Date of Completion

Fall 12-1-2018

Thesis Advisor(s)

Roslyn H. Fitch

Honors Major

Individualized Major

Second Honors Major

Human Rights


Cognitive Psychology | Developmental Psychology | Development Studies | Environmental Public Health | Health Policy | Health Psychology | Influenza Humans | Maternal and Child Health | Medicine and Health | Policy History, Theory, and Methods | Politics and Social Change | Psychology | Public Health | Social and Behavioral Sciences | Women's Health


Core symptoms of Autism Spectrum Disorders (ASD) include deficits in social/communicative behaviors, and repetitive/stereotyped behaviors. Mouse models are a highly established paradigm used to study the phenotypic deficits that result from various inducible genotypic or environmental risk factors for ASD. Previous studies have demonstrated a link between maternal immune activation (MIA) and ASD-like behaviors in mouse models. In this model, the maternal immune system is activated during pregnancy by injecting the viral mimic poly(I:C). The resulting offspring are phenotyped and analyzed with regards to their communicative behaviors.

Previous studies have demonstrated that male pups born to dams with immune activation produce fewer ultrasonic vocalizations (USVs) in testing than do their saline-injected counterparts. It has also been found that MIA produces offspring with hallmark signs of ASD: social deficits and stereotyped, repetitive behaviors. In the present study, the MIA theory was assessed using a mouse model for ASD, and focused on the shapes of the USVs produced. Some significant differences were seen in call types between wild-type and MIA male animals that are indicative of differing levels of complexity in their communicative behaviors. These results provide insight into the impact of models like MIA as an environmental risk factor for autism and suggest a need for further research on ways to improve maternal health during pregnancy, as well as associated infant health outcomes.