Abstract
Neural circuits develop based on homeostatic mechanisms that stabilize the excitability of neurons about a set point. “Scaling up” occurs when a cell increases synaptic strength to compensate for decreased network activity. Underlying these adjustments of excitability are changes in synaptic strength, which is mediated by AMPA receptors. In particular, glutamate receptor-interacting protein 1 (GRIP1) is a protein that binds GluR2 subunits and has been shown to be necessary for synaptic scaling. Here we show that during scaling, GRIP1 accumulates at exocyst sites. Furthermore, we demonstrate a method of assessing the reliability of detecting sites of colocalization. Additionally, we determined that during synaptic scaling, the rates of recycling exocytosis are unaffected. We further establish that GRIP1 is required for recycling processes, but not sufficient to drive it.