| First Author | Li S | Year | 2005 |
| Journal | Mol Cell Neurosci | Volume | 29 |
| Issue | 1 | Pages | 26-39 |
| PubMed ID | 15866044 | Mgi Jnum | J:98115 |
| Mgi Id | MGI:3577161 | Doi | 10.1016/j.mcn.2004.12.008 |
| Citation | Li S, et al. (2005) Transgenic inhibition of Nogo-66 receptor function allows axonal sprouting and improved locomotion after spinal injury. Mol Cell Neurosci 29(1):26-39 |
| abstractText | Axon growth after spinal injury is thought to be limited in part by myelin-derived proteins that act via the Nogo-66 Receptor (NgR). To test this hypothesis, we sought to study recovery from spinal cord injury (SCI) after inhibiting NgR transgenically with a soluble function-blocking NgR fragment. Glial fibrillary acidic protein (gfap) gene regulatory elements were used to generate mice that secrete NgR(310)ecto from astrocytes. After mid-thoracic dorsal over-hemisection injury, gfapColon, two colonsngr(310)ecto mice exhibit enhanced raphespinal and corticospinal axonal sprouting into the lumbar spinal cord. Recovery of locomotion is improved in the gfapColon, two colonsngr(310)ecto mice. These data indicate that the NgR ligands, Nogo-66, MAG, and OMgp, play a role in limiting axonal growth in the injured adult CNS and that NgR(310)ecto might provide a therapeutic means to promote recovery from SCI. |
