Ephrin-B3 coordinates timed axon targeting and amygdala spinogenesis for innate fear behaviour

Xiao-Na Zhu, Xian-Dong Liu, Suya Sun (), Hanyi Zhuang, Jing-Yu Yang, Mark Henkemeyer and Nan-Jie Xu ()
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Xiao-Na Zhu: Institute of Neurology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine
Xian-Dong Liu: Histology and Embryology, Shanghai Jiao Tong University School of Medicine
Suya Sun: Institute of Neurology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine
Hanyi Zhuang: The Institute of Health Sciences, Shanghai Institues for Biological Sciences, Chinese Academy of Sciences/Shanghai Jiao Tong University School of medicine
Jing-Yu Yang: Shenyang Pharmaceutical University
Mark Henkemeyer: Kent Waldrep Center for Basic Research on Nerve Growth and Regeneration, University of Texas Southwestern Medical Center
Nan-Jie Xu: Histology and Embryology, Shanghai Jiao Tong University School of Medicine

Nature Communications, 2016, vol. 7, issue 1, 1-11

Abstract: Abstract Innate emotion response to environmental stimuli is a fundamental brain function that is controlled by specific neural circuits. Dysfunction of early emotional circuits may lead to neurodevelopmental disorders such as autism and schizophrenia. However, how the functional circuits are formed to prime initial emotional behaviours remain elusive. We reveal here using gene-targeted mutations an essential role for ephrin-B3 ligand-like activity in the development of innate fear in the neonatal brain. We further demonstrate that ephrin-B3 controls axon targeting and coordinates spinogenesis and neuronal activity within the amygdala. The morphological and behavioural abnormalities in ephrin-B3 mutant mice are rescued by conditional knock-in of wild-type ephrin-B3 during the critical period when axon targeting and fear responses are initiated. Our results thus define a key axonal molecule that participates in the wiring of amygdala circuits and helps bring about fear emotion during the important adolescence period.

Date: 2016
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DOI: 10.1038/ncomms11096

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