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Studies of neuronal survival and axonal regeneration in birds and mammals have made it clear that the microenvironment of the CNS is critical to the failure of CNS regeneration in these animals. This environment includes growth and trophic factors, ECM components and matrix turnover enzymes, cytokines and other immune system contributions. Urodele amphibians (salamanders and newts) can regenerate spinal cord even as adults, and environmental contributions of glial populations are a major part of the difference between urodele and higher vertebrate spinal cord regeneration. In particular, the behavior of injury-reactive ependymal cells (radial glia) is critical to the regenerative capacity of urodele spinal cord. In this review we examine what is known about cell-cell interactions between ependymal cells and neurons and between ependymal cells and other glial populations. The known contributions of ependymal cell products such as matrix metalloproteinases and trophic factors are discussed. There is evidence in the literature that an ependymal response occurs during embryonic or fetal development in birds and mammals following spinal cord transection, and this review discusses the implications of such a process for future studies of spinal cord injury.
Ellen A.G. Chernoff (Mon,) studied this question.