EFFECT OF NEONATAL NERVE INJURY ON THE EXPRESSION OF MAJOR HISTOCOMPATIBILITY COMPLEX ANTIGENS IN THE RAT SPINAL-CORD

Motoneurones are known to die following nerve lesions in immature animals. We have studied the expression of major histocompatibility complex (MHC) antigens in the spinal cord during the first 2 weeks after sciatic nerve injury in neonatal rats. Following neonatal injury, an increase in MHC class I immunoreactivity was observed, which peaked 7 days after the lesion. Retrograde labelling of ankle flexor motoneurones with fluorescent tracers prior to injury, indicate that motoneurones are degenerating at this time, and that small microglial-like cells take up the label by phagocytosis of dying motoneurones. A number of antibodies were used to examine the phenotype of these cells. The MHC class II monoclonal antibody identified a population of microglial cells displaying morphological features of activated (amoeboid) microglia, whose perineuronal position was identical to that of the fluorescently labelled phagocytic cells. These cells were also recognized with the Ox-1 and 0x-42 antibodies which labelled both resting (ramified) and activated microglial cells and with the MHC class I antibody. Thus, neonatal nerve injury induces a change in the phenotype of injured motoneurones and surrounding glial cells which coincides with the peak period of motoneurone degeneration. It is suggested-that activated microglial cells may not only participate in the phagocytosis of dying motoneurones, but may also be involved in initiating motoneurone death.