Please use this identifier to cite or link to this item: https://hdl.handle.net/10356/81153
Title: Postnatal TrkB ablation in corticolimbic interneurons induces social dominance in male mice
Authors: Chen, Albert I-Ming
Soong, Tuck Wah
Je, H. Shawn
Tan, Shawn
Xiao, Yixin
Yin, Henry H.
Keywords: Social Dominance
Prefrontal Cortex
Science::Biological sciences
Issue Date: 2018
Source: Tan, S., Xiao, Y., Yin, H. H., Chen, A. I-M., Soong, T. W., & Je, H. S. (2018). Postnatal TrkB ablation in corticolimbic interneurons induces social dominance in male mice. Proceedings of the National Academy of Sciences, 115(42), E9909-E9915. doi:10.1073/pnas.1812083115
Series/Report no.: Proceedings of the National Academy of Sciences
Abstract: Our ability to reason, feel, and socialize relies on the development of a tight balance between inhibition and excitation within cortical circuits. The growth factor BDNF and its receptor TrkB are important for inhibitory neuron development and have been implicated in neuropsychiatric disorders. However, the behavioral consequences of impaired BDNF/TrkB signaling are unknown. Using a transgenic mouse line, we show that mice with deletion of BDNF/TrkB signaling from cortical inhibitory neurons exhibit social dominance and decreased inhibition within the prefrontal cortex, a key region regulating social behavior. Reversal of the network imbalance with optogenetic inhibition could rescue the behavior. Our results reveal a previously uncharacterized role of growth factor signaling within cortical interneurons for the development of social cognition.
URI: https://hdl.handle.net/10356/81153
http://hdl.handle.net/10220/50077
ISSN: 0027-8424
DOI: http://dx.doi.org/10.1073/pnas.1812083115
Rights: © 2018 The Author(s) (Published by National Academy of Sciences). All rights reserved. This paper was published in Proceedings of the National Academy of Sciences of the United States of America and is made available with permission of The Author(s) (Published by National Academy of Sciences).
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metadata.item.fulltext: With Fulltext
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