A small penetrating incision made through the sclera, choroid and retina of the adult rat eye creates a unique lesion paradigm. More specifically, by one to two weeks after the incision the wound area stabilizes, leaving a clean inflammation-free degeneration gap or 'die-back zone' (200-300 microns wide) between the cut edges of the intact retina. The dependable formation of a small focal retinal lesion makes this an ideal model for the determination of conditions that may stimulate retinal regeneration, wound repair and/or cell survival. In other words, material may be injected or placed into the lesion site and the retina analyzed for responses to such treatments. Accordingly, the placement of a desheathed peripheral nerve implant (PNI) into the lesioned adult rat eye initiated the rescue of retinal tissue that would normally die due to trauma. In addition, the cut edges of the retina just lateral to the PNI actually touched and fused together, thus demonstrating a wound closure or healing phenomenon which was not observed in control situations. Also the thickness and organization of most retinal layers at the site of lesion were maintained at intact control levels in the presence of the PNI. However, controls not containing the PNI exhibited dramatic reductions in total and individual retinal layer thickness for up to approximately 500 microns lateral to the lesion site. Through the use of a double lesion paradigm, it was also determined that the wound repair phenomena could be influenced over a distance by (a) putative diffusable factor(s) elaborated or initiated by the PNI.