| Abstract: | A qualitative and quantitative light and electron microscopic analysis of the glial cells in the supraventricular part of the corpus callosum of the neonatal and adult homozygous athymic nude (nu/nu) and normal BALB/c (+/+) mice was carried out to determine the possible contribution of nude gene mutation to glial cell development. Quantitative cell counts using toluidine blue stained serial callosal sections of 0.5 μm thickness showed that the overall glial cell population was significantly reduced in both neonatal and adult athymic mice. The number of glioblasts, astrocytes and microglia of 5-day-old athymic mouse was reduced by 10%, 27%, and 39%, respectively, when compared to the 5-day-old normal mouse. The frequency of necrotic cells in the neonatal athymic mouse increased by 70% when compared with the normal mouse. In the 13-week-old adult athymic mouse, the number of oligodendrocytes, astrocytes, and microglia decreased by 19%, 31%, and 33%, respectively, when compared to normal mouse. There was no significant difference in the area covered by the corpus callosum in 5-day-old and adult nude mice versus the normal ones of corresponding ages. Except for microglia and astrocytes, the ultrastructural features of the other glial cell types in both strains were comparable. Most of the microglial cells of the neonatal normal mouse were round and were selectively marked by Mac-1 monoclonal antibody at their plasma membrane. The immunoreactivity appeared to be more intense in the normal than the athymic mouse, suggesting a down regulation of CR3 receptors and reduced phagocytic activity of this cell type in the athymic mouse. It is proposed that the increased number of necrotic cells in the neonatal athymic mouse may be attributed to the delay in the removal of dead cells normally phagocytosed by microglia. The microglia in both strains of mouse showed comparable lectin staining intensity at the plasma membrane, indicating that their glycoprotein binding receptors to lectin remained unchanged. Some astrocytes in the adult athymic mice showed hypertrophy. The reduced number of glial cells may be the direct result of genetic mutation or consequential to the lack of certain trophic factors arising from the genetic mutation. Thus, the reduction of microglial cells in both neonatal and adult athymic mice may be due to the lack of thymic hormones which, together with lymphokines have been shown to affect the maturation of bone marrow derived cells including monocytes, the putative precursor cells of microglia. The reduction in the number of glioblasts and astrocytes may be attributed to the diminution of T lymphocytes or consequential to the reduction of microglia which are known to secrete interleukin-1 that would influence gliogenesis and produce specific growth factors for promoting astrocyte proliferation. Last, as interaction exists between astrocytes and oligodendrocytes, the products of astrocytes may affect the development of oligodendrocytes and vice vasa. The present findings point to a relation between glial cell development and immune network system. © 1995 Wiley-Liss, Inc. |
