Submission Date

7-23-2026

Document Type

Paper- Restricted to Campus Access

Department

Neuroscience

Faculty Mentor

Nathan Vogler

Comments

Presented during the 28th Annual Summer Fellows Symposium, July 24, 2026 at Ursinus College.

Project Description

Autism spectrum disorder (ASD) is a spectrum of complex neurodevelopmental disorders characterized by social deficits and restricted, repetitive behavior with unclear genetic and environmental causes. However, it is suggested that disrupted excitatory/inhibitory (E/I) balance contributes to the pathogenesis of ASD. Specifically, certain cortical regions of those with ASD show a significant reduction in the density of inhibitory parvalbumin-positive (PV) interneurons, which could explain the cortical hyperexcitability in individuals with ASD. In ASD, auditory processing deficits in the less understood sensory cortical region, the primary auditory cortex (AU1), could be explained by this dysregulation of E/I. To study the cellular and molecular changes in the ASD AU1, we used a mouse model of ASD known as SHANK3 knockout (KO). We performed immunohistochemistry on the brain tissue of wildtype (WT), heterozygous KO, and homozygous KO mice to visualize and quantify the number of PV neurons in the primary auditory cortex (AU1). The results of this experiment will illuminate a characteristic of the SHANK3 KO mouse model and indicate a region-specific or cortex-wide relationship between ASD and reduced PV density.

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