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http://purl.uniprot.org/citations/25662838http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/25662838http://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/25662838http://purl.org/dc/terms/identifier"doi:10.1038/npp.2015.26"xsd:string
http://purl.uniprot.org/citations/25662838http://purl.uniprot.org/core/author"Tanaka K."xsd:string
http://purl.uniprot.org/citations/25662838http://purl.uniprot.org/core/author"Aizawa H."xsd:string
http://purl.uniprot.org/citations/25662838http://purl.uniprot.org/core/author"Ito Y."xsd:string
http://purl.uniprot.org/citations/25662838http://purl.uniprot.org/core/author"Nagai T."xsd:string
http://purl.uniprot.org/citations/25662838http://purl.uniprot.org/core/author"Nomura M."xsd:string
http://purl.uniprot.org/citations/25662838http://purl.uniprot.org/core/author"Yanagisawa M."xsd:string
http://purl.uniprot.org/citations/25662838http://purl.uniprot.org/core/author"Takata N."xsd:string
http://purl.uniprot.org/citations/25662838http://purl.uniprot.org/core/author"Cui W."xsd:string
http://purl.uniprot.org/citations/25662838http://purl.uniprot.org/core/author"Iino Y."xsd:string
http://purl.uniprot.org/citations/25662838http://purl.uniprot.org/core/author"Takayanagi R."xsd:string
http://purl.uniprot.org/citations/25662838http://purl.uniprot.org/core/author"Soma M."xsd:string
http://purl.uniprot.org/citations/25662838http://purl.uniprot.org/core/author"Hirase H."xsd:string
http://purl.uniprot.org/citations/25662838http://purl.uniprot.org/core/author"Kano M."xsd:string
http://purl.uniprot.org/citations/25662838http://purl.uniprot.org/core/author"Yoshida J."xsd:string
http://purl.uniprot.org/citations/25662838http://purl.uniprot.org/core/author"Gotz M."xsd:string
http://purl.uniprot.org/citations/25662838http://purl.uniprot.org/core/author"Bai N."xsd:string
http://purl.uniprot.org/citations/25662838http://purl.uniprot.org/core/author"Tanimura A."xsd:string
http://purl.uniprot.org/citations/25662838http://purl.uniprot.org/core/author"Aida T."xsd:string
http://purl.uniprot.org/citations/25662838http://purl.uniprot.org/core/author"Tanaka K.F."xsd:string
http://purl.uniprot.org/citations/25662838http://purl.uniprot.org/core/date"2015"xsd:gYear
http://purl.uniprot.org/citations/25662838http://purl.uniprot.org/core/name"Neuropsychopharmacology"xsd:string
http://purl.uniprot.org/citations/25662838http://purl.uniprot.org/core/pages"1569-1579"xsd:string