Presynaptic inputs of bipolar cells onto retinal ganglion cells

Optic nerve damage often leads to vision loss that is currently untreatable. One example is glaucoma: as the disease progresses there is damage to the optic nerve. Glaucoma affects about 60 million people worldwide. To help those impaired, additional investigation of the retinal synaptic pathways is essential to produce new therapies that address optic nerve damage. The way the synaptic circuitry works is by bipolar cells (BCs) that process and transmit visual information from photoreceptors to retinal ganglion cells (RGC). A novel technique to label presynaptic inputs onto RGCs allowed for the identification of BCs. The RGCs analyzed were junctional adhesion molecule B (JAMB) and bistratified dendrite (BD). BCs found in the RGCs were divided into subtypes based on whether their primary input was from a rod or cone photoreceptor. Additionally, they were divided into their primary synaptic output; either the ON or OFF layer of the inner plexiform layer (IPL). The classification was produced from ten subtypes of cone BCs and one rod BC. Further, BC inputs onto RGCs in CD3ζ mice were analyzed. CD3ζ, the key component of a Major Histocompatibility Complex Class I receptor, is expressed in RGCs. Elimination of CD3ζ causes axon and dendritic morphology changes which results in presynaptic changes. These presynaptic changes may help researchers identify the exact underlying mechanism for how vision occurs. This result may lead innovative therapies or stem cell recovery methods that restore or introduce vision to those persons suffering damaged optic nerves.