Date of Award

Spring 5-2021

Document Type

Honors Thesis

Degree Name

Bachelor of Science



Advisor/Committee Chair

Annalisa Scimemi




With mice identified as an adaptable human disease model, researchers have been able to use genome editing to study a myriad of human disorders and diseases. One of these disorders, Obsessive Compulsive Disorder (OCD), has a prevalence of 2% in humans. At present, its underlying molecular and circuit mechanism remains incompletely understood. Genetic studies identified the gene encoding EAAC1, a neuronal glutamate transporter, as a candidate gene associated with OCD. Therefore, by understanding how EAAC1 shapes synaptic transmission and behavior, we can shed light on how it may ultimately contribute to OCD in humans. Here we show how bacterial artificial chromosome (BAC) transgenic mice can be used to remove EAAC1 either constitutively, or from identified populations of neurons. We show that mice that do not express EAAC1 (EAAC1-/-) display altered timing of reward-based behaviors. These findings confirm a potential implication of EAAC1 in behaviors relying on the activity of brain structure that show hyperactivity in humans with OCD. Our findings open many new areas of study for understanding how OCD and OCD-like behaviors manifest.