviors in iKO mice. These results suggest that astroglial GLT1 has a critical role in controlling the synaptic efficacy at corticostriatal synapses and its dysfunction causes pathological repetitive behaviors."xsd:string |
http://purl.uniprot.org/citations/25662838 | http://purl.org/dc/terms/identifier | "doi:10.1038/npp.2015.26"xsd:string |
http://purl.uniprot.org/citations/25662838 | http://purl.uniprot.org/core/author | "Tanaka K."xsd:string |
http://purl.uniprot.org/citations/25662838 | http://purl.uniprot.org/core/author | "Aizawa H."xsd:string |
http://purl.uniprot.org/citations/25662838 | http://purl.uniprot.org/core/author | "Ito Y."xsd:string |
http://purl.uniprot.org/citations/25662838 | http://purl.uniprot.org/core/author | "Nagai T."xsd:string |
http://purl.uniprot.org/citations/25662838 | http://purl.uniprot.org/core/author | "Nomura M."xsd:string |
http://purl.uniprot.org/citations/25662838 | http://purl.uniprot.org/core/author | "Yanagisawa M."xsd:string |
http://purl.uniprot.org/citations/25662838 | http://purl.uniprot.org/core/author | "Takata N."xsd:string |
http://purl.uniprot.org/citations/25662838 | http://purl.uniprot.org/core/author | "Cui W."xsd:string |
http://purl.uniprot.org/citations/25662838 | http://purl.uniprot.org/core/author | "Iino Y."xsd:string |
http://purl.uniprot.org/citations/25662838 | http://purl.uniprot.org/core/author | "Takayanagi R."xsd:string |
http://purl.uniprot.org/citations/25662838 | http://purl.uniprot.org/core/author | "Soma M."xsd:string |
http://purl.uniprot.org/citations/25662838 | http://purl.uniprot.org/core/author | "Hirase H."xsd:string |
http://purl.uniprot.org/citations/25662838 | http://purl.uniprot.org/core/author | "Kano M."xsd:string |
http://purl.uniprot.org/citations/25662838 | http://purl.uniprot.org/core/author | "Yoshida J."xsd:string |
http://purl.uniprot.org/citations/25662838 | http://purl.uniprot.org/core/author | "Gotz M."xsd:string |
http://purl.uniprot.org/citations/25662838 | http://purl.uniprot.org/core/author | "Bai N."xsd:string |
http://purl.uniprot.org/citations/25662838 | http://purl.uniprot.org/core/author | "Tanimura A."xsd:string |
http://purl.uniprot.org/citations/25662838 | http://purl.uniprot.org/core/author | "Aida T."xsd:string |
http://purl.uniprot.org/citations/25662838 | http://purl.uniprot.org/core/author | "Tanaka K.F."xsd:string |
http://purl.uniprot.org/citations/25662838 | http://purl.uniprot.org/core/date | "2015"xsd:gYear |
http://purl.uniprot.org/citations/25662838 | http://purl.uniprot.org/core/name | "Neuropsychopharmacology"xsd:string |
http://purl.uniprot.org/citations/25662838 | http://purl.uniprot.org/core/pages | "1569-1579"xsd:string |