Please use this identifier to cite or link to this item: https://doi.org/10.1073/pnas.1812083115
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dc.titlePostnatal TrkB Ablation in Corticolimbic Interneurons Induces Social Dominance in Male Mice
dc.contributor.authorTan, S.
dc.contributor.authorXIAO YIXIN
dc.contributor.authorYin, H.H.
dc.contributor.authorChen, A.I.
dc.contributor.authorSOONG TUCK WAH
dc.contributor.authorHYUNSOO SHAWN JE
dc.date.accessioned2020-05-27T08:34:21Z
dc.date.available2020-05-27T08:34:21Z
dc.date.issued2018-10-16
dc.identifier.citationTan, S., XIAO YIXIN, Yin, H.H., Chen, A.I., SOONG TUCK WAH, HYUNSOO SHAWN JE (2018-10-16). Postnatal TrkB Ablation in Corticolimbic Interneurons Induces Social Dominance in Male Mice. Proceedings of the National Academy of Sciences of the United States of America 115 (42) : E9909-E9915. ScholarBank@NUS Repository. https://doi.org/10.1073/pnas.1812083115
dc.identifier.issn0027-8424
dc.identifier.issn1091-6490
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/168527
dc.description.abstractThe tight balance between synaptic excitation and inhibition (E/I) within neocortical circuits in the mammalian brain is important for complex behavior. Many loss-of-function studies have demonstrated that brain-derived neurotrophic factor (BDNF) and its cognate receptor tropomyosin receptor kinase B (TrkB) are essential for the development of inhibitory GABAergic neurons. However, behavioral consequences of impaired BDNF/TrkB signaling in GABAergic neurons remain unclear, largely due to confounding motor function deficits observed in previous animal models. In this study, we generated conditional knockout mice (TrkB cKO) in which TrkB was ablated from a majority of corticolimbic GABAergic interneurons postnatally. These mice showed intact motor coordination and movement, but exhibited enhanced dominance over other mice in a group-housed setting. In addition, immature fast-spiking GABAergic neurons of TrkB cKO mice resulted in an E/I imbalance in layer 5 microcircuits within the medial prefrontal cortex (mPFC), a key region regulating social dominance. Restoring the E/I imbalance via optogenetic modulation in the mPFC of TrkB cKO mice normalized their social dominance behavior. Taken together, our results provide strong evidence for a role of BDNF/TrkB signaling in inhibitory synaptic modulation and social dominance behavior in mice.
dc.description.urihttps://www.pnas.org/content/115/42/E9909
dc.publisherNational Academy of Sciences
dc.subjectBDNF; TrkB; interneurons; prefrontal cortex; social dominance.
dc.typeArticle
dc.contributor.departmentDEPT OF PHYSIOLOGY
dc.contributor.departmentDUKE-NUS MEDICAL SCHOOL
dc.description.doi10.1073/pnas.1812083115
dc.description.sourcetitleProceedings of the National Academy of Sciences of the United States of America
dc.description.volume115
dc.description.issue42
dc.description.pageE9909-E9915
dc.published.statePublished
dc.grant.idMOE2014-T2-2-071
dc.grant.idNMRC/CBRG/0075/2014
dc.grant.idNMRC/OFIRG/0050/2017
dc.grant.id13/1/96/688
dc.grant.idR01MH112883
dc.grant.fundingagencySingapore Ministry of Education
dc.grant.fundingagencyNational Medical Research Council Collaborative Research Grants
dc.grant.fundingagencyA*Star Translational Collaborative Research Partnership Grant
dc.grant.fundingagencyDuke–National University of Singapore (NUS) Signature Research Program Block Grant
dc.grant.fundingagencyNIH Grant
dc.grant.fundingagencyNUS Graduate School for Integrative Sciences and Engineering Scholarship
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