Abstract
BackgroundWe 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.ResultsAs 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.ConclusionsRGC 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.
Highlights
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
We have previously shown that the slow Wallerian degeneration mutation (WldS) delays RGC axon degeneration in adult rats after optic nerve injury, but does not reduce cell body death compared to wildtype animals [10]
RGC axon regeneration Two weeks after optic nerve crush alone, only a small number of adult rat RGC axons were able to grow past the optic nerve lesion site in both wildtype and Slow Wallerian degeneration mutation (WldS) transgenic rats with no significant difference between the two (Figure 1A-C)
Summary
The visual system provides an excellent model for studying neuronal survival and axon regeneration after central nervous system injury. It has been found that RGC survival and axon regeneration past the optic nerve lesion site can be enhanced, for example by lens injury [2,3,4], peripheral nerve injury [1,4], or intravitreal zymosan injection [2]. To test the effects of a combination approach protecting both axons and cell bodies we performed combined optic nerve crush and lens injury, which enhances RGC survival as well as axon regeneration in wildtype rats [2,3,4] This is of particular interest in terms of the effects of the WldS mutation on the axon regeneration potential in the central nervous system (CNS) because previous studies have mainly focused on peripheral. We found that whilst optic nerve crush and lens injury did not lead to enhanced RGC survival in WldS transgenic rats, these cells were able to successfully re-grow RGC axons past the optic nerve lesion site
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