Fig. 3

RGC neurocircuitries in healthy, diseased, and transplanted retinas. Bipolar and amacrine cells establish direct contact with RGCs to relay visual information. Different RGC subtypes extend their dendrites into ON and OFF sublamina in the inner plexiform layer and exhibit different electrophysiological responses. Glaucoma causes dendrite retraction and eventual death of RGCs and the activation of astrocytes, microglia, and Müller glia, while photoreceptor, bipolar, amacrine, and horizontal cells are relatively unaffected. RGC transplantation must replace lost RGCs, return the diseased retina to a homeostatic state, and establish neurocircuitry between host and donor cells. While donor RGCs have been shown to survive in the retina, few are currently able to migrate into the ganglion cell layer, with the inner limiting membrane (ILM) serving as a major barrier for intravitreal (IVT) delivery, and even fewer form de novo neurocircuits in the retina