This is also supported by our neurochemical analysis of the extracellular dopamine metabolite3-MT which decreases, indicative of dopamine release defects.38 The FSCV-based computational model also predicted dopamine release defects, suggesting defective SV sequestration of dopamine in auxilin KO mice, which is seen in patients with PD.57 Although our CCV proteomic analysis was not sufficiently sensitive to detect VMAT2, it could be downregulated in auxilin KO CCVs considering the decrease of two other key vesicular neurotransmitter transporters, VGLUT1 and VGLUT2. This evidence concerns the gene SLC18A2 and Parkinson disease.