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Journal of Neuroscience, Vol 11, 3398-3411, Copyright © 1991 by Society for Neuroscience
Reduction of neurite outgrowth in a model of glial scarring following CNS injury is correlated with the expression of inhibitory molecules on reactive astrocytes
RJ McKeon, RC Schreiber, JS Rudge and J Silver
Department of Neurosciences, Case Western Reserve University, Cleveland, Ohio 44106.
The extracellular matrix (ECM) molecules chondroitin-6-sulfate proteoglycan
(CS-PG) and cytotactin/tenascin (CT), present on subpopulations of
astroglia or their precursors during development, can inhibit neurite
outgrowth in vitro. However, it is not known whether these molecules are
expressed within the mature CNS following injury, where they could
contribute to regenerative failure. Thus, the expression of various ECM
molecules that affect axon growth was examined in areas of reactive gliosis
caused by implanting a piece of nitrocellulose into the cortex of neonatal
and adult animals. The expression of these molecules was compared to the
amount of neurite outgrowth that occurred in vitro when the damaged CNS
tissue from animals of various ages was removed intact and used as a
substrate in explant culture. The results demonstrate that the
growth-promoting molecules laminin, collagen type IV, and fibronectin were
present around the implant in all experimental groups. In comparison, CS-PG
and CT were present within and around the area of the lesion only in adult
animals. In vivo, these molecules were colocalized with intensely glial
fibrillary acidic protein (GFAP)-positive astrocytes in and immediately
adjacent to the scar, but not with other equally intensely GFAP- positive
astrocytes in the cortex away from the site of injury. CT and CS-PG were
present in gray matter areas of the cortex that had been directly damaged
during the implant procedure and in the corpus callosum when lesioned
during implantation. In vitro, the glial tissue removed from the lesion
site of neonatal animals supported neurite outgrowth, while scars removed
from adult animals did not. The inability of the adult glial scar tissue to
support neurite outgrowth was best correlated with the expression of CS-PG
and CT, suggesting that these molecules may be involved in limiting the
growth of regenerating axons in the CNS after injury.
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