The Journal of Neuroscience, August 20, 2008, 28(34):8510-8516; doi:10.1523/JNEUROSCI.1189-08.2008
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Brief Communications
Motor Neuron Regeneration in Adult Zebrafish
Michell M. Reimer,1
Inga Sörensen,2
Veronika Kuscha,1
Rebecca E. Frank,1
Chong Liu,1
Catherina G. Becker,1 * and
Thomas Becker1 *
1Centre for Neuroscience Research, Royal (Dick) School of Veterinary Studies, University of Edinburgh, Summerhall, Edinburgh EH9 1QH, United Kingdom, and 2Medizinische Hochschule Hannover, Molekularbiologie, 30625 Hannover, Germany
Correspondence should be addressed to Thomas Becker, Centre for Neuroscience Research, Royal (Dick) School of Veterinary Studies, University of Edinburgh, Summerhall, Edinburgh EH9 1QH, UK. Email: thomas.becker{at}ed.ac.uk
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.
Key words: endogenous stem cells; radial glia; BrdU; PCNA; SV2; adult neurogenesis
Received March 19, 2008;
revised June 18, 2008;
accepted July 11, 2008.
Correspondence should be addressed to Thomas Becker, Centre for Neuroscience Research, Royal (Dick) School of Veterinary Studies, University of Edinburgh, Summerhall, Edinburgh EH9 1QH, UK. Email: thomas.becker{at}ed.ac.uk