Elevated intraocular pressure (IOP) increases production of the pro-inflammatory cytokines interleukin-1α (IL-1α), tumor necrosis factor α (TNF-α), and complement component 1q (C1q) by activated microglia and recruited macrophages. These cytokines activate neurotoxic astrocytes, and results in retinal ganglion cell (RGC) death. Our lab has shown that the GLP-1R agonist NLY01 inhibits activation of microglia, macrophages, and astrocytes, and prevents RGC death in eyes with microbead-induced IOP elevation. However, the mechanism behind NLY01-induced RGC rescue, including the cell types mediating its protective effects as well as the relative contribution of macrophages versus microglia, has not been examined.