An immunohistochemical study of the intraventricular macrophages in induced hydrocephalus in prenatal rats following a maternal injection of 6-aminonicotinamide.

Hydrocephalus was induced experimentally in prenatal rats following an injection of 6-aminonicotinamide (6-AN) into pregnant rats. The most remarkable change of the dilated lateral ventricles was in a marked increase in the number of intraventricular macrophages, some of which were laden with ingested erythrocytes. The immunoreactivity of the intraventricular macrophages was noticeably enhanced with the monoclonal antibodies OX-42 and OX-18 which marked the complement type 3 receptors (CR3) and major histocompatibility complex (MHC) class I antigen, respectively. Many immunoreactive cells with similar external morphology were observed to penetrate the ependymal lining at the roof of the ventricles. This, coupled with the concomitant depletion of the conglomeration of amoeboid microglia in the supraventricular corpus callosum, suggests that the upsurge of immunoreactive intraventricular macrophages in hydrocephalus was partly due to the influx of amoeboid microglia probably in response to the damage of the ventricular walls and possible alteration in the contents of the cerebrospinal fluid. The significance of the upregulation of complement type 3 receptors and major histocompatibility complex class I antigens on epiplexus cells in hydrocephalic rats remains to be explored, although our results suggest that the surface antigens may be involved in increased phagocytosis and/or a possible immune response.