We analyzed the ability of microglia to transform into phagocytic cells in the rat facial nucleus by administering the protein synthesis inhibitor cycloheximide at the transected facial nerve. Immunoblotting revealed that a phagocytic marker, the cluster of differentiation 68 (CD68) protein, was induced in the transected and cycloheximide-treated facial nucleus on day 5 post-insult, but not significantly induced in either the normal facial nucleus or simply transected facial nucleus. The time-course experiment indicated that the levels of CD68 protein peaked 5-7 days after transection and cycloheximide-administration. Avidin-biotin peroxidase complex staining revealed that the CD68-expressing cells appeared at the transected and cycloheximide-treated facial nucleus, and were located in the vicinity of motoneuron cell bodies. Fluorescent double-staining revealed that the CD68-expressing cells were almost positive for ionized Ca²⁺-binding adapter molecule 1 (a microglial marker). Collectively, these results demonstrated that the resident microglia can transform into phagocytic cells in response to injury and cycloheximide-treatment of motoneurons in the facial nucleus.