Loss of Foxg1 Impairs the Development of Cortical SST-Interneurons Leading to Abnormal Emotional and Social Behaviors.

FOXG1 syndrome is a severe encephalopathy that exhibit intellectual disability, emotional disorder, and limited social communication. To elucidate the contribution of somatostatin-expressing interneurons to the cellular basis underlying FOXG1 syndrome, here, by crossing with a Foxg1fl/fl line, we selectively ablated Foxg1. Loss of Foxg1 resulted in an obvious reduction in the number of accompanied by an altered ratio of subtypes. Foxg1-deficient 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 development to the aberrant emotion, cognition, and social capacities in patients. Our findings identify a novel role of Foxg1 in duanyu1942-IN development and put new insights into the cellular basis of FOXG1 syndrome.

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