Experiential modulation of social dominance in a SYNGAP1 rat model of ASD



Data in support of the article entitled Experiential modulation of social dominance in a SYNGAP1 rat model of ASD in the European Journal of Neuroscience
Advances in our understanding of developmental brain disorders such as autism spectrum disorders (ASD) are being achieved through human neurogenetics in, for example, identifying de novo mutations in SYNGAP1 as one relatively common cause of ASD. A recently developed rat line lacking the calcium/lipid binding (C2) and GTPase activation protein (GAP) domain may further help understanding the neurobiology of deficits seen in children with ASD. This study focused on social dominance in the tube test using Syngap+/Δ-GAP (rats heterozygous for the ) as alterations in social behaviour are a key facet of the human phenotype. Male animals of this line living together formed a stable intra- cage hierarchy but when living with WT cage-mates, they were submissive, modelling the social withdrawal seen in ASD, with detailed analysis of the specific behaviours shown in social interactions by dominant and submissive animals. A further suggestive observation was that when the Syngap+/Δ-GAP mutants that had been living together had dominance encounters with WT animals from other cages, the two higher ranking Syngap+/Δ-GAP rats were dominant whereas the two lower ranking mutants showed the opposite pattern of being submissive. These findings confirm earlier observations with a rat model of Fragile-X indicating that although genotype may be a major determinant of intra-cage hierarchies, the experience of winning or losing can have an influence on subsequent encounters with others. Our results highlight and model that even with single-gene mutations, dominance phenotypes reflect an interaction between genotypic and environmental factors.

Data Citation

Morris, Richard; Saxena, Kapil. (2021). Experiential modulation of social dominance in a SYNGAP1 rat model of ASD, [dataset]. University of Edinburgh. Centre for Discovery Brain Sciences. https://doi.org/10.7488/ds/3121.
Date made available15 Sep 2021
PublisherEdinburgh DataShare

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