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well as changes in the pattern genes that the neuron expresses. The main
metabolic activity of the cell is shifted from synthesizing neurotransmitter-
related proteins to the synthesis of structural materials needed for axon repair
and growth. For example, choline acetyltransferase is downregulated,
whereas the neuropeptide, calcitonin gene-related peptide, the fast trans-
ported growth-associated protein, GAP-43, and the slowly transported
cytoskeletal proteins, actin and tubulin, are upregulated (
Haas, Donath, &
Kreutzberg, 1993; Tetzlaff, Gilad, Leonard, Bisby, & Gilad, 1988
).
Glucose-6-phosphate dehydrogenase and hydrolytic enzyme are also
upregulated (
Davis, Taylor, & Anastakis, 2011; Fawcett & Keynes, 1990
).
The success of nerve regeneration and functional reinnervation of targets
first depend on the capacity of axotomized neurons to survive and shift
toward the regenerative phenotype (
Navarro et al., 2007
). Results of studies
on the changes in DRG neuron number following a nerve injury show a
wide variation in results. Most of the authors report that peripheral nerve
transection induces the primary sensory neuronal death (
Himes & Tessler,
1989; Terenghi, 1999; Vestergaard, Tandrup, & Jakobsen, 1997
), showing
that between 7% and 50% of primary sensory neurons (more small than large
neurons) die after injury (
Himes & Tessler, 1989; McKay Hart, Brannstrom,
Wiberg, & Terenghi, 2002
). Other authors report no significant neuron loss
(
Swett, Hong, &Miller, 1995
) or no detectable loss of dorsal root axons until
4 months (
Coggeshall, Lekan, Doubell, Allchorne, &Woolf, 1997; Cohen,
Yachnis, Arai, Davis, & Scherer, 1992
) after injury to the spinal or
sciatic nerve.
Further, during regeneration, the cell body undergoes visible changes
that mark the reversal of chromatolysis. Indeed, the nucleus returns to the
cell center and nucleoproteins reorganize into the compact Nissl granules.
A complex and incompletely understood interaction occurs between the cell
body and the regenerating axon tip. Axoplasm, which serves to regenerate
the axon tip, arises from the proximal axon segment and cell body. Both fast
and slow components of axoplasmic transport supply materials from the cell
body to the sites of axonal regeneration. The rate of increase in protein and
lipid synthesis in the cell body influences the rate of advance and the final
caliber of the regenerating axon (
Burnett & Zager, 2004
).
4.2. CNS plasticity induced by peripheral nerve injury and
regeneration
Until recently, it was thought that no new neural connections could be
formed in the adult brain (
Kandel & Squire, 2000
). It was assumed that, once
