Activation and re-expression of surface antigen in microglia following an epidural application of kainic acid in the rat brain.

Following an epidural application of kainic acid over the sensorimotor cortex in rats, the ipsilateral hippocampus and the ventrobasal nuclear complex of the thalamus showed extensive neural degeneration. The neuronal death, either as a result of direct neurotoxic destruction or wallerian and retrograde degeneration, elicited a dramatic expression of immunoreactivity on numerous cells bearing the external morphology of microglia. Thus, with the monoclonal antibody OX-42, many amoeboid immunoreactive cells bearing stout processes were observed in the above-mentioned lesioned sites. The present electron microscopic immunocytochemical study confirmed that these OX-42 positive cells were activated microglia characterised by an abundant cytoplasm containing a variable number of lysosomes and phagosomes. The surfaces of these activated microglial cells were thrown into pseudopodial processes engaged in the phagocytosis of cellular debris. Immunoreactivity was also observed in these cells with the monoclonal antibodies OX-18 and OX-6, although in the latter the immunoreactive cells were fewer and less intensely stained. With OX-42, the corresponding areas on the contralateral side showed some widely scattered typical microglial cells bearing extremely fine processes. They were not stained with either OX-18 or OX-6. It was concluded from this study that neural degeneration induced the expression of CR3 receptors (marked by OX-42) and MHC encoded antigens (marked by OX-18 and OX-6) in microglia. The elevation of the former antigen was related to their active phagocytic activity. The latter, on the other hand, would facilitate the capability of interaction between the activated microglia and T lymphocytes in a possible immune response.