| Description |
In humans and other adult mammals, spinal cord injury leads to a permanent loss of motor and sensory function. The biggest obstacle to recovery is the inability of severed axons and neurons to regenerate. During embryogenesis, all vertebrates have a population of neural stem cells called radial glia in their spinal cord. These radial glia can self-renew as well as give rise to committed neural progenitors, which further differentiate into molecularly and anatomically distinct neural sub-types, forming the post-embryonic spinal cord. Zebrafish differ from mammals in that radial glial persist past embryogenesis into adulthood. After spinal cord injury, these cells facilitate axon regrowth, rewiring of existing circuits and local neurogenesis, allowing zebrafish to make a near full recovery of sensory and motor function. Following injury, radial glia proliferate and migrate into the injured region, forming a bridge, across which ascending and descending axons can regrow. Additionally, radial glia in the injured region have been shown to differentiate into newly born neurons after injury. Previous work from our lab has shown that Wnt signaling is vital to axon regrowth and neurogenesis in injured larval zebrafish. The specific processes and genes regulated by Wnt signaling during recovery, however, remain largely unknown. In this study, we used in situ hybridization to identify newly born neurons that have adopted specific neuronal sub-types, in a Wnt dependent manner. We have also used RNA-seq to identify a candidate group of genes regulated by Wnt signaling that promote neurogenesis and recovery from spinal cord injury. |
