In a previous study, we found immunoreactivity for
complement factors C3, C3d, and C4d, as well as endogenous
IgG in the hypoglossal nucleus following
hypoglossal nerve transection, suggesting that activation of the
complement cascade had taken place in the vicinity of the axotomized motorneurons. In the present study, we found increased immunoreactivity for
complement factor C1 and C1q in reactive microglia, indicating an increased potential for initiation of the classical pathway by binding of
IgG to C1q. Furthermore, we found immunoreactivity for C9, which contributes to the formation of
C5b-9, the final lytic product of the
complement cascade close to the axotomized neurons and perineuronal glia. In addition, immunoreactivity and
mRNA labeling of sulfated
glycoprotein (SGP-2), a putative
complement inhibitor, was increased in a subpopulation of the axotomized motorneurons. SGP-2 immunoreactivity was also increased in astroglial cells ipsilateral to the nerve injury. The results lend further support to the hypothesis that the
complement cascade is activated in the vicinity of axotomized neurons, which in turn may be protected by
complement inhibitors. The balance between activation of
complement and
complement inhibitors might have an impact on the degenerative components of the
axon reaction and, in particular, the events leading to nerve cell death.