Mitochondrial ROS signaling during synaptic potentiation

Abstract

Exacerbated emission of reactive oxygen species (ROS) from presynaptic mitochondria 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 measurement of synaptic potentiation in drosophila neuromuscular preparations.