Summer Research Description: Integrins, made up of α and β subunits, are involved in cell adhesion and migration in synapses. The integrin β3 subunit of the αvβ3 receptor modulates SERT function by differentially affecting serotonin (5-HT) uptake within distinct mouse brain regions. Integrin β3 knock-in (Pro33) mice express an activated form of integrin β3 associated with elevated blood 5-HT levels, an endophenotype of autism spectrum disorder (ASD). Pro33 mice have enhanced SERT function in the midbrain, as well as particular ASD-like social deficits. Here, we hypothesize that direct modulation of SERT by integrin αvβ3 receptors, which can be characterized by changes in co-localization of SERT and αvβ3 receptors, is brain-region dependent. Super resolution images acquired through structured illumination microscopy of midbrain and hippocampal slices will reveal variations in SERT/β3 co-localization along axons and within pre-synaptic terminals. We will also compare SERT localization along axons versus within synapses and SERT vesicle size dependent on the presence of integrin β3. Next, we will compare SERT/β3 co-localization between wild-type and Pro33 mouse models to examine a possible correlation between altered integrin β3 expression and ASD-like social behaviors. Findings from these morphological measurements will lead to a broader understanding of the brain 5-HT system.