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Editors Selection IGR 12-1

Experimental Glaucoma: Optic nerve head astrocytes

Comment by Chris Leung on:

53194 Morphology of astrocytes in a glaucomatous optic nerve, Lye-Barthel M; Sun D; Jakobs TC, Investigative Ophthalmology and Visual Science, 2013; 54: 909-917

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Although the optic nerve head astrocytes have been implicated in regulating axon loss in glaucoma, it remains difficult to examine the cellular interaction between astrocytes and retinal ganglion cell axons. Lye-Barthel and colleagues backcrossed the hGFAPpr-GFP transgene into the DBA/2J mice, producing a strain of transgenic animals (D2.hGFAPpr-GFP) that allowed visualization of the morphologic changes of individual astrocytes in the glial lamina. The intraocular pressure (IOP) elevation profile and retinal ganglion cell damage of this strain are similar to those of the DBA/2J mice. The processes and cell bodies can be distinctively identified in the GFAP-expressing astrocytes because only a small proportion of astrocytes are labeled. As axon damage in glaucoma is often localized, the authors set out to investigate whether astrocytes showed compartmentalized reactivity in some of their processes. They demonstrated that in glaucoma, glial lamina astrocytes had thickened processes and a reduced ramification pattern. With volume reconstructions of individual astrocytes, they showed that there were localized protrusions sprouting out from the processes of astrocytes in five optic nerves from animals of six months of age. As there was no detectable retinal ganglion cell loss in these eyes, the authors suggested that the localized astrocytic remodeling could be the initial response before retinal ganglion cell damage in glaucoma.

While visualization of individual astrocytes at the glial lamina provides a powerful tool to study the mechanisms of axon damage in glaucoma, the association between the localized astrocytic remodeling and axon damage has not been confirmed. Specifically, it remains unclear whether the sprouting of astrocyte processes represents a response secondary to IOP elevation (the authors did not report the IOP profiles in the eyes showing astrocytic remodeling). It is also uncertain if similar changes would be observed in animals without IOP elevation. It has been proposed that the damage to the astrocytes is mechanical and that the link between astrocyte reactivity and retinal ganglion cell axon damage is metabolic. Understanding the mechanistic interaction between astrocytes and retinal ganglion cell axons would be pivotal to unfold the pathogenesis of axon degeneration in glaucoma.

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