Left dorsal cordotomy at the 11th thoracic vertebra was performed in mature female rats. Local exposures of 1,000 R of 280 kvp x rays were made within 10 min, 12, 24 36 or 48 hrs after injury. Tritiated thymidine (1 μCi/g body wt.) was injected i. v. 1 hr before death and necropsy examination 5, 18 or 30 days after surgery. Hematoxylin-stained sagittal sections (5 μ) of the spinal cord were prepared for radioautographic examination. The parameters of magnitude and duration of changes in cell numbers and numbers of cells incorporating tritiated thymidine were determined for scar parenchymal cells (neuroglia and fibroblasts), macrophage, endothelia and mitotic cells. Irradiation modified the cellular composition of the developing scar tissue. These changes were due to a delay of proliferation in scar parenchymal and endothelial cell populations. A concomitant suppression of the number of cells incorporating tritiated thymidine occurred in 5-day old irradiated lesions. The magnitude and duration of these delays varied with the cell type and the time of irradiation after injury. These changes indicate that scar parenchymal and endothelial cells proliferatein situ from progenitor cell populations that were in the lesions at the time of irradiation. Macrophage cell numbers and numbers of these cells incorporating tritiated thymidine were not decreased after irradiation. It is, therefore, probable that the majority of the macrophage cells did not originate from a local progenitor cell population.