Cited by 606Nerve injury and regenerationNeurogenesis and neuroplasticity mechanismsSpinal Cord Injury Research

The DOI matches its Crossref record; 53 of the 54 references it cites were found in a registry or an index.

Robust regeneration of adult sensory axons in degenerating white matter of the adult rat spinal cord.

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Abstract

We have recently reported that minimally disturbed adult CNS white matter can support regeneration of adult axons by using a novel microtransplantation technique to inject minute volumes of dissociated adult rat dorsal root ganglion neurons directly into adult rat CNS pathways (Davies et al., 1997). This atraumatic injection procedure minimized scarring and allowed considerable numbers of regenerating adult axons immediate access to the adult CNS glial terrain where they rapidly extended for long distances. A critical question remained as to whether degenerating white matter at acute and chronic stages (up to 3 months) after injury could still support regeneration. To investigate this, we have microtransplanted adult sensory neurons into degenerating white matter of the adult rat spinal cord several millimeters rostral to a severe lesion of the dorsal columns. Regeneration of donor sensory axons in both directions away from the site of transplantation was robust even within white matter undergoing fulminant Wallerian degeneration despite intimate contact with myelin. Along their route, the regrowing axons extended large numbers of collaterals into the adjacent dorsal horn. However, after entering the lesion, the rapidly extending growth cones stopped and became dystrophic within high concentrations of reactive glial matrix. Our results offer compelling evidence that the major environmental impediment to regeneration in the adult CNS is the molecular barrier that forms directly at the lesion site, and that degenerating white matter beyond the glial scar has a far greater intrinsic ability to support axon regeneration than previously thought possible.

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Crossref · 10.1523/jneurosci.19-14-05810.1999

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Research works printed but not linked: 2

  1. Huber, 1998, Developmental expression pattern and functional analysis of NOGO (formerly NI-35/250), a major inhibitor of CNS regeneration., Soc Neurosci Abstr, 24, 616.6
  2. McKeon, 1997, Gene expression in glial scars following CNS injury., Soc Neurosci Abstr, 23, 777.1

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Metadata

Authors
Davies, S. J. A., Goucher, D. R., Doller, C., & Silver, J.
Affiliations
Case Western Reserve University (US)
Venue
The Journal of Neuroscience
Published
1999-07-15
Volume
19
Issue
14
Pages
5810-5822
ISSN
  • 0270-6474 (ISSN-L)
  • 1529-2401
OpenAlex
W1826719783
Cited by
606
References
54
Citations by year
2026: 2 · 2025: 6 · 2024: 5 · 2023: 7 · 2022: 11 · 2021: 13 · 2020: 9 · 2019: 11 · 2018: 13 · 2017: 13 · 2016: 13 · 2015: 13 · 2014: 27 · 2013: 22 · 2012: 39
FWCI
14.12
Type
journal article
Language
en
Open access
Locations
  • Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Institute of Neurological Disorders and Stroke (NS 25713)
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
  • Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
  • Health Sciences › Medicine › Clinical Neurology › Spinal Cord Injury Research
Keywords
axon regeneration, spinal cord injury, dorsal root ganglion neurons, microtransplantation, Wallerian degeneration, glial scar, sensory axons, dorsal horn, myelin, dorsal column lesion
MeSH terms
Animals, Astrocytes, Axons, Cells, Cultured, Chickens, Ganglia, Spinal, Luminescent Proteins, Mice, Inbred C57BL, Mice, Transgenic, Myelin Sheath, Nerve Degeneration, Nerve Regeneration, Neurons, Neurons, Afferent, Oligodendroglia, Spinal Cord, Time Factors, Rats, Sprague-Dawley, Coculture Techniques, Green Fluorescent Proteins, Mice, Rats

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