Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/12633
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dc.contributor.authorJiang, Luningen
dc.contributor.authorO'Leary, Claireen
dc.contributor.authorKim, Hyun Ahen
dc.contributor.authorParish, Clare Len
dc.contributor.authorMassalas, Jimen
dc.contributor.authorWaddington, John Len
dc.contributor.authorEhrlich, Michelle Een
dc.contributor.authorSchütz, Günteren
dc.contributor.authorGantois, Ilseen
dc.contributor.authorLawrence, Andrew Jen
dc.contributor.authorDrago, Johnen
dc.date.accessioned2015-05-16T02:21:32Z
dc.date.available2015-05-16T02:21:32Z
dc.date.issued2015-02-12en
dc.identifier.citationNeurobiology of Disease 2015; 76(): 137-58en
dc.identifier.govdoc25684539en
dc.identifier.otherPUBMEDen
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/12633en
dc.description.abstractD1-dopamine receptors (Drd1a) are highly expressed in the deep layers of the cerebral cortex and the striatum. A number of human diseases such as Huntington disease and schizophrenia are known to have cortical pathology involving dopamine receptor expressing neurons. To illuminate their functional role, we exploited a Cre/Lox molecular paradigm to generate Emx-1(tox) MUT mice, a transgenic line in which cortical Drd1a-expressing pyramidal neurons were selectively ablated. Emx-1(tox) MUT mice displayed prominent forelimb dystonia, hyperkinesia, ataxia on rotarod testing, heightened anxiety-like behavior, and age-dependent abnormalities in a test of social interaction. The latter occurred in the context of normal working memory on testing in the Y-maze and for novel object recognition. Some motor and behavioral abnormalities in Emx-1(tox) MUT mice overlapped with those in CamKIIα(tox) MUT transgenic mice, a line in which both striatal and cortical Drd1a-expressing cells were ablated. Although Emx-1(tox) MUT mice had normal striatal anatomy, both Emx-1(tox) MUT and CamKIIα(tox) MUT mice displayed selective neuronal loss in cortical layers V and VI. This study shows that loss of cortical Drd1a-expressing cells is sufficient to produce deficits in multiple motor and behavioral domains, independent of striatal mechanisms. Primary cortical changes in the D1 dopamine receptor compartment are therefore likely to model a number of core clinical features in disorders such as Huntington disease and schizophrenia.en
dc.language.isoenen
dc.subject.otherD1-dopamine receptoren
dc.subject.otherDystoniaen
dc.subject.otherHuntington diseaseen
dc.subject.otherSchizophreniaen
dc.subject.otherTargeted cell deletionen
dc.titleMotor and behavioral phenotype in conditional mutants with targeted ablation of cortical D1 dopamine receptor-expressing cells.en
dc.typeJournal Articleen
dc.identifier.journaltitleNeurobiology of diseaseen
dc.identifier.affiliationFlorey Institute of Neuroscience and Mental Health, University of Melbourne, Melbourne, Australiaen
dc.identifier.affiliationSt Vincent's Hospital, Melbourne, Victoria, Australiaen
dc.identifier.affiliationDepartment of Neurology, Mount Sinai School of Medicine, New York, NY, USAen
dc.identifier.affiliationMolecular and Cellular Therapeutics, Royal College of Surgeons in Ireland, Dublin 2, Ireland.en
dc.identifier.affiliationDeutsches Krebsforschungszentrum, Heidelberg, Germany.en
dc.identifier.doi10.1016/j.nbd.2015.02.006en
dc.description.pages137-58en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/25684539en
dc.type.austinJournal Articleen
item.openairetypeJournal Article-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.grantfulltextnone-
item.fulltextNo Fulltext-
item.cerifentitytypePublications-
item.languageiso639-1en-
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