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Editors Selection IGR 9-1

Basic research: Retinal ganglion cells

Comment by Keith Martin on:

13747 Retinal ganglion cell axotomy induces an increase in intracellular superoxide anion, Lieven CJ; Hoegger MJ; Schlieve CR et al., Investigative Ophthalmology and Visual Science, 2006; 47: 1477-1485

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The signalling mechanisms by which axonal injury triggers retinal ganglion cell (RGC) death in diseases such as glaucoma remain illusive. There has been much recent interest in the possibility that mitochondrial dysfunction following axonal injury is a key cause of neuronal death. High levels of reactive oxygen species (ROS) have been proposed as an important death signal and ROS scavengers are of interest as potential therapeutic agents.

Lieven et al. (378) hypothesized that a specific ROS, superoxide anion, acts as an intracellular signalling molecule for RGC death after axotomy. In an elegant series of experiments, they used dyes that change fluoresence specifically when oxidised by superoxide anion to explore the timecourse of changes in this particular ROS after axonal injury (both after retinal dissociation and optic nerve crush). They found that optic nerve crush caused a surprisingly asynchronous superoxide burst that could not be prevented by exposure to neurotrophic factors.

Neurotrophin factor deprivation is unlikely to be the only signal triggering cell death after axotomy

This finding suggests that neurotrophin factor deprivation is unlikely to be the only signal triggering cell death after axotomy. The authors suggest that the asynchronous superoxide burst after axotomy could explain the delayed death of RGC that follows optic nerve transection, and this interesting idea warrants further investigation. However, it remains to be seen whether ROS signalling occurs upstream of apoptosis or as part of a parallel cell death pathway.

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