Influence of cortisone on amoeboid microglia and microglial cells in the corpus callosum in postnatal rats

Abstract

Amoeboid microglia and typical microglial cells in the corpus callosum of rats were studied following a subcutaneous injection of cortisone at birth. The rats were killed 2, 5, 10 and 20 days after the injection. The most striking change in the corpus callosum was the great reduction in the number of amoeboid microglial cells as shown by the silver carbonate stain of Rio-Hortega. The change was sustained throughout the period studied. Ramified and typical microglial cells which do not normally appear until between the fifth and tenth postnatal day, were observed on the second postnatal day after the cortisone administration. Cell enumeration in semithin sections showed that the proportion of amoboid microglial cells was reduced to 50% of their normal value soon (2 days) after the cortisone injection. This proportion was further decreased and the cells were absent from the fifth postnatal day onwards. Typical microglial cells were developed prematurely and they constituted more than 2% of the total glial population 2 days after the cortisone injection. Another striking change noted in the semithin section was the increase in the compactness of the axons in the corpus callosum in the experimental animals. Electron microscopic observations were in general agreement with the light microscopy. The amoeboid microglial cells appeared less active; they contained small Golgi apparatus, accumulations of lipid droplets and sparse lysosomes. The cell outline was regular. The reduction in the number of amoeboid microglia after the cortisone injection was explained by the fact that the drug suppressed the production of their precursor cells, i.e. circulating monocytes, Moreover, it was suggested that cortisone probably interfered with the phagocytic activity of the amoeboid microglial cells which would normally undergo structural changes to become the quiescent microglia which were observed in the early postnatal animals.