In our previous studies on studies on spinal cord regeneration in the adult lizard and the newt, we observed that the radial processes of the regenerating ependyma form between them channels which are subsequently invaded by growing neurites. In the present study we compare embryogenesis of the newt spinal cord with regeneration in the adult. Except for minor differences, we observed that the germinal neuroepithelium of the embryo and larva patterns the longitudinal neural tracts in a similar manner. With these facts in mind we propose the blueprint hypothesis which asserts that inherent in the primitive germinal neuroepithelium and its derivative primitive glia is the pattern of the primary neuronal pathways which is expressed in neurogenesis as formed channels or spaces between the processes of the epithelial cells, the surfaces of which contain trace pathways which the growing neurites follow toward their destination. The trace pathways are envisoned as mechanical-chemical itineraries which the neurities follow according to their individual affinities. The hypothesis is compared to extant theories and the limitations in central nervous regeneration of vertebrates is compared.

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Changes in intermediate fiiament content and extracellular matrix material showed that the injury response of ependymal cells in lesioned axolotl spinal cord involves an epithelial-to-mesenchymal transformation, and that fibrous astrocytes are excluded from the remodeling lesion site. Antibody localization was used to visualize cytokeratin-, vimentin-, and glial fibrillary acidic protein-(GFAP-) containing intermediate filaments, as well as the adhesive glycoprotein fibronectin. In normal axolotl spinal cord cytokeratins were found near the apical surface of the ependymal cells. Transmission electron microscopic examination suggested that these cytokeratins were in tonofilaments. Cytokeratin expression was lost and vimentin production was initiated in ependymal cells 23 weeks following spinal cord injury. There was a period of approximately 1-2 weeks when cytokeratins and vimentin were co-expressed in vivo. This co-expression was maintained in vitro by culture on a fibronectin-coated substratum. As the central canal reformed, vimentin expression was lost. Ependymal cells lacked GFAP intermediate filaments, but GFAP was present in fibrous astrocytes of the neuropil and white matter. Following injury, GFAP localization showed that fibrous astrocytes disappeared from the remodeling lesion site and reappeared only after the ependymal epithelium reformed and newly myelinated axons were found. Fibronectin expression closely followed the expression of vimentin during mesenchymal ependymal cell outgrowth. These results suggest that the ependymal cell outgrowth requires changes in cell shape followed by changes in production of extracellular matrix.

The present work describes the ultrastructure of the spinal cord in the regenerating tail of the lizard, Anolis. The distal growing region of the tail contains the advancing ependymal tube which is relatively devoid of axons but already contains channels between ependymal cell processes which anticipate their ingrowth, More proximally, fascicles of naked axons having their origin in the stump are present in the ependymal channels. Therefore, the pattern of fiber regeneration in the spinal cord is prescribed by the ependyma and not by the growing axons. Details of the ultrastructure of proximal, intermediate, and distal regions of the regenerate are reported. Particular attention is paid to the structure and differentiation of the ependymal cells and the relation of the ependyma to other glial cells, to nerve fibers, and to meningeal tissues.