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ZFIN ID: ZDB-PUB-080826-36
Motor neuron regeneration in adult zebrafish
Reimer, M.M., Sörensen, I., Kuscha, V., Frank, R.E., Liu, C., Becker, C.G., and Becker, T.
Date: 2008
Source: The Journal of neuroscience : the official journal of the Society for Neuroscience   28(34): 8510-8516 (Journal)
Registered Authors: Becker, Catherina G., Becker, Thomas, Frank, Rebecca E., Kuscha, Veronika, Reimer, Michell M.
Keywords: endogenous stem cells, radial glia, BrdU, PCNA, SV2, adult neurogenesis
MeSH Terms:
  • Animals
  • Animals, Genetically Modified
  • Basic Helix-Loop-Helix Transcription Factors/genetics
  • Basic Helix-Loop-Helix Transcription Factors/metabolism
  • Bromodeoxyuridine
  • Cell Count
  • Cell Differentiation
  • Cell Lineage
  • Cell Proliferation
  • Green Fluorescent Proteins/genetics
  • Homeodomain Proteins/genetics
  • Homeodomain Proteins/metabolism
  • LIM-Homeodomain Proteins
  • Microscopy, Electron
  • Motor Neurons*/pathology
  • Nerve Regeneration*
  • Nerve Tissue Proteins/genetics
  • Nerve Tissue Proteins/metabolism
  • Neuroglia/metabolism
  • Neuroglia/pathology
  • Phenotype
  • Recombinant Fusion Proteins/genetics
  • Spinal Cord/metabolism
  • Spinal Cord/pathology
  • Spinal Cord Injuries/pathology
  • Spinal Cord Injuries/physiopathology*
  • Stem Cells/metabolism
  • Stem Cells/pathology
  • Transcription Factors/genetics
  • Transcription Factors/metabolism
  • Zebrafish*
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism
PubMed: 18716209 Full text @ J. Neurosci.
FIGURES
ABSTRACT
The mammalian spinal cord does not regenerate motor neurons that are lost as a result of injury or disease. Here we demonstrate that adult zebrafish, which show functional spinal cord regeneration, are capable of motor neuron regeneration. After a spinal lesion, the ventricular zone shows a widespread increase in proliferation, including slowly proliferating olig2-positive (olig2+) ependymo-radial glial progenitor cells. Lineage tracing in olig2:green fluorescent protein transgenic fish indicates that these cells switch from a gliogenic phenotype to motor neuron production. Numbers of undifferentiated small HB9+ and islet-1+ motor neurons, which are double labeled with the proliferation marker 5-bromo-2-deoxyuridine (BrdU), are transiently strongly increased in the lesioned spinal cord. Large differentiated motor neurons, which are lost after a lesion, reappear at 6-8 weeks after lesion, and we detected ChAT+/BrdU+ motor neurons that were covered by contacts immunopositive for the synaptic marker SV2. These observations suggest that, after a lesion, plasticity of olig2+ progenitor cells may allow them to generate motor neurons, some of which exhibit markers for terminal differentiation and integration into the existing adult spinal circuitry.
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