Summer Research Description: Serotonin (5-HT) is known to be important for cortical connectivity during neural development, and has long been a biomarker for autism spectrum disorders (ASD), making it a primary focus in the search for ASD’s etiology. People with ASD tend to have stereotyped deficits in social communication, and sensory processes. Recent experiments have proposed that deficits in sensory processing, specifically multisensory, could lead to difficulties with social communication. We hypothesize that altered 5-HT regulation during development could underpin abnormal audio-visual sensory processing in ASD. To test this hypothesis, we are using a mouse model with a knock-in of a mutated human serotonin transporter (SERT) with a Gly56Ala substitution, encoded by the SLC6A4 gene. This mutation is associated with ASD, and causes an increase in 5-HT reuptake. We are immunolabeling 10-week-old fixed mouse brains for 5-HT, vesicular glutamate transporter 2 (vGluT2), and parvalbumin (PV). Preliminary results show changes in cortical layering using the 5-HT and vGluT2 labels in audio-visual area V2L. PV is expected to be reduced, as has been shown in other mouse models of autism. These experiments will help provide a greater understanding of the neural network development in ASD, which could lead to improved therapies for people with ASD.