Student Presenter(s): William Shin, Yamini Nori, Himani Jani, Aaron Miller, Mac Josh Reandelar
Faculty Mentor: Randy F. Stout
Department: Biomedical Sciences
School/College: College of Osteopathic Medicine, Long Island

Olfactory deficit is characteristic of Autism Spectrum Disorder (ASD) and can lead to malnutrition. The Contactin-Associated Protein-like 2 (Cntnap2) gene is associated with ASD. Recent work (Li et al 2020) has shown that olfactory discrimination of odors in Cntnap2 mice was similar to that of Wild-type (WT) mice, but was severely impaired in the presence of novel background odors. Cntnap2-/- mice express decreased glutamate decarboxylase thereby decreasing the number of GABAergic interneurons in the neocortex. This reduction suggests a possible mechanism for the observed odor discrimination deficit in the presence of novel odors. Herein, we evaluated the number of inhibitory interneurons in Cntnap2-/- mice within the piriform cortex, a brain region associated with olfaction, by staining for GAD67, a marker for GABAergic neurons. Using the software Fiji-Image J, we analyzed images of brain samples and counted the number of neurons in layer 1 of the piriform cortex expressing GAD67 and compared the cell number between Cntnap2-/- mice and WT mice. Preliminary results show that there was not a statistically significant difference between the two groups. The next steps will be testing for any morphological differences in piriform cortex inhibitory neurons and comparing the number of inhibitory neurons in other brain regions of WT and Cntnap2-/- mice. By localizing the cause of olfactory deficit, more targeted treatments can be developed to alleviate olfactory symptoms in ASD.