Altered expression of immune-related antigens by neuronophages does not improve neuronal survival after severe lesion of the facial nerve in rats.

Injection of Fluoro-Gold (FG) into the whiskerpad muscles of rats yields a permanent retrograde labeling of motoneurons in the facial nucleus. Following subsequent resection of 10 mm of the facial nerve, one-third of the facial motoneurons die and the microglia phagocytize the dead FG-labeled neurons, take up FG, and get labeled in vivo. The resulting identification of all FG-labeled cells allows long-term comparative investigations on the behavior of neuronophages. In this study, we used two groups of rats to test whether the quantified expression of five immune-related antigens by neuronophages was related to quantified decline in neuron number (counts after immunostaining for neuron-specific enolase) 3 to 224 days after resection of the facial nerve. Rats of the first group received standard food and those of the second group, pellets containing 1,000 ppm of the calcium channel blocker nimodipine. Image analysis of the number of FG-containing cells and the number and projection area of immunopositive neuronophages in serial sections for each antigen showed that nimodipine significantly attenuated the immunostaining for CR3, MHC class I, and class II antigens (monoclonal antibodies [MAbs] OX-42, OX-18, and OX-6); enhanced the expression of monocyte-macrophage-specific antigen (MAb ED1); and did not change the expression of rat macrophage differentiation antigen (MAb ED2). The altered expressions, however, had no effect on the loss of motoneurons in the lesioned facial nucleus. We conclude that the degree of expression of immune-related antigens by neuronophages has no influence on the delayed neuronal cell death induced by permanent target deprivation.