Loss of Satb2 in the Cortex and Hippocampus Leads to Abnormal Behaviors in Mice

Frontiers in Molecular Neuroscience

Qiong Zhang¹  Ying Huang¹  Lei Zhang¹  Yu-Qiang Ding²  Ning-Ning Song⁴ 

[1] Department of Anatomy and Neurobiology, Tongji University School of Medicine, Shanghai, China;Department of Laboratory Animal Science, Fudan University, Shanghai, China;Key Laboratory of Arrhythmias, Ministry of Education of China, East Hospital, Tongji University School of Medicine, Shanghai, China;State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Institutes of Brain Science, Fudan University, Shanghai, China;

关键词: Satb2;    cerebral cortex;    hippocampus;    Satb2-associated syndrome;    mouse behavior;   

DOI  :  10.3389/fnmol.2019.00033

来源: DOAJ

【 摘 要 】

Satb2-associated syndrome (SAS) is a genetic disorder that results from the deletion or mutation of one allele within the Satb2 locus. Patients with SAS show behavioral abnormalities, including developmental delay/intellectual disability, hyperactivity, and symptoms of autism. To address the role of Satb2 in SAS-related behaviors and generate an SAS mouse model, Satb2 was deleted in the cortex and hippocampus of Emx1-Cre; Satb2flox/flox [Satb2 conditional knockout (CKO)] mice. Satb2 CKO mice showed hyperactivity, increased impulsivity, abnormal social novelty, and impaired spatial learning and memory. Furthermore, we also found that the development of neurons in cortical layer IV was defective in Satb2 CKO mice, as shown by the loss of layer-specific gene expression and abnormal thalamocortical projections. In summary, the abnormal behaviors revealed in Satb2 CKO mice may reflect the SAS symptoms associated with Satb2 mutation in human patients, possibly due to defective development of cortical neurons in multiple layers including alterations of their inputs/outputs.

【 授权许可】

Unknown