Shear forces inflicted by explosion or head impact may result in traumatic retinopathy due to damage of retinal pigment epithelium (RPE) and photoreceptors, leading to loss of sight. Similar injury to photoreceptors and RPE can be induced by exposure to a short pulse laser. Currently there is no therapy for such blind spots (scotomata), and the loss of sight is permanent. This study is focused on development of the animal model of traumatic retinopathy and evaluation of the role of constructive retinal plasticity in elimination or reduction of retinal scotomata and scarring. We established a model of traumatic retinopathy using selective laser coagulation of RPE and photoreceptors in rabbits, based on rapid scanning with a continuous laser. This approach allows creation of the very uniform damage to RPE and photoreceptors over wide areas, sparing the inner retinal neurons in any pigmented animal. We explored the extent of migration of the RPE and photoreceptors from the adjacent non-damaged areas into the damage zone and rewiring of the migrating photoreceptors to local inner retinal neurons. The shift of the photoreceptors into the damage zone over time was monitored with optical coherence tomography and histology. The extent of rewiring was assessed using electrophysiology on a multielectrode array. Within the 4 months we observed complete recovery of the 100 and 200um-wide lines of damage. However, larger damage zones (400um) contracted only partially.