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 neurological disorder that is characterized by social deficits as well as repetitive behaviors and limited interests. There have been many genetic mutations known to be connected to the development of ASD. However, the neurological mechanisms underlying the phenotypes remain unclear. To study synaptic changes, we will use transgenic SHANK3 knockout (KO) mouse models. Shank3 KO mice have a mutation that leads to deficits in postsynaptic signaling complexes, which are thought to cause behavioral abnormalities, such as a lack of interest in social interactions and repetitive behaviors including overgrooming. SHANK3 mutations have among the strongest links to ASD. Despite numerous prior studies on the SHANK3 mutation, it remains unclear how it leads to these phenotypes. This study will compare the phenotypes of wild-type, heterozygous, and homozygous Shank3 KO mice using behavioral tests. Then we will track protein expression using immunohistochemistry, using antibodies to visualize and map proteins and neurotransmitters. The main protein to be examined is vesicular glutamate transporter 1 (vGLUT1), which transports glutamate into synaptic vesicles within neurons before releasing it into the synapse. In the heterozygous and homozygous Shank3 KO mice compared to the wild-type mice, we expect to observe a greater number of vGLUT1-positive excitatory synapses and an imbalance of glutamate in the hippocampus. Results from this study will aid in understanding the neurobiological effects of the Shank3 mutation in relation to ASD.

Download

Restricted

Available to Ursinus community only.

Share

COinS