|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.
|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|
|PubMed:||18716209 Full text @ J. Neurosci.|
Reimer, M.M., Sörensen, I., Kuscha, V., Frank, R.E., Liu, C., Becker, C.G., and Becker, T. (2008) Motor neuron regeneration in adult zebrafish. The Journal of neuroscience : the official journal of the Society for Neuroscience. 28(34):8510-8516.
ABSTRACTThe 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.