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- Author or Editor: James E. Madl x
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Abstract
Objective—To determine whether glutamate contents are decreased in the ganglion cell layer (GCL) of retinas of DBA/2J mice with glaucoma, compared with unaffected control mice.
Sample Population—20 eyes from DBA/2J mice (9-week-old mice [n = 8] and 4- [4], 6- [4], and 12-month-old [4] mice) and 17 eyes from control CD-1 (7) and C57/BL6 (10) mice of similar age.
Procedure—After euthanasia, the eyes were rapidly dissected and fixed. Serial 0.5-μm sections were prepared from eyecups and stained with toluidine blue (to identify damaged cells) or immunogold (to localize glutamate). Microscopic images were captured digitally for comparison; immunostaining densities were assessed via special software.
Results—In the GCL of control mice, few cells appeared damaged; large amounts of glutamate were detected in 83 ± 8.3% of cells. In DBA/2J mice ≥ 9 weeks of age, damaged neurons were observed in retinal sections; the level of glutamate immunoreactivity was high in a few cells near areas of damage (13 ± 3.2%) and in many cells in less-damaged regions of the same sections (82 ± 4.2%). Many neurons with low amounts of glutamate in damaged regions did not appear damaged histologically.
Conclusions and Clinical Relevance—In retinas of young DBA/2J mice, damaged and undamaged GCL cells had decreased levels of immunostaining for glutamate, compared with less-damaged adjacent regions or retinas from control mice. The loss of neuronal glutamate in damaged retinal regions suggests that glutamate is contributing to early retinal damage prior to changes in intraocular pressure.
Abstract
Objective—To determine whether taurine and glutamate contents are reduced in damaged photoreceptors in dogs with primary glaucoma (PG) in a manner consistent with an ischemia-like release of both of these amino acids from damaged cells.
Sample Population—Retinas from 6 dogs with PG and 3 control dogs.
Procedure—Serial, semithin sections of each canine retina were stained with toluidine blue to identify damaged photoreceptors or via immunogold techniques to quantify taurine and glutamate content in retinal cells.
Results—Regions with a thin outer nuclear layer and pathologic nuclear changes in photoreceptors were evident in retinas of dogs with PG. The density of immunostaining for taurine in damaged photoreceptors was significantly reduced to (mean ± SEM) 37.5 ± 2.6% of the density in adjacent undamaged photoreceptors. Photoreceptors with decreased taurine immunostaining also had decreased glutamate immunostaining, consistent with ischemia-like release of both of these amino acids from damaged cells. Immunostaining for glutamate, but not taurine, was increased in presumptive radial glial cells (ie, Müller cells) in damaged regions, consistent with an ischemia-induced redistribution of amino acids in dogs with PG.
Conclusions and Clinical Relevance—Retinal damage in dogs with PG includes ischemia-like losses of taurine and glutamate from photoreceptors and accumulation of glutamate, but not taurine, in nearby Müller cells. These changes are consistent with glutamate release and depletion of intracellular taurine in damaged regions, perhaps contributing to progressive damage in these areas. (Am J Vet Res 2005;66:791–799)
Abstract
Objective—To determine whether retinal damage in dogs with primary glaucoma (PG) is consistent with ischemia-induced glutamate toxicosis.
Sample Population—Retinal tissue sections from 25 dogs with PG and 12 normotensive control dogs.
Procedure—Retinal sections from control and glaucomatous dogs were stained for morphometric and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) analyses to determine whether retinal damage was consistent with glutamate toxicosis. Immunohistochemical analysis was performed to detect ischemia-like loss of glutamate from neurons in damaged areas.
Results—In severely damaged glaucomatous retinas, all neurosensory layers had focal regions that were thin or disrupted. There was less thinning of the outer nuclear layer (ONL) and inner nuclear layer (INL) in moderately damaged retinas than in severely damaged retinas. Acute signs of damage in the INL included cells with dark, condensed chromatin and lightly stained cytoplasm interspersed with a few TUNELpositive cells, which was consistent with glutamate toxicosis. Glutamate immunoreactivity was reduced in thin areas and in damaged cells of the INL and ONL, which was consistent with glutamate release in damaged areas. Glutamate immunoreactivity was increased in putative Müller cells in damaged areas, which also was consistent with glutamate release.
Conclusions and Clinical Relevance—Retinal damage in dogs with PG differs in intensity in focal areas. Damage in affected regions resembles damage induced by glutamate. Glutamate is lost from damaged neurons and accumulates in Müller cells, which is consistent with increased glutamate release contributing to the damage. Glutamate antagonists may protect INL cells in dogs with glaucoma. (Am J Vet Res 2004;65:776–786)
