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Exacerbated emission of reactive oxygen species (ROS) from presynaptic mito- chondria is a well-studied hallmark of several neurodegenerative diseases, including amyotrophic lateral sclerosis. Outside the context of pathology, the potential physiological role of mitochondrial ROS in presynaptic function and plasticity remains largely understudied. Here, we investigated this potential role by combining optogenetic techniques, electrophysiological recordings, confocal microscopy, and a well-established protocol for induction and mea- surement of synaptic potentiation in drosophila neuromuscular preparations. We observed an expected increase in spontaneous miniature excitatory junction potentials (mEJP), accompanied by a temporary increase in ROS emission seen by confocal imaging of presynaptic motor neuron mitochondria expressing roGFP2-Orp1. Furthermore, we were able to replicate this increase in mEJP frequency after optogenetic induction of ROS emission from pre-synaptic mito- chondria expressing mito-killer red. These preliminary but exiting results may indicate a potential role of mitochondrial ROS signaling in synaptic potentia- tion. Further studies will inquire about this role, as well as the potential signaling targets of mitochondrial ROS in the presynaptic structure of drosophila neuromuscular junctions.