the retinohypothalamic tract for setting and maintaining circadian rhythms. Other retinal ganglion cells projecting to the lateral geniculate nucleus (LGN) include cells making connections with the Edinger-Westphal nucleus (EW), for control of the pupillary light reflex, and giant retinal ganglion cells. Physiology Most mature ganglion cells are able to fire action potentials at a high frequency because of their expression of Kv3 potassium channels. Pathology Degeneration of axons of the retinal ganglion cells (the optic nerve) is a hallmark of glaucoma. Developmental biology Retinal growth: the beginning Retinal ganglion cells (RGCs) are born between embryonic day 11 and post-natal day zero in the mouse and between week 5 and week 18 in utero in human development. In mammals, RGCs are typically added at the beginning in the dorsal central aspect of the optic cup, or eye primordium. Then RC growth sweeps out ventrally and peripherally from there in a wave-like pattern. This process depends on a host of factors, ranging from signaling factors like FGF3 and FGF8 to proper inhibition of the Notch signaling pathway. 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. 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. Growth within the retinal ganglion cell (optic fiber) layer Early progenitor RGCs will typically extend processes connecting to the inner and outer limiting membranes of the retina with the outer layer adjacent to the retinal pigment epithelium and inner adjacent to the future vitreous humor. The cell soma will pull towards the pigment epithelium, undergo a terminal cell division and differentiation, and then migrate backwards towards the inner limiting membrane in a process called somal translocation. The kinetics of RGC somal translocation and underlying mechanisms are best understood in the zebrafish. The RGC will then extend an axon in the retinal ganglion cell layer, which is directed by laminin contact. The retraction of the apical process of the RGC is likely mediated by Slit–Robo signaling. RGCs will grow along glial end feet positioned on the inner surface (side closest to the future vitreous humor). Neural cell adhesion molecule (N-CAM) will mediate this attachment via homophilic interactions between molecules of like isoforms (A or B). Slit signaling also plays a role,