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dc.contributor.authorBarros, Claudia
dc.contributor.authorCalabrese, B
dc.contributor.authorChamero, P
dc.contributor.authorRoberts, AJ
dc.contributor.authorKorzus, E
dc.contributor.authorLloyd, K
dc.contributor.authorStowers, L
dc.contributor.authorMayford, M
dc.contributor.authorHalpain, S
dc.contributor.authorMüller, U
dc.date.accessioned2016-10-26T21:35:52Z
dc.date.available2016-10-26T21:35:52Z
dc.date.issued2009-03-17
dc.identifier.issn0027-8424
dc.identifier.issn1091-6490
dc.identifier.urihttp://hdl.handle.net/10026.1/6648
dc.description.abstract

<jats:p> Neuregulin-1 (NRG1) and its ErbB2/B4 receptors are encoded by candidate susceptibility genes for schizophrenia, yet the essential functions of NRG1 signaling in the CNS are still unclear. Using CRE/LOX technology, we have inactivated ErbB2/B4-mediated NRG1 signaling specifically in the CNS. In contrast to expectations, cell layers in the cerebral cortex, hippocampus, and cerebellum develop normally in the mutant mice. Instead, loss of ErbB2/B4 impairs dendritic spine maturation and perturbs interactions of postsynaptic scaffold proteins with glutamate receptors. Conversely, increased NRG1 levels promote spine maturation. <jats:italic>ErbB2/B4</jats:italic> -deficient mice show increased aggression and reduced prepulse inhibition. Treatment with the antipsychotic drug clozapine reverses the behavioral and spine defects. We conclude that ErbB2/B4-mediated NRG1 signaling modulates dendritic spine maturation, and that defects at glutamatergic synapses likely contribute to the behavioral abnormalities in <jats:italic>ErbB2</jats:italic> / <jats:italic>B4</jats:italic> -deficient mice. </jats:p>

dc.format.extent4507-4512
dc.format.mediumPrint-Electronic
dc.languageen
dc.language.isoeng
dc.publisherProceedings of the National Academy of Sciences
dc.subjectcerebral cortex
dc.subjectdendritic spines
dc.subjectmigration
dc.subjectneuregulin
dc.subjectschizophrenia
dc.titleImpaired maturation of dendritic spines without disorganization of cortical cell layers in mice lacking NRG1/ErbB signaling in the central nervous system
dc.typejournal-article
dc.typeJournal Article
dc.typeResearch Support, N.I.H., Extramural
dc.typeResearch Support, Non-U.S. Gov't
plymouth.author-urlhttps://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000264278800081&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=11bb513d99f797142bcfeffcc58ea008
plymouth.issue11
plymouth.volume106
plymouth.publication-statusPublished
plymouth.journalProceedings of the National Academy of Sciences
dc.identifier.doi10.1073/pnas.0900355106
plymouth.organisational-group/Plymouth
plymouth.organisational-group/Plymouth/Faculty of Health
plymouth.organisational-group/Plymouth/Faculty of Health/Peninsula Medical School
plymouth.organisational-group/Plymouth/REF 2021 Researchers by UoA
plymouth.organisational-group/Plymouth/REF 2021 Researchers by UoA/UoA01 Clinical Medicine
plymouth.organisational-group/Plymouth/Users by role
plymouth.organisational-group/Plymouth/Users by role/Academics
plymouth.organisational-group/Plymouth/Users by role/Researchers in ResearchFish submission
dc.publisher.placeUnited States
dc.identifier.eissn1091-6490
dc.rights.embargoperiodNot known
rioxxterms.versionofrecord10.1073/pnas.0900355106
rioxxterms.licenseref.urihttp://www.rioxx.net/licenses/all-rights-reserved
rioxxterms.typeJournal Article/Review
plymouth.oa-locationhttp://www.pnas.org/content/106/11/4507.full.pdf?with-ds=yes


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