The Visual System(Report on Session 25.0)

The goal of the session on the visual system, as described by Dr. R. Lund in his introductory remarks, was to integrate the biology of the visual system with transplantation studies. The presentations were selected as examples of different approaches to transplantation which would bring together problems from both spheres. Dr. G. Bray, speaking in place of Dr. A. Aguayo on responses of injured retinal ganglion cells, considered the theme of injury-related phenomena. Dr. Bray introduced his talk by outlining experiments done in Dr. Aguayo’s laboratory which formed the basis for the topic at hand. These experiments dealt with the results of axotomy in the optic nerve in rodents /1/. When transected, optic nerve axons do not regenerate, and the target (the superior colliculus, for over 90% of the fibers originating in the optic nerve in the rodent) remains denervated. In studies by Dr. Vidal-Sanz, it was shown that peripheral nerve, grafted to a totally transected optic nerve, survived and axons were shown to grow to the end of the graft/17/. Grafts could also be used to guide axons from the transected optic nerve back to the superior colliculus (SC). Grafts inserted in the SC survived and extended fibers which were shown to form well-differentiated synapses, and which activated neurons in the SC in response to light flashed on the retina. The reconnectivity potential of this model was limited by the fact that many neurons died as a result of retrograde degeneration following transection of the optic nerve. The experiments which followed were designed to explore the extent and pattern of death after axotomy in the hope of elucidating the mechanisms responsible. In the first set of these experiments, by VidalSanz and Villegas-Perez/18/, lesions of the optic nerve were made at four distances from the eye, two close to the eye, intraorbitally, and two far from the eye, intracranially. The survival of the retinal ganglion cell (RGC) was determined and quantified two weeks to 20 months post-lesion. Two phases of cell loss were observed, an initial, acute phase which took place between 7 and 10 days following axotomy, and a second, protracted phase. The number of surviving RGCs varied with the distance of the axotomy from the eye. More distal lesions resulted in less cell death. It was speculated that RGCs may be temporarily sustained by trophic mechanisms originating within the optic nerve stump itself. Work by Lu et al. /13/ was cited, in which lesions of the optic nerve were found to result in an 8-fold increase in amounts of NGF mRNA on the first day following transection. This finding suggests that the injured portion of the nerve is capable of producing trophic molecules, at least for a brief period, which may play a role in the transient survival of the RGCs. The type of lesion may also affect cell survival. As Dr. Bray noted, a cut as opposed to a crush results in greater cell loss, possibly due to the production of molecules which are damaging to the cell. Thus, the cytological reaction at the site of injury may affect cell survival in either a positive or a negative way. In discussing the second phase of cell death following axotomy, Dr. Bray described data from studies by Vidal-Sanz and David Carter with peripheral nerve grafts in the superior colliculus, which suggested that RGCs that have formed synapses by means of a graft may be sustained and do not die following transection/2,17/. In summary, the degree of cell loss occurring during the initial phase following axotomy appears to be related to the distance of the lesion from the