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Journal of Neuroscience, Vol 15, 8053-8066, Copyright © 1995 by Society for Neuroscience
Differential effects of glycosaminoglycans on neurite growth on laminin and L1 substrates
CL Dou and JM Levine
Department of Neurobiology and Behavior, State University of New York at Stony Brook 11794, USA.
Glycosaminoglycans (GAGs), the carbohydrate moieties of proteoglycans, are
thought to be positive and negative regulators of axonal growth. The
physiological role of GAGs is controversial as some studies have shown that
GAGs inhibit cell adhesion and neurite elongation (Exp Neurol 109:111,
1990) whereas other studies have reported a growth stimulatory effect of
GAGs (Development 114:17, 1992). These and other studies have examined the
effects of GAGs using different types of neurons and different substrate
conditions thereby making a direct comparison of the experimental data
difficult. To resolve the controversy concerning the ability of exogenous
GAGs to modulate neurite growth, we examined the effects of a panel of
structurally different GAGs on the growth of postnatal rat cerebellar
granule neurons and embryonic rat dorsal root ganglia (DRG) neurons on
substrates of either laminin or the L1 glycoprotein. Here we show that
chondroitin 4-sulfate (CS4), chondroitin 6-sulfate (CS6), and keratan
sulfate (KS) inhibit neurite growth from both cerebellar and DRG neurons on
laminin-coated surfaces. On L1 surfaces, however, these GAGs are either
extremely weak inhibitors of neurite extension or, in the case of CS4, a
modest stimulator of neurite growth. Heparan sulfate (HS) and dermatan
sulfate (DS) inhibited the growth of cerebellar neurons but not the growth
of DRG neurons on L1-coated surfaces. On laminin surfaces, DS and HS had no
effect on neurite growth from both cerebellar and DRG neurons. These
results demonstrate a cellular and a substrate specificity to the effects
of exogenous GAGs on neurite extension in vitro. They suggest that while CS
and KS GAGs may not exert strong negative influences over axonal growth in
regions of the developing CNS where the L1 glycoprotein is abundant, these
GAGs are capable of inhibiting the growth of axons that extend within an
environment rich in laminin.
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