Spinal Cord Repair: Is Tissue Oxygenation an Important Variable?

Abstract

It is now clear that a broad range of grafting techniques can be used to successfully introduce fetal homografts of the vertebrate spinal cord into an adult injury site (Sladek and Gash, 1984; Houle and Reier, 1988). In general, these grafts are capable of long-term survival, and undergo extensive differentiation even to the extent that many exhibit features characteristic of homologous sites of the normal adult CNS. Furthermore, these grafts can form axonal interactions in varying degrees with the recipient spinal cord; host axons often project to the transplants, and dorsal root afferents penetrate the graft neuropil (Tessler et al., 1988). Thus, fetal spinal grafts also provide an excellent experimental condition in which to investigate problems of development, plasticity, and regeneration (Sladek and Gash, 1984). Although important questions remain about the mechanism by which such repair processes take place, various lines of evidence suggest that this could occur either by restoration of neurotransmitter stores, by provision of a cellular bridge which can facilitate axonal elongation across a lesion, or by anatomical and physiological reconstruction of damaged synaptic circuitries. In this regard, transplantation seems to offer great promise as a possible therapeutic approach to a variety of brain disorders related to disease and trauma.