| First Author | Chen D | Year | 2019 |
| Journal | Cereb Cortex | Volume | 29 |
| Issue | 8 | Pages | 3666-3682 |
| PubMed ID | 31237323 | Mgi Jnum | J:333603 |
| Mgi Id | MGI:6754689 | Doi | 10.1093/cercor/bhz114 |
| Citation | Chen D, et al. (2019) Loss of Foxg1 Impairs the Development of Cortical SST-Interneurons Leading to Abnormal Emotional and Social Behaviors. Cereb Cortex 29(8):3666-3682 |
| abstractText | FOXG1 syndrome is a severe encephalopathy that exhibit intellectual disability, emotional disorder, and limited social communication. To elucidate the contribution of somatostatin-expressing interneurons (SST-INs) to the cellular basis underlying FOXG1 syndrome, here, by crossing SST-cre with a Foxg1fl/fl line, we selectively ablated Foxg1. Loss of Foxg1 resulted in an obvious reduction in the number of SST-INs, accompanied by an altered ratio of subtypes. Foxg1-deficient SST-INs exhibited decreased membrane excitability and a changed ratio of electrophysiological firing patterns, which subsequently led to an excitatory/inhibitory imbalance. Moreover, cognitive defects, limited social interactions, and depression-like behaviors were detected in Foxg1 cKO mice. Treatment with low-dose of clonazepam effectively alleviated the defects. These results identify a link of SST-IN development to the aberrant emotion, cognition, and social capacities in patients. Our findings identify a novel role of Foxg1 in SST-IN development and put new insights into the cellular basis of FOXG1 syndrome. |
