INTERCELLULAR-ADHESION MOLECULE-1 (ICAM-1) IN THE MOUSE FACIAL MOTOR NUCLEUS AFTER AXONAL INJURY AND DURING REGENERATION

Intercellular adhesion molecule 1 (ICAM-1, CD54) is a widely expressed glycoprotein, which plays an important role in leukocyte extravasatio n and in the interaction of lymphocytes with antigen-presenting cells. In the current study we examined the regulation of ICAM-1 in the mous e facial motor nucleus after facial nerve transection, using immunohis tochemistry, confocal laser microscopy and electron microscopy. In the normal facial nucleus ICAM-1 immunoreactivity was restricted to vascu lar endothelium. Transection of the facial nerve led to a strong and s elective upregulation of ICAM-1 on activated microglia. Quantitation o f microglial ICAM-1 immunoreactivity revealed a biphasic increase. The first peak 1-2 days post operation paralleling the early stage of mic roglial activation was followed by a decline at 4-7 days. The second i nduction of ICAM-1 occured at day 14 accompanying the period of neuron al cell death and microglial phagocytosis of neuronal debris. Immunoel ectron microscopy showed strong ICAM-1 reactivity on the cell membrane of activated microglia at day 2. During the second peak (day 14), ICA M-1 was also observed on lymphocytes adhering to phagocytotic microgli a forming aggregates around neuronal debris. No immunolabelling was ob served on neurons, astrocytes or oligodendroglia. These data suggest t he involvement of ICAM-1 in the adhesion of activated microglia, in th eir phagocytosis of neuronal debris, and also in the interaction with infiltrating lymphocytes following this injury.