Editors Selection (IGR: 8-1) | International Glaucoma Review #283

Editors Selection IGR 8-1

Basic science: Cortisol

Comment by Leonard A. Levin on:

15120 Cortisol promotes survival and regeneration of axotomised retinal ganglion cells and enhances effects of aurintricarboxylic acid, Heiduschka P; Thanos S, Graefe's Archive for Clinical and Experimental Ophthalmology, 2006; 244: 1512-1521

It is controversial whether high-dose corticosteroids are neuro-protective for retinal ganglion cells in traumatic optic neuropathy. Based on spinal cord injury studies, several neuro-ophthalmologists routinely advised using doses of several grams per day of methyl-prednisolone intravenously to treat acute traumatic optic neuropathy. However, this is changing, based on recent studies by Steinsapir et al.,¹ Diem et al.,² and Ohlsson et al.³ which suggest that these doses may actually be toxic to the optic nerve and/or the retinal ganglion cell. The present study by Heiduschka and Thanos (1254) is ingenious, in that the corticosteroid is delivered to the retinal ganglion cell (and not the optic nerve) directly via intravitreal injection. They found that high-dose cortisol dramatically increased retinal ganglion cell survival after optic nerve transection, at the same time decreasing the number of microglial cells. Not surprisingly, there was also increased regeneration into a peripheral nerve graft, which was even greater when the endonuclease inhibitor ATA was coadministered.

High-dose cortisol dramatically increased retinal ganglion cell survival after optic nerve transection, at the same time decreasing the number of microglial cells

The authors hypothesized three different mechanisms by which cortisol could increase retinal ganglion cell survival, including inhibition of microglia, up-regulation of the astrocyte enzyme glutamine synthetase, and induction of heat shock proteins, which maintain protein conformation and may be cytoprotective. The finding that cortisol was so very neuroprotective, while studies by other groups using methylprednisolone showed toxic effects, strongly implies that the exact corticosteroid used may be an important factor in the mechanism of neuroprotection of retinal ganglion cells.

References

Steinsapir et al., Restor Neurol Neurosci 2000; 17: 157-163
Diem et al., J Neurosci 2003; 23: 6993-7000
Ohlsson et al., J Neuroophthalmol 2004; 24: 11-18

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Issue 8-1

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