Abstract
Autism spectrum disorder (ASD) is a neurodevelopmental condition primarily characterised by alterations in social interaction and communication combined with the presence of restricted interests and stereotyped behaviours. Mutations in several genes have been associated with ASD resulting in the generation of corresponding mouse models. Here, we focus on the behavioural (social and stereotyped behaviours), functional and structural traits of mice with mutations in genes encoding defined synaptic proteins including adhesion proteins, scaffolding proteins and subunits of channels and receptors. A meta-analysis on ASD mouse models shows that they can be divided into two subgroups. Cluster I gathered models highly impaired in social interest, stereotyped behaviours, synaptic physiology and protein composition, while Cluster II regrouped much less impaired models, with typical social interactions. This distribution was not related to gene families. Even within the large panel of mouse models carrying mutations in Shank3, the number of mutated isoforms was not related to the severity of the phenotype. Our study points that the majority of structural or functional analyses were performed in the hippocampus. However, to robustly link the structural and functional impairments with the behavioural deficits observed, brain structures forming relevant nodes in networks involved in social and stereotyped behaviours should be targeted in the future. In addition, the characterisation of core ASD-like behaviours needs to be more detailed using new approaches quantifying the variations in social motivation, recognition and stereotyped behaviours.
Allain-Thibeault Ferhat and Sonja Halbedl are equally contributing authors.
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Acknowledgements
We thank Jean-Pierre Bourgeois for his helpful comments and discussion on the manuscript. This work was supported by the Fondation de France, the ANR FLEXNEURIM [ANR09BLAN034003], the ANR [ANR-08-MNPS-037-01–SynGen], the Neuron-ERANET (EUHF-AUTISM), the Fondation Orange, the Fondation FondaMental, the Fondation de France and the Fondation Bettencourt Schueller. The research leading to this article has also received support from EU-AIMS, which receives support from the Innovative Medicines Initiative Joint Undertaking under grant agreement no.115300, resources of which are composed of financial contributions from the European Union’s Seventh Framework Programme (P7/2007–2013), from EFPIA companies in kind contribution and from Autism Speaks. MJS was further supported by the Baustein programme of Ulm University (L.SBN.0081), the Care-for-Rare Foundation, the Elite programme of the Baden-Wuerttemberg Foundation and together with EE by the PROCOPE programme.
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Ferhat, AT., Halbedl, S., Schmeisser, M.J., Kas, M.J., Bourgeron, T., Ey, E. (2017). Behavioural Phenotypes and Neural Circuit Dysfunctions in Mouse Models of Autism Spectrum Disorder. In: Schmeisser, M., Boeckers, T. (eds) Translational Anatomy and Cell Biology of Autism Spectrum Disorder. Advances in Anatomy, Embryology and Cell Biology, vol 224. Springer, Cham. https://doi.org/10.1007/978-3-319-52498-6_5
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