Changes in the neuroglial cell populations of the rat spinal cord after local X-irradiation

Abstract

A 16 mm length of cervical spinal cord of young adult female rats was irradiated with 4000 rad of 250 kV X rays. Counts of astrocyte and oligodendrocyte nuclei were made in the dorsal columns of both irradiated and control cervical cords during the latent period before the onset of radionecrosis. The numbers of both astrocyte and oligodendrocyte nuclei were reduced one month after exposure to radiation. Both cell populations showed an apparent recovery but this was subsequently followed by a rapid loss of cells prior to the development of white-matter necrosis. The oligodendrocyte population in unirradiated spinal cords increased with age, and mitotic figures were observed among the neuroglia of both irradiated and control cervical spinal cords. A slow, natural turnover of neuroglial cells in the cervical spinal cord is proposed and the relevance of this to the manifestation of delayed white matter necrosis is discussed.

Time- and dose-related changes in the white matter of the rat brain after single doses of X rays

“…Recent studies, in which the influence of field size on the radiation response of the rat spinal cord was investigated (Hopewell et al, 1987b), have also supported the existence of the two independent pathologies. Evidence from a number of other sources provides support for the view that the relatively early white matter lesions, which develop within 6-7 months, result from an effect of radiation on oligodendrocytes (Zeman, 1963;Hubbard & Hopewell, 1979;Hornsey et al, 1981b). The more diffusely distributed vascular abnormalities, which develop in the spinal cord after a longer latent period following lower doses than those that produced necrosis, had a similar appearance to those previously reported in the irradiated brain (van der Kogel, 1983).…”

Tolerance Dose and Morphologic Changes in Murine Spinal Cord after Fractioned Irradiation with Fast Neutrons

“…Even the animals receiving the highest total dose of 15 Gy failed to show any parenchymal changes after the period of six months, which suggests that, in our experimental set-up, any radiation-induced damage is primarily manifested by chronic inflammatory infiltration and perivascular inflammation. Our results agree with those of Hopewell [8] and are also sup ported by the fact that the to date known individual factors predisposing for the development of postactinic myelopathy, are seen in general hypertension and diabetes mellitus [2], The occurrence of early, primary, inflammatory vascular changes during the so-called asymptomatic latency period be tween the stop of irradiation and the clinical manifestation of myelopathy is another fact substantiated by our study, although it has been disputed in other recent publications [9,10,15,20], That irradiation may cause larger necroses and demyelination of white matter, is so far uncontested. Electron microscopic studies have helped to identify oligodendrocytes as the critical cells responsible for those changes [5,6], It is further known that necroses may occur without vascular changes, but also that vascular changes may be clinically manifest without necroses.…”

Pathophysiological Mechanisms Leading to the Development of Late Radiation-Induced Damage to the Central Nervous System

“…These studies showed no time-related changes in oligodendrocyte number, even in areas adjacent to regions of necrosis. This apparently conflicts with earlier studies in the irradiated rat spinal cord where oligodendrocyte numbers were reduced prior to the onset of white matter necrosis [5]. However, this was after a single dose of 40 Gy, well above the ED 50 for white matter necrosis in that model, i.e.…”