Date
2021
Abstract
Impairments in social relationships and awareness are features observed in autism spectrum disorders (ASDs). However, the under lying mechanisms remain poorly understood. Shank2 is a high-confi dence ASD candidate gene and localizes primarily to postsynaptic densities (PSDs) of excitatory synapses in the central nervous system (CNS). We show here that loss of Shank2 in mice leads to a lack of social attachment and bonding behavior towards pubs independent of hormonal, cognitive, or sensitive deficits. Shank2 / mice display functional changes in nuclei of the social attachment circuit that were most prominent in the medial preoptic area (MPOA) of the hypothalamus. Selective enhancement of MPOA activity by DREADD technology re-established social bonding behavior in Shank2 / mice, providing evidence that the identified circuit might be crucial for explaining how social deficits in ASD can arise.
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Description
peer-reviewed
Publisher
EMBO Press
Citation
The EMBO Journal;40: e104267
Collections
Biological Sciences
Bernal Institute
Health Research Institute (HRI)
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Grabrucker_2021_Activation.pdf
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Keywords
autism spectrum disorders, bonding, SHANK3, social behavior
ULRR Identifiers
https://hdl.handle.net/10344/9886
 https://doi.org/10.34961/15146
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Funding Information
European Union (EU), Horizon 2020, Comitato Telethon Fondazione Onlus
Sustainable Development Goals
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