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Exposure of the lumbar spinal cord of rats to X-rays 3 days after birth results in changes in the composition of central glia. Shortly after irradiation, there is both retardation of central myelin formation and a loss of integrity of the astrocyte-derived glia limitans on the dorsal surface of the cord. Subsequently, Schwann cells invade, undergo division and myelinate axons in the dorsal funiculi in the irradiated region of the cord, creating there an environment similar to that of peripheral nerve. The present study was undertaken to compare the ability of lesioned dorsal root axons to grow back into the altered glial environments that exist within the spinal cord after irradiation. This regrowth was assessed by injecting Fluoro-Gold into the spinal cord and subsequently examining neurons in the dorsal root ganglia (DRG) for the presence of this label. Numbers of retrogradely labeled neurons were counted in the DRG in both injured and contralateral non-injured sides. Non-irradiated control rats had almost no labeled DRG neurons on the injured side, whereas Fluoro-Gold labeled neurons were observed in substantial numbers in the DRG on the injured side of irradiated rats. There was a definite trend in the data, indicating that the longer the interval between irradiation and root injury, the greater the number of labeled neurons. Since the Fluoro-Gold labeling technique does not allow for visualization of the labeled axons within the spinal cord, a few animals were used to assess anterograde labeling with wheat germ agglutinin-conjugated horseradish peroxidase (WGA-HRP/HRP) from the dorsal root into the spinal cord. HRP-filled regenerating axons were visualized in dorsal white and gray matter of the irradiated spinal cord. Such axons were not present in the non-irradiated spinal cords. Radiation-induced changes in glial populations are discussed, particularly with regard to the temporal sequence of these changes and their possible relationship to the conversion of a normally non-permissive environment into one conducive to axonal regrowth. [ABSTRACT FROM AUTHOR]

Irradiation of the rat spinal cord during the first postnatal week results in a profound reduction of oligodendrocyte myelin formation in the dorsal funiculi (DF). Despite this absence of myelin, however, axons in the irradiated region in the DF increase in diameter and approximate the size distribution seen in the control spinal cord. By 25 days of age Schwann cells are present in the irradiated DF where they undergo cell division and myelinate the axons. During the early stages of this myelin formation, these intraspinal Schwann cells exhibit a relationship to axons that is somewhat different from that seen in the normal developing peripheral nervous system (PNS). For example, within a given region, intraspinal Schwann cells myelinate axons of large diameter prior to ensheathing bundles of small diameter axons. Additionally, during myelination a Schwann cell will surround a single axon with multiple processes which appear to compete for contact with the axolemma. On axons of larger diameter, the elaboration of these processes is so excessive that it is often difficult to trace them back to the parent Schwann cell. Later, when a single process establishes several spirals about an axon, additional processes are no longer elaborated, and the 'extra' processes disappear as myelin formation advances to the stage of compact lamellae. Thereafter, the myelin sheath continues to form in a normal manner. Excess processes have been observed during myelinogenesis in the normal developing PNS, but their frequency in that environment is much less than in the irradiated cord. These observations support the hypothesis that the signal(s) to initiate myelin formation are expressed on the axolemmal surface and are controlled by the neuron. In addition, these observations suggest that the delay in myelination results in an affinity or tropism between axons and Schwann cells which exceeds the level existing at the normal time of myelin formation. [ABSTRACT FROM AUTHOR]