Date of Award

Winter 1-15-2021

Author's School

Graduate School of Arts and Sciences

Author's Department

Biology & Biomedical Sciences (Neurosciences)

Degree Name

Doctor of Philosophy (PhD)

Degree Type



Autism spectrum disorder (ASD) is a heterogeneous neurodevelopmental condition characterized by social impairments and restricted, repetitive behaviors. Despite its growing prevalence, ASD remains poorly understood. One explanation for its social symptoms that has gained prominence in recent years is the Social Motivation Theory, which proposes a reduced motivation for social engagement as the underlying cause of impaired social functioning in ASD. While typically developing individuals find social interaction inherently rewarding, this theory suggests that people who develop ASD do not experience the same attraction to social stimuli and therefore miss out on critical social learning opportunities, hampering the development of social skills. However, testing this theory has been impeded by the lack of standardized measures to assess social motivation, particularly in ways that allow for meaningful comparison across species; though animal models of ASD are widely employed to investigate neurobiological mechanisms, their utility to explain a behaviorally defined disorder such as ASD is limited without adequate methods assess comparable behavioral phenotypes. Therefore, in this dissertation I present two novel behavioral assays validated in human toddlers and genetic mouse models respectively, which aim quantify the social orienting and social reward components of social motivation. In my first study, I adapt a simple behavioral test from prior work in dogs to assess social attention during object engagement among young children with and without ASD. I demonstrate that this brief play session pitting a high-interest object against the innate draw of social engagement can serve as a rapid, feasible measure of social orienting and that children with ASD show reduced social interest compared to typically developing peers. In my second study, I design an add-on device to allow delivery of social contact as a reward in the classic operant conditioning assay and demonstrate that mice will exert effort to obtain this social reward. I present preliminary evidence suggesting that the value of social reward may be differentially affected by two ASD-associated mutations, based on initial data from genetic mouse models harboring mutations in the Nf1 and Shank3B genes. Together, these findings in both human subjects and mouse models provide some support for the Social Motivation Theory but suggest a more nuanced revision may be needed to account for the apparent variability in social motivation among ASD genetic liabilities. Moreover, these cross-species measures of social motivation will enable more effective translational studies to elucidate the underlying mechanisms of ASD and other neurodevelopmental disorders.


English (en)

Chair and Committee

Joseph Dougherty John Constantino

Committee Members

Alexxai Kravitz, Lori Markson, Natasha Marrus, Karen O’Malley,