Abstract
Reactive oxygen species (ROS) are chemically reactive molecules normally produced during cellular respiration. High ROS levels negatively impact forms of synaptic plasticity that rely on changes in the number of ionotropic glutamate receptors (iGluRs) at synapses. More recently, we have shown that physiological increases in ROS reduce iGluR transport to synapses by acting on activity-dependent calcium signaling. Here, we show that decreasing mitochondria-derived ROS decrease iGluR transport albeit in a calcium-independent manner. These data demonstrate differential regulatory mechanisms by elevated or diminished ROS levels which further support a physiological signaling role for ROS in regulating iGluR transport to synapses.