L. Liu et al., GLIAL-CELL RESPONSES, COMPLEMENT, AND CLUSTERIN IN THE CENTRAL-NERVOUS-SYSTEM FOLLOWING DORSAL-ROOT TRANSECTION, Glia, 23(3), 1998, pp. 221-238
We have examined the glial cell response, the possible expression of c
ompounds associated with the complement cascade, including the putativ
e complement inhibitor clustering and their cellular association durin
g Wallerian degeneration in the central nervous system. Examination of
the proliferation pattern revealed an overall greater mitotic activit
y after rhizotomy, an exclusive involvement of microglia in this proli
feration after peripheral nerve injury, but, in addition, a small frac
tion of proliferating astrocytes after rhizotomy. Immunostaining with
the phagocytic cell marker ED1 gradually became very prominent after r
hizotomy, possibly reflecting a response to the extensive nerve fiber
disintegration. Lumbar dorsal rhizotomy did not induce endogenous immu
noglobulin G (IgG) deposition or complement expression in the spinal c
ord dorsal horn, dorsal funiculus, or gracile nucleus. This is in mark
ed contrast to the situation after peripheral nerve injury, which appe
ars to activate the entire complement cascade in the vicinity of the c
entral sensory processes. Clusterin, a multifunctional protein with co
mplement inhibitory effects, was markedly upregulated in the dorsal fu
niculus in astrocytes. In addition, there was an intense induction of
clusterin expression in the degenerating white matter in oligodendrocy
tes, possibly reflecting a degeneration process in these cells. The fi
ndings suggest that 1) complement expression by microglial cells is in
timately associated with IgG deposition; 2) axotomized neuronal perika
rya, but not degenerating central fibers, undergo changes which induce
such deposition; and 3) clusterin is not related to complement expres
sion following neuronal injury but participates in regulating the stat
e of oligodendrocytes during Wallerian degeneration. (C) 1998 Wiley-Li
ss, Inc.