Abstract

In the course of our study on Wallerian degeneration in the young rat optic nerve after unilateral enucleation, cell proliferation was measured by quantitative radio-autography. Ninety-two newborn rats were separated into four groups which were operated at 2, 5, 8 and 20 days postnatal (key stages) respectively. In each of these groups, the animals were sacrificed after progressive delays ranging from 3 h to 30 days (DPO). They received, 3 h before the sacrifice, an intraperitoneal injection of 2 μCi/g weight of tritiated thymidine. After the radio-autographic procedure, semi-thin sections were examined, and labeled as well as unlabeled cells were counted on the whole cross section of the operated nerve, as well as on the contralateral nerve. In the operated nerve, the four key stages may be separated into two reactive patterns, depending on whether the enucleation is performed before or after the myelination gliosis. The two first key stages (2 and 5 DPN) show leveling down of the curve of their proliferative indices, when compared with the control, whereas the two other key stages (8 and 20 DPN) showed a leveling up of the curve. The comparison of these data with those of previous work (Fulerand and Privat, 1977; Valat et al., 1978) permitted the evaluation of cell death, which is specially evident at the key stage 8 DPN. The proliferative ability of neuroglial cells thus appear no to be closely dependent upon an intrinsic genetic program, but rather to be modulated by epigenetic events. The early absence of the axonic signal induces a decrease of this proliferation, whereas the more or less belated interruption of the same signal induces a reactive gliosis, with a net increase of proliferative indices over the control.

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