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Editors Selection IGR 7-1

Basic research: Endothelin and astrocytes

Comment by Rosario Hernandez on:

13731 Endothelin B receptor in human glaucoma and experimentally induced optic nerve damage, Wang L; Fortune B; Cull G et al., Archives of Ophthalmology, 2006; 124: 717-724

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Although glutamate is an important neurotransmitter in the central nervous system, it is toxic to neurons including ganglion cells when there is excessive stimulation or it is present in excessive amounts. Protection of ganglion cells from injury by NMDA type glutamate channel blockers provides evidence for the role of glutamate toxicity in experimental glaucoma. However the source of this excess extracellular glutamate is not known. In the retina glutamate is used as neurotransmitter by photoreceptors, bipolar cells and ganglion cells.

Low et al. (379) discuss the possibility that glutamate released from ganglion cells may cause damage to neighboring cells even before increase in IOP in DBA/2J mice. These mice develop pigmentary glaucoma within nine to twelve months after birth and eventually lose all their ganglion cells. In retinas of nine-week old mice they observed some signs of damage described as cells with irregularly shaped nuclei with foamy cytoplasm. Some of these cells also appeared swollen. However, they did not do tests to show whether these cells were undergoing apoptosis or necrosis. Immunostaining for glutamate in nine- week old DBA/2J mice showed that some regions had a high number of damaged cells and these cells showed low amounts of glutamate. Some of the neighboring cells which had normal morphology, also had low amount of glutamate suggesting that the decrease in glutamate was not associated with damaged morphology. They interpret this to be a signal of early injury before the increase in IOP which happens several months later. They do not describe the reason for the decrease in ganglion cell glutamate nor have they evaluated the harmful effect of the possibly released glutamate. This study does not give adequate information on the fate of the 'damaged' cells. The fact that the expression of GFAP (sign of retinal stress) is apparent after six months and not at nine weeks is puzzling, especially if glutamate is released and is causing cell death.

The methods and experimental approaches in this paper limit its value in addressing the important questions on the role of glutamate in glaucoma or the source of this glutamate in glaucoma. Nor does it help us to understand this particular genetic glaucoma model.

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