UC Riverside Undergraduate Research Journal

Fragile X Syndrome (FXS) is a genetic neurodevelopmental disorder that causes autism and intellectual disabilities: exhibiting hyperactivity, elevated anxiety, and impaired cognitive/sensory processing. These deficits result from mutations in the X-linked gene Fragile X messenger ribonucleoprotein 1 (Fmr1). Fmr1-knock- out (KO) mouse models have shown consistency with observations in humans, displaying seizures and sensory processing deficits. Utilizing Fmr1-KO mice to identify a potential treatment for these symptoms, we administered a drug called 2-chloro-4-((2,5-dimethyl-1-(4-trifluoromethoxy)phenyl)-1H-imidazole-4-yl) ethynyl)pyridine (CTEP) to KO mice and measured behavioral changes. CTEP in- hibits metabotropic glutamate receptor pathways, which are upregulated in FXS. Two types of experiments were run: open field test (OFT) and elevated plus maze (EPM), commonly used to study anxiety and hyperactivity. Experimental mice with higher anxiety depict decreased exploration and more time spent near the arena’s wall or closed arms. We found that CTEP reduces the distance traveled in the OFT across both wild-type (WT) and KO groups, suggesting reduced locomotion. There were no statistically significant differences in time spent in EPM closed arms between WT and KO mice, indicating no treatment of anxiety. These results suggest that more effective intervention is needed to target anxiety deficits related to FXS.