We review and comment on Grimbert & Cang's (2012) model of the development of topographically ordered maps from the retina to the superior colliculus. This model posits a phase in which arbours are created in zones permitted by Eph and ephrin signalling, followed by a phase in which activity-dependent synaptic plasticity refines the map. We show that it is not possible to generate the arborization probability functions used in Grimbert & Cang's simulations using gradients of Ephs and ephrins and the interaction mechanism that Grimbert & Cang propose in their results. Furthermore, the arborization probabilities we do generate are far less sharp than we imagine truly "permissive" ones would be. It remains to be seen if maps can be generated from the non-permissive arborization probabilities generated from gradients.Keywords visual system; topography; computational modelling; chemoaffinity; retinal waves
CommentaryThe extensive experimental and theoretical investigation of the development of topographically ordered maps from the retina to its targets ( Figure 1A) has led to two important theories of map development: molecular signalling and activity-dependent synaptic plasticity (Goodhill & Xu, 2005). In theories of molecular signalling, retinal ganglion cell (RGC) growth cones bear receptors in different densities depending on the location of the RGC soma in the retina, and these receptors are activated by ligands expressed in cells in the superior colliculus (SC) at levels depending on their location. This confers on each RGC a preferred location in the SC, which, depending on the pattern of receptor and ligand expression, is not necessarily its correct topographical position. Activitydependent synaptic plasticity of RGC-SC synapses along with correlated activity in the retina can also, in theory, lead to map formation, though extra cues are needed to ensure the orientation of the map is correct (Willshaw & von der Malsburg, 1976). In both theories other mechanisms, such as competition, may be required for a normal topographic map to form.There is experimental evidence that both molecular signalling and activity-dependent synaptic plasticity are involved in map formation. In support of molecular signalling, the Eph and ephrin families of molecules are expressed in gradients along the axes of the retina and colliculus, and their disruption genetically leads to disrupted maps (Feldheim & O'Leary, 2010;Cang & Feldheim, 2013). In support of activity-dependent synaptic plasticity, correlated activity exists in the retina in the form of retinal waves, and its disruption leads to impaired map precision (Torborg & Feller, 2005). Thus the two theories are complementary and the questions centre around the exact form and role of each mechanism and how they interact.Grimbert & Cang (2012) use a computational model to address the roles of activitydependent synaptic plasticity and molecular signalling in the development of topographically ordered maps from the retina to the SC. In contrast to previous models where mole...