Retinal ganglion cell survival and axon regeneration in Wld S transgenic rats after optic nerve crush and lens injury
1 Centre for Brain Repair, University of Cambridge, Cambridge, UK
2 First Department of Ophthalmology, Evgenidion Hospital, University of Athens, Athens, Greece
3 Cambridge NIHR Biomedical Research Centre, Cambridge, UK
4 Eye Department, Addenbrooke's Hospital, Cambridge, UK
5 Cambridge Centre for Brain Repair, University of Cambridge, Cambridge, CB2 0PY, United Kingdom
BMC Neuroscience 2012, 13:56 doi:10.1186/1471-2202-13-56Published: 6 June 2012
We have previously shown that the slow Wallerian degeneration mutation, whilst delaying axonal degeneration after optic nerve crush, does not protect retinal ganglion cell (RGC) bodies in adult rats. To test the effects of a combination approach protecting both axons and cell bodies we performed combined optic nerve crush and lens injury, which results in both enhanced RGC survival as well as axon regeneration past the lesion site in wildtype animals.
As previously reported we found that the WldS mutation does not protect RGC bodies after optic nerve crush alone. Surprisingly, we found that WldS transgenic rats did not exhibit the enhanced RGC survival response after combined optic nerve crush and lens injury that was observed in wildtype rats. RGC axon regeneration past the optic nerve lesion site was, however, similar in WldS and wildtypes. Furthermore, activation of retinal glia, previously shown to be associated with enhanced RGC survival and axon regeneration after optic nerve crush and lens injury, was unaffected in WldS transgenic rats.
RGC axon regeneration is similar between WldS transgenic and wildtype rats, but WldS transgenic rats do not exhibit enhanced RGC survival after combined optic nerve crush and lens injury suggesting that the neuroprotective effects of lens injury on RGC survival may be limited by the WldS protein.