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The Journal of Neuroscience, May 15, 2001, 21(10):3457-3475
Neurotrophic Factors and Receptors in the Immature and Adult
Spinal Cord after Mechanical Injury or Kainic Acid
Johan
Widenfalk,
Karin
Lundströmer,
Marie
Jubran,
Stefan
Brené, and
Lars
Olson
Department of Neuroscience, Karolinska Institute, S-171 77 Stockholm, Sweden
Delivery of neurotrophic factors to the injured spinal cord has
been shown to stimulate neuronal survival and regeneration. This
indicates that a lack of sufficient trophic support is one factor
contributing to the absence of spontaneous regeneration in the
mammalian spinal cord. Regulation of the expression of neurotrophic
factors and receptors after spinal cord injury has not been studied in
detail. We investigated levels of mRNA-encoding neurotrophins, glial
cell line-derived neurotrophic factor (GDNF) family members and
related receptors, ciliary neurotrophic factor (CNTF), and c-fos
in normal and injured spinal cord. Injuries in adult rats included
weight-drop, transection, and excitotoxic kainic acid delivery; in
newborn rats, partial transection was performed. The regulation of
expression patterns in the adult spinal cord was compared with that in
the PNS and the neonate spinal cord. After mechanical injury of the
adult rat spinal cord, upregulations of NGF and GDNF mRNA occurred in
meningeal cells adjacent to the lesion. BDNF and p75 mRNA increased in
neurons, GDNF mRNA increased in astrocytes close to the lesion, and
GFR -1 and truncated TrkB mRNA increased in astrocytes of
degenerating white matter. The relatively limited upregulation of
neurotrophic factors in the spinal cord contrasted with the response of
affected nerve roots, in which marked increases of NGF and GDNF mRNA
levels were observed in Schwann cells. The difference between the
ability of the PNS and CNS to provide trophic support correlates with their different abilities to regenerate. Kainic acid delivery led to
only weak upregulations of BDNF and CNTF mRNA. Compared with several
brain regions, the overall response of the spinal cord tissue to kainic
acid was weak. The relative sparseness of upregulations of endogenous
neurotrophic factors after injury strengthens the hypothesis that lack
of regeneration in the spinal cord is attributable at least partly to
lack of trophic support.
Key words:
rat; GFR; NGF; BDNF; NT3; NT4; GDNF; NTN; CNTF; PSP; TrkA; TrkB; truncated TrkB; TrkC; p75; in situ
hybridization; spinal cord injury; kainic acid; weight-drop; motoneuron
Copyright © 2001 Society for Neuroscience 0270-6474/01/21103457-19$05.00/0
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