期刊
JOURNAL OF NEUROSCIENCE
卷 32, 期 9, 页码 3245-3252出版社
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.6398-11.2012
关键词
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资金
- Biotechnology and Biological Sciences Research Council [BB/H003304/1]
- Robert Packard Center for ALS Research at Johns Hopkins
- Euan MacDonald Centre for Motor Neurone Disease Research
- TENOVUS Scotland
- BBSRC [BB/H003304/1] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BB/H003304/1] Funding Source: researchfish
In mammals, increased Notch signaling is held partly responsible for a lack of neurogenesis after a spinal injury. However, this is difficult to test in an essentially nonregenerating system. We show that in adult zebrafish, which exhibit lesion-induced neurogenesis, e.g., of motor neurons, the Notch pathway is also reactivated. Although apparently compatible with neuronal regeneration in zebrafish, forced activity of the pathway significantly decreased progenitor proliferation and motor neuron generation. Conversely, pharmacological inhibition of the pathway increased proliferation and motor neuron numbers. This demonstrates that Notch is a negative signal for regenerative neurogenesis, and, importantly, that spinal motor neuron regeneration can be augmented in an adult vertebrate by inhibiting Notch signaling.
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