The DOI matches its Crossref record; 113 of the 113 references it cites were found in a registry or an index.
Neurotrophic Factors and Receptors in the Immature and Adult Spinal Cord after Mechanical Injury or Kainic Acid
Open accessAbstract
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 GFRα-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.
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Cites
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Spinal shock revisited: a four-phase model
Ditunno, J. F., Little, J. W., Tessler, A., & Burns, A. S. (2004) · Spinal Cord · doi:10.1038/sj.sc.3101603 · Cited by 441
ProNGF Induces p75-Mediated Death of Oligodendrocytes following Spinal Cord Injury
Beattie, M. S., Harrington, A. W., Lee, R., Kim, J. Y., Boyce, S. L., Longo, F. M., Bresnahan, J. C., Hempstead, B. L., & Yoon, S. O. (2002) · Neuron · doi:10.1016/s0896-6273(02)01005-x · Cited by 414
Chondroitinase ABC Promotes Sprouting of Intact and Injured Spinal Systems after Spinal Cord Injury
Barritt, A. W., Davies, M., Marchand, F., Hartley, R., Grist, J., Yip, P., McMahon, S. B., & Bradbury, E. J. (2006) · The Journal of Neuroscience · doi:10.1523/jneurosci.2980-06.2006 · Cited by 413
Prolonged Microgliosis in the Rhesus Monkey Central Nervous System after Traumatic Brain Injury
Nagamoto-Combs, K., McNeal, D. W., Morecraft, R. J., & Combs, C. K. (2007) · Journal of Neurotrauma · doi:10.1089/neu.2007.0377 · Cited by 156
Colombo, E., Cordiglieri, C., Melli, G., Newcombe, J., Krumbholz, M., Parada, L. F., Medico, E., Hohlfeld, R., Meinl, E., & Farina, C. (2012) · Journal of Experimental Medicine · doi:10.1084/jem.20110698 · Cited by 146
Metadata
- Authors
- Widenfalk, J., Lundströmer, K., Jubran, M., Brené, S., & Olson, L.
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2001-05-15
- Volume
- 21
- Issue
- 10
- Pages
- 3457-3475
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- OpenAlex
- W1916238061
- Cited by
- 289
- References
- 113
- FWCI
- 5.22
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- Widenfalk, J., Lundströmer, K., Jubran, M., Brené, S., & Olson, L. (2001). Neurotrophic Factors and Receptors in the Immature and Adult Spinal Cord after Mechanical Injury or Kainic Acid. The Journal of Neuroscience. https://doi.org/10.1523/jneurosci.21-10-03457.2001
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