The Journal of Neuroscience, 2012 · DOI: 10.1523/JNEUROSCI.6398-11.2012 · Published: February 29, 2012
In mammals, increased Notch signaling is thought to contribute to the lack of neurogenesis after spinal cord injury. This study investigates this in zebrafish, which can regenerate neurons after spinal injuries. The researchers found that the Notch pathway is reactivated in zebrafish after spinal cord injury. However, when they increased Notch activity, it reduced the production of new motor neurons. Conversely, blocking the Notch pathway increased the number of new motor neurons. This suggests that Notch signaling normally inhibits motor neuron regeneration in the zebrafish spinal cord.
Inhibiting Notch signaling may promote motor neuron regeneration after spinal cord injury.
Precise regulation of Notch activity is necessary to allow neurogenesis while maintaining the progenitor pool in the lesioned CNS.
Pharmacological intervention with the Notch inhibitor DAPT may inform future therapeutic interventions in the lesioned spinal cord of mammals.