Spinal Cord Transplantation(Report on Session 41.0)

The symposium on spinal cord transplantation has been shadowed, this year, by the loss of Dr. Michael Goldberger (Medical College of Pennsylvania, Philadelphia, USA) who passed away in January 1992. Michael Goldberger’s contribution to the field of spinal cord plasticity and restoration, including transplantation, has been enormous. His impact on the field is best exemplified by the fact that all speakers in this symposium had, at one point or another, collaborated with him. It was therefore decided that this symposium would be dedicated to his memory. Five speakers presented their latest data in the symposium. Four of them dealt with various aspects of transplantation after mechanical lesions of spinal cord neuronal populations and pathways while the last speaker considered the potential for therapeutic transplantation in motoneuronal diseases. Dr. Barbara Bregman (Georgetown University, Washington, D.C., USA) presented a summary of her work devoted to the comparative analysis of plastic phenomena in the developing and adult spinal cord/1/. After spinal cord lesions at birth, fetal CNS transplants are able to support the regeneration of all spinal projections. In the long term, specific connections between regrowing afferents and appropriate grafted targets are required for maintenance of projections when fibers originate from supraspinal structures, whereas a similar specificity is not required when fibers originate from the dorsal root ganglia. Projections from the dorsal root ganglia can be maintained even by non-target tissue transplants. Behavioral experiments indicate that the regrowth of severed afferents from supraspinal structures allows some recovery of motor function at this stage. Some plasticity of afferent systems in the adult is observed, but to a much lesser extent as concerns supraspinal fibers. Altogether, these data point to the fact that different sets of afferents display varying degrees of plasticity, and that responses are largely, but not entirely, dependent upon the stage of maturation. Dr. Alan Tessler and colleagues (Medical College of Pennsylvania, Philadelphia, USA) analyzed another aspect of the same model by looking at the prevention of retrograde cell death after axotomy that can be provided by transplants /8/. They showed two different phenomena. The first is a regeneration of severed fibers comparable to that described by Dr. Bregman. This phenomenon, studied using both anatomical and electrophysiological techniques, can be best observed after rhizotomy, when transplants can allow calcitonin gene-related peptide (CGRP) fibers to regrow. The second phenomenon is a rescue of axotomized neurons that do not send axons to their appropriate targets, but survive due to the presence of the transplant. This was shown by comparing the effect of an axotomy at the T8 level, with or without a concurrent transplant, on the survival of Clarke’s nucleus neurons at L1. Normally, 30 to 40% of these neurons die after axotomy, while different types of transplants (spinal, cerebellar or cortical) provide the neurons with enough survival factors for them to survive for several months after the lesion. By examining the relevant literature, the authors concluded neurotrophin 3 (NT3) was enriched in all three tissues that provided efficient transplants. In order to determine the possible role of this factor in the neuronal survival, the authors used another tissue, the kidney, which contains high levels of NT3 but is not of neural origin. They thus demonstrated that