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Deconstruction of the retrosplenial granular cortex for social behavior in the mouse model of fragile X syndrome

Hui-Fang Shang, Ruonan Cai, Hao Sun, Tao Sheng, Yan-Na Lian, Li Liu, Wei Chen, Lixia Gao, Han Xu, Chen Zhang, Jian-Hong Luo, Xinjian Li, Xiang-Yao Li
doi: https://doi.org/10.1101/2021.01.24.428008
Hui-Fang Shang
1Department of Neurobiology and Department of Anesthesiology, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou 310058, China
2NHC and CAMS Key Laboratory of Medical Neurobiology, Ministry of Education Frontier Science Center for Brain Research and Brain-Machine Integration, School of Brain Science and Brain Medicine, Zhejiang University, Hangzhou 310058, China
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Ruonan Cai
3Department of Neurology of the Second Affiliated Hospital, Interdisciplinary Institute of Neuroscience and Technology, Zhejiang University School of Medicine, Hangzhou 310029, China
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Hao Sun
3Department of Neurology of the Second Affiliated Hospital, Interdisciplinary Institute of Neuroscience and Technology, Zhejiang University School of Medicine, Hangzhou 310029, China
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Tao Sheng
2NHC and CAMS Key Laboratory of Medical Neurobiology, Ministry of Education Frontier Science Center for Brain Research and Brain-Machine Integration, School of Brain Science and Brain Medicine, Zhejiang University, Hangzhou 310058, China
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Yan-Na Lian
2NHC and CAMS Key Laboratory of Medical Neurobiology, Ministry of Education Frontier Science Center for Brain Research and Brain-Machine Integration, School of Brain Science and Brain Medicine, Zhejiang University, Hangzhou 310058, China
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Li Liu
4Core Facilities of the School of Medicine, Zhejiang University, Hangzhou 310058, China
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Wei Chen
5Department of Psychiatry, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou 310016, China
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Lixia Gao
3Department of Neurology of the Second Affiliated Hospital, Interdisciplinary Institute of Neuroscience and Technology, Zhejiang University School of Medicine, Hangzhou 310029, China
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Han Xu
2NHC and CAMS Key Laboratory of Medical Neurobiology, Ministry of Education Frontier Science Center for Brain Research and Brain-Machine Integration, School of Brain Science and Brain Medicine, Zhejiang University, Hangzhou 310058, China
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Chen Zhang
6School of Basic Medical Sciences, Capital Medical University, Beijing 100069, China
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Jian-Hong Luo
2NHC and CAMS Key Laboratory of Medical Neurobiology, Ministry of Education Frontier Science Center for Brain Research and Brain-Machine Integration, School of Brain Science and Brain Medicine, Zhejiang University, Hangzhou 310058, China
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Xinjian Li
3Department of Neurology of the Second Affiliated Hospital, Interdisciplinary Institute of Neuroscience and Technology, Zhejiang University School of Medicine, Hangzhou 310029, China
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  • For correspondence: Lixiangy@zju.edu.cn lxjbio@zju.edu.cn
Xiang-Yao Li
1Department of Neurobiology and Department of Anesthesiology, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou 310058, China
2NHC and CAMS Key Laboratory of Medical Neurobiology, Ministry of Education Frontier Science Center for Brain Research and Brain-Machine Integration, School of Brain Science and Brain Medicine, Zhejiang University, Hangzhou 310058, China
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  • For correspondence: Lixiangy@zju.edu.cn lxjbio@zju.edu.cn
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ABSTRACT

Deficits in fragile X mental retardation 1 protein lead to fragile X syndrome (FXS) with mental retardation and social activity disorder. Until now, the neuronal circuits that mediate the social impairments of FXS were mostly unclear. Accidently, we found fewer c-fos expression in RSG of KO than WT mice after social behavior test. Inactivation of RSG neurons decreased social novelty but not the sociability of naive mice. Interestingly, although the RSG neurons of KO mice had higher background activity, fewer social contact-related Ca2+ neurons were observed during social interaction test via one-photon Ca2+ imaging in freely-behaving mice. Strikingly, enhancing the activity of RSG neurons rescued the abnormal social novelty in KO mice. Further studies proved that the innervations from the subiculum and ACC to RSG contributes to the social behavior. Take together, we found that abnormal activity in the retrosplenial granular cortex (RSG) led to social novelty deficits in Fmr1-knockout (KO) mice. Moreover, selective manipulation of RSG neurons may be an effective strategy to treat the social deficits in FXS.

One Sentence Summary Deletion of FMRP leads to lower social-related neuronal activity in the RSG; this causes social novelty deficits in Fmr1-KO mice.

Competing Interest Statement

The authors have declared no competing interest.

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Posted January 26, 2021.
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Deconstruction of the retrosplenial granular cortex for social behavior in the mouse model of fragile X syndrome
Hui-Fang Shang, Ruonan Cai, Hao Sun, Tao Sheng, Yan-Na Lian, Li Liu, Wei Chen, Lixia Gao, Han Xu, Chen Zhang, Jian-Hong Luo, Xinjian Li, Xiang-Yao Li
bioRxiv 2021.01.24.428008; doi: https://doi.org/10.1101/2021.01.24.428008
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Deconstruction of the retrosplenial granular cortex for social behavior in the mouse model of fragile X syndrome
Hui-Fang Shang, Ruonan Cai, Hao Sun, Tao Sheng, Yan-Na Lian, Li Liu, Wei Chen, Lixia Gao, Han Xu, Chen Zhang, Jian-Hong Luo, Xinjian Li, Xiang-Yao Li
bioRxiv 2021.01.24.428008; doi: https://doi.org/10.1101/2021.01.24.428008

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