Visualization and correction of social abnormalities-associat

AAV-SaCas9 was used to investigate whether the social deficit of MECP2-TG mice might be rescued by genome editing targeting human MECP2 transgene in adulthood. VSV-GFP was used to investigate the synaptic downstream partners of CA1 neurons. (From BrainVTA)

The viruses used from BrainVTA in this article are in the table below

Custom-Made AAVs	AAV-SaCas9-SghMECP2 AAV-SaCas9-SgLacZ
VSV	VSV-EGFP

Le Sun, Ruiguo Chen, Long Li, Bo Yuan, Kun Song, Na Pan, Tian-Lin Cheng, Shiyang Chang, Kunzhang Lin, Xiaobin He, Qian Wu, Fuqiang Xu, Zilong Qiu, Xiaoqun Wang
Pub Date: 2020-03-26, DOI: 10.1016/j.scib.2020.03.026, Email: sales@brainvta.com

Duplications of MECP2-containing genomic segments led to severe autistic symptoms in male. Transgenic mice overexpressing the human MECP2 gene exhibit autistic-like behaviors. Neural circuits underlying social defects in MECP2 transgenic (MECP2-TG) mice remain unknown. To observe neural activity of MECP2-TG mice in vivo, we performed calcium imaging by implantation of microendoscope in the hippocampal CA1 regions of MECP2-TG and wild type (WT) mice. We identified neurons whose activities were tightly associated with social interaction, which activity patterns were compromised in MECP2-TG mice. Strikingly, we rescued the social-related neural activity in CA1 and social defects in MECP2-TG mice by deleting the human MECP2 transgene using the CRISPR/Cas9 method during adulthood. Our data points to the neural circuitry responsible for social interactions and provides potential therapeutic targets for autism in adulthood.

This study is aimed to explore neural circuits underlying social defects in MECP2 transgenic (MECP2-TG) mice. These experiments provide compelling evidences that the neural activity of hippocampal CA1 neurons is essential for social interactions. More importantly, specific deletion of human MECP2 transgene (Rescue) in CA1 regions of MECP2-TG mice could totally restore the deficits of social interactions and social zone cells activity during adulthood. The data suggested that the neural circuitry in CA1 is responsible for deficit social interactions and provides potential therapeutic intervention targets for autism in adulthood.

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