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Expression of excitatory amino acid transporter interacting protein transcripts in the thalamus in schizophrenia

dc.contributor.authorHuerta, Iboneen_US
dc.contributor.authorMcCullumsmith, Robert E.en_US
dc.contributor.authorHaroutunian, Vahramen_US
dc.contributor.authorGiménez-Amaya, José Manuelen_US
dc.contributor.authorMeador-Woodruff, James H.en_US
dc.date.accessioned2007-07-11T18:12:38Z
dc.date.available2007-07-11T18:12:38Z
dc.date.issued2006-06-01en_US
dc.identifier.citationHuerta, Ibone; McCullumsmith, Robert E.; Haroutunian, Vahram; GimÉnez-Amaya, JosÉ Manuel; Meador-Woodruff, James H. (2006). "Expression of excitatory amino acid transporter interacting protein transcripts in the thalamus in schizophrenia." Synapse 59(7): 394-402. <http://hdl.handle.net/2027.42/55214>en_US
dc.identifier.issn0887-4476en_US
dc.identifier.issn1098-2396en_US
dc.identifier.urihttps://hdl.handle.net/2027.42/55214
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=16485262&dopt=citationen_US
dc.description.abstractThe excitatory amino acid transporters (EAATs) are a family of plasma membrane proteins that maintain synaptic glutamate concentration by removing glutamate from the synaptic cleft. EAATs are expressed by glia (EAAT1 and EAAT2) and neurons (EAAT3 and EAAT4) throughout the brain. Glutamate reuptake is regulated, in part, by EAAT-interacting proteins that modulate subcellular localization and glutamate transport activity of the EAATs. Several lines of investigation support the hypothesis of glutamatergic abnormalities in schizophrenia. Previous work in our laboratory demonstrated increased expression of EAAT1 and EAAT2 transcripts in the thalamus, suggesting that alterations in synaptic glutamate levels may contribute to the pathophysiology of schizophrenia. Since EAAT-interacting proteins regulate EAAT function, directly impacting glutamatergic neurotransmission, we hypothesized that expression of EAAT-interacting proteins may also be altered in schizophrenia. Using in situ hybridization in subjects with schizophrenia and a comparison group, we detected increased expression of JWA and KIAA0302, molecules that regulate EAAT3 and EAAT4, respectively, in the thalamus in schizophrenia. In contrast, we did not find changes in the expression of transcripts for the EAAT2 and EAAT4 regulatory proteins GPS-1 and ARHGEF11. To address prior antipsychotic treatment in our schizophrenic subjects, we treated rats with haloperidol and clozapine for 4 weeks, and found changes in transcript expression of the EAAT-interacting proteins in clozapine-, but not haloperidol-, treated rats. These findings suggest that proteins associated with the regulation of glutamate reuptake may be abnormal in this illness, supporting the hypothesis of altered thalamic glutamatergic neurotransmission in schizophrenia. Synapse 59:394–402, 2006. © 2006 Wiley-Liss, Inc.en_US
dc.format.extent290953 bytes
dc.format.extent3118 bytes
dc.format.mimetypeapplication/pdf
dc.format.mimetypetext/plain
dc.publisherWiley Subscription Services, Inc., A Wiley Companyen_US
dc.subject.otherLife and Medical Sciencesen_US
dc.subject.otherNeuroscience, Neurology and Psychiatryen_US
dc.titleExpression of excitatory amino acid transporter interacting protein transcripts in the thalamus in schizophreniaen_US
dc.typeArticleen_US
dc.rights.robotsIndexNoFollowen_US
dc.subject.hlbsecondlevelMolecular, Cellular and Developmental Biologyen_US
dc.subject.hlbsecondlevelNeurosciencesen_US
dc.subject.hlbsecondlevelPublic Healthen_US
dc.subject.hlbtoplevelHealth Sciencesen_US
dc.subject.hlbtoplevelScienceen_US
dc.description.peerreviewedPeer Revieweden_US
dc.contributor.affiliationumMolecular and Behavioral Neuroscience Institute and Department of Psychiatry, University of Michigan Medical School, Ann Arbor, Michigan 48109 ; Departamento de MorfologÍa, Facultad de Medicina Universidad AutÓnoma de Madrid, 28029 Madrid, Spainen_US
dc.contributor.affiliationumMolecular and Behavioral Neuroscience Institute and Department of Psychiatry, University of Michigan Medical School, Ann Arbor, Michigan 48109 ; 205 Zina Pitcher Place, Molecular and Behavioral Neuroscience Institute, University of Michigan, Ann Arbor, MI 48109, USAen_US
dc.contributor.affiliationumMolecular and Behavioral Neuroscience Institute and Department of Psychiatry, University of Michigan Medical School, Ann Arbor, Michigan 48109en_US
dc.contributor.affiliationotherDepartment of Psychiatry, Mount Sinai School of Medicine, New York, New York 10029en_US
dc.contributor.affiliationotherDepartamento de MorfologÍa, Facultad de Medicina Universidad AutÓnoma de Madrid, 28029 Madrid, Spainen_US
dc.identifier.pmid16485262en_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/55214/1/20250_ftp.pdfen_US
dc.identifier.doihttp://dx.doi.org/10.1002/syn.20250en_US
dc.identifier.sourceSynapseen_US
dc.owningcollnameInterdisciplinary and Peer-Reviewed


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