ED2-POSITIVE PERIVASCULAR PHAGOCYTES PRODUCE INTERLEUKIN-1-BETA DURING DELAYED NEURONAL LOSS IN THE FACIAL NUCLEUS OF THE RAT

Injection of Fluoro-Gold (FG) into the whisker pad of rats yields stab le retrograde labeling of facial motoneurons, Subsequent removal of 10 mm from all facial nerve branches permanently deprives the FG-labeled motoneurons from their targets and the motoneurons gradually die. Neu ronal debris is phagocytized by two types of neuronophages: parenchyma l microglia (monoclonal antibody [MAb] OX42-positive, MAb ED2-negative ) and perivascular phagocytes (OX42-negative, ED2-positive), Because b oth types of neuronophages express major histocompatibility complex (M HC) class II glycoproteins (MAb OX6-positive), they are considered to be the potential antigen-presenting cells of the brain. To check this hypothesis, we tested whether both types of neuronophages also synthet ize the co-stimulatory cytokine interleukin-1 beta (IL-1 beta) immunoc ytochemically visualized by MAbs SILK-5/6, Employing combined fluoresc ent visualization of antigens (OX6, ED2, and SILK-5/6) in sections con taining fluorescent (FG-prelabeled) neuronophages, we found that, duri ng slowly occurring neuronal loss, the vast majority of IL-1 beta immu noreactive neuronophages were of perivascular (ED2-positive) origin, W e concluded that, during delayed neuronal death ''behind'' an intact b lood-brain barrier, the perivascular phagocytes were more likely to fu nction as antigen-presenting cells than the parenchymal microglia. J. Neurosci. Res. 54:820-827, 1998. (C) 1998 Wiley-Liss, Inc.