PubMed1990
In each of 6 mature rats, unilateral rubrospinal tractotomy and hypoglossal neurectomy were done at one operative sitting. Paired operated animals were killed by formaldehyde and ethanol-acetic acid perfusion 3, 14 and 28 days later. One pair of unoperated control rats was perfused also. All rats were injected i.p. with [3H]thymidine 24 h before death. Immunohistochemical methods were applied to paraffin sections to visualize glial fibrillary acidic protein (GFAP) and transferrin in astrocytes and oligodendroglia, respectively. Microglia were demonstrated by both lectin-binding and histoautoradiographic methods. Neuroglia and nerve cells were counted in hematoxylin-eosin and azure B stains. Cell areas and the RNA concentration of hypoglossal neurons were determined by the Zeiss Image Scan System. Three days after hypoglossal neurectomy, increased astroglial staining (GFAP) and microglial hyperplasia (radiolabeled nuclei) were evident in the ipsilateral hypoglossal nucleus (HN). Microglial hyperplasia waned rapidly after 3 days and microglial numbers decreased. However, astroglial hypertrophy, demonstrable by GFAP staining, persisted 4 weeks postoperatively when astroglial processes were concentrated in a perineuronal position. Oligodendroglia were unaltered. In contrast to the HN, the axotomized red nucleus (RN) contained few radiolabeled microglia while a slight increase in GFAP-positive astroglial processes was seen only in animals killed 28 days postoperatively. Again, oligodendroglia were unchanged. In neither HN nor RN did axotomy cause nerve cell death. Although axotomized rubral neurons atrophy and become depleted of RNA, no statistically significant changes in somal size and RNA content of axotomized hypoglossal neurons occurred. The apparent absence of a neuroglial response of putatively supportive nature in the environs of axotomized rubral neurons may relate to their failure to regenerate. The neuroglial response likely is originated by the axotomized neuron and its absence may be an innate defect in the reaction of intrinsic neurons to axonic severance. Somas of axotomized peripherally projecting nerve cells appear to have the capacity to summon a neuroglial response.