PubMed1999
Initial experimental transplantations and attempts to induce regeneration in the nerve tissue were done during the last decades of the 19th century. Though experiments were partly successful, the Cajal's doctrine about the unchanging adult nervous system overbalanced those promising findings for long period thereafter. Only during the last thirty years requirements of clinicians moved neuroscientists to study the problems of regeneration and transplantation in the CNS again. The possibility of transferring nerve cells from a donor to the host CNS, their survival, and formation of functional contacts has been fully established. Recent findings has shown that techniques of molecular biology can overcome some of the essential problems of transplantation, e.g. the glial scar. It is evident that the key role in plastic processes accompanying integration of the transplanted cells have neurotrophic factors produced both by the host and the graft. The entire microenvironment within the transplanted tissue is altered. Some specific features of the graft may be also significant. As the implant is mostly an embryonic tissue, processes of differentiation have to be considered. Accordingly, transplantation can be used as a model in the studies of neuroontogeny. In our experiments structural association of neurones transplanted as a suspension of embryonic cells into the dorsal blade of the dentate gyrus where granule cells were eliminated was described. Differentiation and signs of synapse formation were observed. Using Timm staining method, changes in the distribution of mossy fibres were identified. In thirty-day-old grafts, high number of NADPH-d positive neurones was found. Some nitric oxide producing neurones formed long processes extending into the host tissue. Such long fibres also produced nitric oxide synthase. In order to influence the process of the graft integration we induced extreme hyperfunction by a metrazol kindling. In kindled animals, more neurones survived, however, the density of apoptotic cells was similar to control animals. Our findings may be related to the hyperfunction or to the effect of metrazol on the nerve cells of both the host and the graft. They may result from microenvironmental changes or from the activation of genes participating on the mechanism of priming.