The main model to study the development of topographic maps is the retinal ganglion cell projection to the optic tectum or superior colliculus, which is organized in two orthogonally oriented axes. Nasal RGCs project to the caudal tectum and temporal RGCs project to the rostral tectum, whereas dorsal RGCs project to the ventral tectum and ventral RGCs project to the dorsal tectum. RGC axons invade the chicken tectum from the rostral pole and follow its developmental Ginsenoside-F2 gradient axis toward the caudal pole. These axons overshoot their future target areas along the rostro-caudal axis but form branches around the position of their future termination zones, which are formed by the arborization of the appropriately located branches and the pruning of the overshooting axonal leading tips. The branches invade deeper retino-recipient layers, where they establish synaptic connections. The molecular mechanisms involved in topographic mapping agree with Sperry’s theory of chemoaffinity. Sperry predicted that RGC axons find their targets throughout interactions involving recognition molecules that are differentially expressed on their growth cones and on tectal cells. Furthermore, he proposed that each location in the tectum has a unique molecular address determined by the graded distribution of the topographic recognition molecules. Each RGC has a unique profile of receptors for those molecules, resulting in a position-dependent, differential response. It has been later proposed that activityindependent and -dependent interaxonal competition refines this topographic map. Eph receptors and their ephrin ligands are expressed in gradients in both the retina and the tectum/colliculus, and several groups have shown that they represent the main molecular system controlling the mapping of retinal projections onto the tectum/ colliculus. The Eph receptors are a family of widely expressed receptor tyrosine kinases comprising ten EphA and six EphB members. EphA and EphB receptors promiscuously bind the six glycosylphosphatidylinositol -linked ephrin-A ligands and the three transmembrane ephrin-B ligands respectively. The fact that the ephrins are membrane-bound proteins allows the Eph-ephrin interaction to produce bidirectional signaling with morphologic consequences in both interacting cells. EphA receptors and ephrin-As define the topographic retinotectal/ collicular connections along the 
rostro-caudal axis, whereas EphB receptors and ephrin-Bs have been found to be involved in guidance along the dorso-ventral axis. This is achieved through opposing gradients of Ephs and ephrins in both the retina and the tectum. Thus, EphA3, A5 and A6 are expressed in an increasing naso-temporal gradient, whereas EphA4 presents an even distribution along the retina, with a decreasing naso-dorsal to temporo-ventral gradient of phosphorylation. EphA3, A4, A7 and A8 are expressed in a decreasing rostro-caudal gradient in the tectum/colliculus while ephrin-A2, -A5 and �CA6 are expressed in a decreasing naso-temporal retinal gradient and in an increasing rostro-caudal tectal gradient. Ephrin-A2 and ephrin-A5 expressed in the caudal tectum/ colliculus are growth cone repellents and interstitial branching inhibitors that preferentially affect temporal RGC axons by activating their EphA receptors. Thus, tectal ephrin-As prevent temporal RGC axons from branching caudally to their appropriate target area. It has been shown that ephrin-As of RGC axons diminish the repulsive Lomitapide Mesylate response of axonal EphA receptors to tectal ephrin-As, preventing repulsion of nasal RGC axons from the caudal tectum.