Figure 6.

Simulation of retinocollicular map development for an ephrinA deficient mouse. (A) and (B) Exponential curves for EphA and ephrinA across the (A) nasal–temporal (N-T) axis of the retina and (B) anterior–posterior (A-P) axis of the SC for simulations of ephrinA deficient mice. EphrinA curves are reduced by 50% in retina and SC of ephrinA mutants, compared to wild-type, reflecting the continued presence of ephrinAs but at a diminished level, as in an ephrinA single mutant mouse. EphA levels are increased compared to wild-type, due to decreased receptor inactivation by ephrinA in the knockout. (C) Branch probability shown from three locations across the retina. At the start of the simulation there is only a slight bias for branching in topographically correct locations. (D) Simulation of an ephrinA deficient mouse, with examples at three time points during the simulation. Branching along 300 RGC axons was simulated for 200 iterations with branching patterns shown for 10 axons chosen randomly from three different retinal locations (nasal, N; central, C; temporal, T). Early in the simulation there is essentially no topographic bias in branching along RGC axons (iteration 2). However, as arborization proceeds a topographic bias is quickly established and a TZ becomes evident (iteration 20). At the end of the simulation a topographically appropriate TZ has formed for all retinal locations. However, in addition to an appropriately located TZ, nasal and temporal RGCs maintain elaborate ectopic arbors anterior and posterior to their correct TZ, respectively, similar to phenotypes reported for ephrinA single mutants (Frisen et al., 1998; Feldheim et al., 2000).