Disruptions in neuronal function resulting from improper central nervous system development and maintenance have been implicated in a wide array of neurological diseases, including Parkinson’s disease. Oxidative stress has been shown to damage neural fibers in model systems that simulate Parkinson’s disease via an increase in reactive oxygen species; paraquat (PQ) is the canonical method by which to induce oxidative stress in many models, including the fruit fly, Drosophila melanogaster. The present study examined the stomatogastric feeding circuit in Drosophila larvae to correlate its functional output (i.e., feeding) with changes in the axonal architecture innervating the foregut. Second instar larvae were exposed to PQ (i.e., a viologen) for 24 hr to induce oxidative stress, and the effects on both feeding and neurite architecture of the foregut examined. At PQ exposures of 30 mM and below, a depression in feeding without other obvious physiological impairments, as well as a significant increase in the number and size of serotonergic presynaptic vesicles along the neurite length, was observed. The results from this study show that acute oxidative stress, induced by PQ exposure, directly affects the size and number of serotonergic presynaptic vesicles within this neural circuit, correlating with functional behavioral consequences.