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Journal of Neuroscience, Vol 15, 3594-3611, Copyright © 1995 by Society for Neuroscience
The effects of a lesion or a peripheral nerve graft on GAP-43 upregulation in the adult rat brain: an in situ hybridization and immunocytochemical study
E Vaudano, G Campbell, PN Anderson, AP Davies, C Woolhead, DJ Schreyer and AR Lieberman
Department of Anatomy and Developmental Biology, University College London, United Kingdom.
We have sought to determine (1) if thalamic neurons upregulate the growth
associated protein GAP-43 as a response to injury, or if a peripheral nerve
graft is required to induce, enhance or sustain such a response, and (2) if
thalamic neurons with different regenerative potentials also display
different GAP-43 responses. Levels of GAP-43 protein (detected by LM and EM
immunohistochemistry) and of GAP-43 mRNA (detected by in situ
hybridization) were compared in the thalamus of adult rats between 1 d and
180 d after making a stab lesion or after implanting a peripheral nerve
autograft. Stab injury is a sufficient stimulus to cause a transient
upregulation in GAP-43 expression by neurons in the thalamus (both around
the graft tip and in particular in the thalamic reticular nucleus) in the
first week after injury but this response is both prolonged, and enhanced
in the presence of a peripheral nerve graft. In addition, we demonstrate
directly, by double labelling, that neurons of the thalamic reticular
nucleus displaying high levels of the mRNA for GAP-43, have axons
regenerating in the distal portion of the graft. These findings lend direct
support to the hypothesis that upregulation of the GAP-43 gene is essential
for prolonged regenerative axonal growth. We also demonstrate GAP-43
protein in graft Schwann cells and in brain astrocytes close to the site of
graft implantation.
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