RT Journal Article
SR Electronic
T1 Deconstruction of the retrosplenial granular cortex for social behavior in the mouse model of fragile X syndrome
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 2021.01.24.428008
DO 10.1101/2021.01.24.428008
A1 Hui-Fang Shang
A1 Ruonan Cai
A1 Hao Sun
A1 Tao Sheng
A1 Yan-Na Lian
A1 Li Liu
A1 Wei Chen
A1 Lixia Gao
A1 Han Xu
A1 Chen Zhang
A1 Jian-Hong Luo
A1 Xinjian Li
A1 Xiang-Yao Li
YR 2021
UL http://biorxiv.org/content/early/2021/01/26/2021.01.24.428008.abstract
AB 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 StatementThe authors have declared no competing interest.