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Journal of Neuroscience, Vol 11, 3738-3751, Copyright © 1991 by Society for Neuroscience
Fate of GAP-43 in ascending spinal axons of DRG neurons after peripheral nerve injury: delayed accumulation and correlation with regenerative potential
DJ Schreyer and JH Skene
Department of Neurobiology, Stanford University School of Medicine, California 94305-5401.
Proteins characteristic of growing axons often fail to be induced or
transported along axons that have been interrupted far from their cell
bodies in the adult mammalian CNS. Here, we inquire whether long axons in
the mammalian CNS can support efficient axonal transport and deposition of
one such protein, GAP-43, when the protein is induced in neuron cell
bodies. We have used immunocytochemistry to follow the fate of GAP-43 in
dorsal column axons ascending the rat spinal cord from dorsal column axons
ascending the rat spinal cord from dorsal root ganglion (DRG) neurons,
after synthesis of the protein is induced in these cells by peripheral
nerve injury. Sciatic nerve lesions do lead to an accumulation of GAP-43 in
dorsal column axons derived from the lumbar DRG. However, in distal
segments of these CNS axons, accumulation of GAP-43 is apparent only after
a delay of 1-2 weeks, in contrast to its rapid accumulation in axon
segments within the PNS environment, suggesting that deposition and
stabilization of GAP-43 can be limited by local, posttranslational
regulation. GAP-43 immunoreactivity subsides to control levels within 8
weeks after crush lesions that permit peripheral axon regeneration, but
remains robust 8 weeks after resection lesions that prevent peripheral
regeneration. Accumulation of GAP-43 in cervical dorsal column axons after
peripheral nerve injury is closely correlated with the ability of these
axons to respond to local cues capable of eliciting axon growth (Richardson
and Verge, 1986).
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