Undergraduate Honors Theses

Thesis Defended

Spring 2019

Document Type


Type of Thesis

Departmental Honors


Psychology & Neuroscience

First Advisor

Daniel S. Barth, Ph.D

Second Advisor

Christopher A. Lowry, Ph.D

Third Advisor

Michael P. Saddoris, Ph.D


The comorbidity of autism and epilepsy has been studied for many years. The exact mechanism for this comorbidity is still unknown, but it is hypothesized that inflammatory mediators, such as dysregulated microglia, serve a significant role. Maternal stress and terbutaline (ST) have previously been shown to result in prolonged CNS inflammation and can be used as an animal model for the comorbidity of ASD and epilepsy. Injections of a heat killed bacterium, Mycobacterium vaccae, has been shown to protect against stress-induced inflammation in the periphery and CNS. To test the potential mitigating effects of M. vaccaein this model, we measured microglial density across development in certain areas of the brain commonly associated with autism and epilepsy. Three experimental groups (ST+ M. vaccae, ST + vehicle, and control unstressed) were perfused at two time points (P15 and P30). Brains were stained for the marker Iba1 and cell counts were analyzed. Data showed significant differences in microglial density in the insula, motor cortex, and molecular layer of the dentate gyrus between the different groups, with M. vaccaeappearing to have protective effect on the disruptions caused by stress and terbutaline for certain brain regions. These differences are important because they show that these disruptions could lead to the abnormalities in the brain regions that are associated with the two disorders.

Available for download on Wednesday, April 07, 2021