Journal of Neuroscience, Vol 6, 2563-2570, Copyright © 1986 by Society for Neuroscience
Elevated synthesis of an axonally transported protein correlates with axon outgrowth in normal and injured pyramidal tracts
K Kalil and JH Skene
Axons of the adult mammalian CNS typically fail to regenerate after injury.
Among the hypotheses to account for this failure is the proposition that
certain axonal proteins necessary for axon growth are expressed in much
greater abundance in developing than in mature neurons, and that these
proteins are not reinduced after injury to mature axons (Skene and Willard,
1981b). In the present experiments, we have found that hamster pyramidal
tract neurons synthesize an acidic, 43K protein that is transported into
growing axons during the first 2 weeks of postnatal development, and then
declines at least an order of magnitude by the fourth postnatal week. The
decline in synthesis of the 43K protein coincides with the cessation of
pyramidal tract axon elongation. This protein resembles a
"growth-associated protein," GAP- 43, which is induced during regeneration
of CNS axons in lower vertebrates. The 43K protein in hamster pyramidal
tract neurons is not reinduced after axotomy in adult animals, which
correlates with the failure of the injured axons to regenerate. Injury to
neonatal pyramidal tract axons does not reverse or delay the decline in 43K
protein synthesis. This is consistent with previous findings (Kalil and
Reh, 1982) that pyramidal tract axons regrow for only a brief period after
neonatal injury. Taken together, these results lend support to the
hypothesis that synthesis of GAP-43 is important for axon growth in
development and regeneration.
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