Retinal ganglion cells vary significantly in terms of their size, connections, and responses to visual stimulation but they all share the defining property of having a long axon that extends into the brain.

In the extreme periphery (edge of the retina), a single ganglion cell will receive information from many thousands of photoreceptors.

[citation needed] Retinal ganglion cells spontaneously fire action potentials at a base rate while at rest.

In primates, including humans, there are generally three classes of RGCs: The W, X and Y retinal ganglion types arose from studies of the cat.

M-type retinal ganglion cells project to the magnocellular layers of the lateral geniculate nucleus.

BiK-type retinal ganglion cells project to the koniocellular layers of the lateral geniculate nucleus.

They project to, among other areas, the suprachiasmatic nucleus (SCN) via the retinohypothalamic tract for setting and maintaining circadian rhythms.

Most mature ganglion cells are able to fire action potentials at a high frequency because of their expression of Kv3 potassium channels.

[9][10][11] Degeneration of axons of the retinal ganglion cells (the optic nerve) is a hallmark of glaucoma.

[13][14][15] In mammals, RGCs are typically added at the beginning in the dorsal central aspect of the optic cup, or eye primordium.

Most importantly, the bHLH (basic helix-loop-helix)-domain containing transcription factor Atoh7 and its downstream effectors, such as Brn3b and Isl-1, work to promote RGC survival and differentiation.

[13] The "differentiation wave" that drives RGC development across the retina is also regulated in particular of the bHLH factors Neurog2 and Ascl1 and FGF/Shh signaling, deriving from the periphery.

[18] The RGC will then extend an axon in the retinal ganglion cell layer, which is directed by laminin contact.

[13] RGCs will grow along glial end feet positioned on the inner surface (side closest to the future vitreous humor).

CSPGs exist along the retinal neuroepithelium (surface over which the RGCs lie) in a peripheral high–central low gradient.

[20] Adhesion molecules, like N-CAM and L1, will promote growth centrally and will also help to properly fasciculate (bundle) the RGC axons together.

[21] RGCs exit the retinal ganglion cell layer through the optic disc, which requires a 45° turn.

Once RGCs reach the chiasm, the glial cells supporting them will change from an intrafascicular to radial morphology.

[27] The only component in mice projecting ipsilaterally are RGCs from the ventral-temporal crescent in the retina, and only because they express the Zic2 transcription factor.

Some VTc RGCs will project contralaterally because they express the transcription factor Islet-2, which is a negative regulator of Zic2 production.

[21] Other factors influencing ipsilateral RGC growth include the Teneurin family, which are transmembrane adhesion proteins that use homophilic interactions to control guidance, and Nogo, which is expressed by midline radial glia.

This myelination pattern is functionally explained by the relatively high opacity of myelin—myelinated axons passing over the retina would absorb some of the light before it reaches the photoreceptor layer, reducing the quality of vision.