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dc.contributor.authorFeliciano, C.
dc.contributor.authorItohara, S.
dc.contributor.authorDong, X.
dc.contributor.authorZhang, Qiangge
dc.contributor.authorGao, Xian
dc.contributor.authorLi, Chenchen
dc.contributor.authorWang, Dongqing
dc.contributor.authorZhou, Dingxi
dc.contributor.authorMei, Yuan
dc.contributor.authorMonteiro, Patricia
dc.contributor.authorAnand, Michelle S.
dc.contributor.authorFu, Zhanyan
dc.contributor.authorFeng, Guoping
dc.date.accessioned2017-01-30T21:05:10Z
dc.date.available2017-01-30T21:05:10Z
dc.date.issued2016-02
dc.date.submitted2015-12
dc.identifier.issn0270-6474
dc.identifier.issn1529-2401
dc.identifier.urihttp://hdl.handle.net/1721.1/106797
dc.description.abstractIntellectual disability is a common neurodevelopmental disorder characterized by impaired intellectual and adaptive functioning. Both environmental insults and genetic defects contribute to the etiology of intellectual disability. Copy number variations of SORBS2 have been linked to intellectual disability. However, the neurobiological function of SORBS2 in the brain is unknown. The SORBS2 gene encodes ArgBP2 (Arg/c-Abl kinase binding protein 2) protein in non-neuronal tissues and is alternatively spliced in the brain to encode nArgBP2 protein. We found nArgBP2 colocalized with F-actin at dendritic spines and growth cones in cultured hippocampal neurons. In the mouse brain, nArgBP2 was highly expressed in the cortex, amygdala, and hippocampus, and enriched in the outer one-third of the molecular layer in dentate gyrus. Genetic deletion of Sorbs2 in mice led to reduced dendritic complexity and decreased frequency of AMPAR-miniature spontaneous EPSCs in dentate gyrus granule cells. Behavioral characterization revealed that Sorbs2 deletion led to a reduced acoustic startle response, and defective long-term object recognition memory and contextual fear memory. Together, our findings demonstrate, for the first time, an important role for nArgBP2 in neuronal dendritic development and excitatory synaptic transmission, which may thus inform exploration of neurobiological basis of SORBS2 deficiency in intellectual disability.en_US
dc.description.sponsorshipMassachusetts Institute of Technology. Poitras Center for Affective Disorders Researchen_US
dc.description.sponsorshipBroad Institute of MIT and Harvard. Stanley Center for Psychiatric Researchen_US
dc.description.sponsorshipNational Institute of Mental Health (U.S.) (Grant R01MH081201to)en_US
dc.description.sponsorshipChina Scholarship Council (Graduate Fellowship)en_US
dc.description.sponsorshipNational Science Foundation (U.S.). Graduate Research Fellowship Programen_US
dc.description.sponsorshipHarvard Universityen_US
dc.description.sponsorshipFundação para a Ciência e a Tecnologia (Portugal) (Doctoral Fellowship SFRH/BD/33894/2009)en_US
dc.description.sponsorshipBrain & Behavior Research Foundation (National Institute of Mental Health Young Investigator Grant)en_US
dc.description.sponsorshipDuke Institute for Brain Sciencesen_US
dc.language.isoen_US
dc.publisherSociety for Neuroscienceen_US
dc.relation.isversionofhttp://dx.doi.org/10.1523/jneurosci.2528-15.2016en_US
dc.rightsCreative Commons Attribution 4.0 International Licenseen_US
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/en_US
dc.sourceSociety for Neuroscienceen_US
dc.titleImpaired Dendritic Development and Memory in Sorbs2 Knock-Out Miceen_US
dc.typeArticleen_US
dc.identifier.citationZhang, Q. et al. “Impaired Dendritic Development and Memory in Sorbs2 Knock-Out Mice.” Journal of Neuroscience 36.7 (2016): 2247–2260.en_US
dc.contributor.departmentMassachusetts Institute of Technology. Department of Brain and Cognitive Sciencesen_US
dc.contributor.departmentMcGovern Institute for Brain Research at MITen_US
dc.contributor.mitauthorZhang, Qiangge
dc.contributor.mitauthorGao, Xian
dc.contributor.mitauthorLi, Chenchen
dc.contributor.mitauthorWang, Dongqing
dc.contributor.mitauthorZhou, Dingxi
dc.contributor.mitauthorMei, Yuan
dc.contributor.mitauthorMonteiro, Patricia
dc.contributor.mitauthorAnand, Michelle S.
dc.contributor.mitauthorFu, Zhanyan
dc.contributor.mitauthorFeng, Guoping
dc.relation.journalJournal of Neuroscienceen_US
dc.eprint.versionFinal published versionen_US
dc.type.urihttp://purl.org/eprint/type/JournalArticleen_US
eprint.statushttp://purl.org/eprint/status/PeerRevieweden_US
dspace.orderedauthorsZhang, Q.; Gao, X.; Li, C.; Feliciano, C.; Wang, D.; Zhou, D.; Mei, Y.; Monteiro, P.; Anand, M.; Itohara, S.; Dong, X.; Fu, Z.; Feng, G.en_US
dspace.embargo.termsNen_US
dc.identifier.orcidhttps://orcid.org/0000-0002-1069-235X
dc.identifier.orcidhttps://orcid.org/0000-0002-3546-4740
dc.identifier.orcidhttps://orcid.org/0000-0002-5596-1269
dc.identifier.orcidhttps://orcid.org/0000-0003-3288-4560
dc.identifier.orcidhttps://orcid.org/0000-0001-9473-2402
dc.identifier.orcidhttps://orcid.org/0000-0002-8021-277X
mit.licensePUBLISHER_CCen_US
mit.metadata.statusComplete


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