Nature Neuroscience. 2019 May 27
Baolin Guo , Jing Chen, Qian Chen, Keke Ren, Dayun Feng, Honghui Mao, Han Yao, Jing Yang, Haiying Liu, Yingying Liu, Fan Jia, Chuchu Qi, Taylor Lynn-Jones, Hailan Hu ,Zhanyan Fu, Guoping Feng , Wenting Wang  and Shengxi Wu 
Products used in the paper Details Operation
AAV vector packaging We then chose gRNA2, which had the best efficiency, to package in AAV serotype 8 (PackGene Biotech) for administration to the mice. Request Quote

Research Field: CNS

AAV Serotype: AAV2/8

Dose: the viral titer was (2–5) × 10^12 particles per ml. For optical activation behavioral experiments, 350 nl of AAV2/8-CaMKIIa-ChR2-EYFP, AAV2/8-CaMKIIa-eNpHR3.0-EYFP or AAV2/8-CaMKIIa-EYFP was unilaterally injected into the ACC. For the DREADDs activation behavioral experiments, a 350-nl mixture of AAV2/8- CaMKIIa-Cre-EGFP and AAV2/8-EF1a-DIO-hM3D(Gq)-mCherry or AAV2/8- CaMKIIa-EYFP and AAV2/8-EF1a-DIO-hM3D(Gq)—mCherry was unilaterally injected into the ACC. For the conditional knockout and rescue experiments, 300 nl of AAV2/9-SaCas9-GFP or AAV2/8-CaMKIIa-Cre-EGFP was bilaterally injected into the ACC.

Routes of Administration: AAll skull measurements were made relative to Bregma, and viral injection into the ACC was performed using a microinjection needle with a 10-μl microsyringe (Gaoge) to deliver the virus at a rate of 50 nl min−1 using a microsyringe pump

Targeted organ: brain

Animal or cell line strain: The Shank3B−/−, CKI (Shank3fx/fx) and Thy1-GCaMP3 mouse strains have been previously characterized 15,21,50, and all mice had a pure C57BL/6J background. Male and female mice aged 2–6 months old were used in the electrophysiological experiments. All virus injections were administered to mice aged 2–3 months old.


Social deficit is a core clinical feature of autism spectrum disorder (ASD) but the underlying neural mechanisms remain largely unclear. We demonstrate that structural and functional impairments occur in glutamatergic synapses in the pyramidal neurons of the anterior cingulate cortex (ACC) in mice with a mutation in Shank3, a high-confidence candidate ASD gene. Conditional knockout of Shank3 in the ACC was sufficient to generate excitatory synaptic dysfunction and social interaction deficits, whereas selective enhancement of ACC activity, restoration of SHANK3 expression in the ACC, or systemic administration of an α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptor positive modulator improved social behavior in Shank3 mutant mice. Our findings provide direct evidence for the notion that the ACC has a role in the regulation of social behavior in mice and indicate that ACC dysfunction may be involved in social impairments in ASD.

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