Anterior cingulate cortex dysfunction underlies social deficits in Shank3 mutant mice.
Baolin Guo1, Jing Chen2, Qian Chen3
1Department of Neurobiology, School of Basic Medicine, Fourth Military Medical University, Xi'an, China.
Nature Neuroscience
|July 24, 2019
Summary
Autism spectrum disorder (ASD) social deficits stem from impaired Shank3 protein in the anterior cingulate cortex (ACC). Restoring ACC function or Shank3 expression improves social behavior in mouse models.
Area of Science:
- Neuroscience
- Genetics
- Autism Spectrum Disorder Research
Background:
- Social deficit is a core feature of autism spectrum disorder (ASD).
- Neural mechanisms underlying ASD social deficits remain unclear.
- Shank3 is a high-confidence candidate gene for ASD.
Purpose of the Study:
- To investigate the role of Shank3 in the anterior cingulate cortex (ACC) in social behavior.
- To elucidate the neural mechanisms of social deficits in ASD.
- To identify potential therapeutic targets for ASD-related social impairments.
Main Methods:
- Utilized Shank3 mutant mice with conditional knockout in the ACC.
- Examined structural and functional properties of glutamatergic synapses in ACC pyramidal neurons.
- Assessed social interaction deficits and the effects of interventions like ACC activity enhancement and Shank3 restoration.
Main Results:
- Shank3 mutation in ACC pyramidal neurons caused excitatory synaptic dysfunction.
- Conditional Shank3 knockout in the ACC led to social interaction deficits.
- Enhancing ACC activity, restoring Shank3, or using an AMPAkine modulator improved social behavior in mutant mice.
Conclusions:
- The ACC plays a crucial role in regulating social behavior in mice.
- ACC dysfunction, specifically involving Shank3, is implicated in ASD social impairments.
- Targeting ACC activity and Shank3 expression may offer therapeutic strategies for ASD.
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