Notch signaling controls generation of motor neurons in the lesioned spinal cord of adult zebrafish
- Authors
- Dias, T.B., Yang, Y.J., Ogai, K., Becker, T., and Becker, C.G.
- ID
- ZDB-PUB-120306-6
- Date
- 2012
- Source
- The Journal of neuroscience : the official journal of the Society for Neuroscience 32(9): 3245-3252 (Journal)
- Registered Authors
- Becker, Thomas, Dias, Tatyana
- Keywords
- none
- MeSH Terms
-
- Age Factors
- Animals
- Animals, Genetically Modified
- Female
- Homeodomain Proteins/physiology*
- Male
- Motor Neurons/physiology*
- Nerve Regeneration/physiology*
- Nerve Tissue Proteins/physiology*
- Receptor, Notch1/physiology*
- Receptors, Notch/physiology*
- Signal Transduction/physiology*
- Spinal Cord Injuries/metabolism*
- Spinal Cord Injuries/pathology
- Zebrafish
- Zebrafish Proteins/physiology*
- PubMed
- 22378895 Full text @ J. Neurosci.
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.