Neuroretinal Rim Response to Transient Intraocular Pressure Challenge Predicts the Extent of Retinal Ganglion Cell Loss in Experimental Glaucoma.

Purpose: To determine if the optic nerve head (ONH) response to transient elevated intraocular pressure (IOP) can predict the extent of neural loss in the nonhuman primate experimental glaucoma model.

Methods: The anterior chamber pressure of 21 healthy animals (5.4 ± 1.

The Relationship Between Macula Retinal Ganglion Cell Density and Visual Function in the Nonhuman Primate.

Purpose: Loss of ganglion cell inner plexiform layer (GCIPL) and visual sensitivity in the macula region are known to occur at all stages of glaucoma. While both are dependent on the underlying retinal ganglion cells (RGCs), the relationship between structure and function is modest. We hypothesize that the imprecise relationship is due to a lack of direct correspondence between in vivo measures and RGC counts, as well as the relatively large stimulus size used by standard perimetry, which exceeds spatial summation.

Detrimental effects of adenosine signaling in sickle cell disease.

Hypoxia can act as an initial trigger to induce erythrocyte sickling and eventual end organ damage in sickle cell disease (SCD). Many factors and metabolites are altered in response to hypoxia and may contribute to the pathogenesis of the disease. Using metabolomic profiling, we found that the steady-state concentration of adenosine in the blood was elevated in a transgenic mouse model of SCD.

Elevated albumin in retinas of monkeys with experimental glaucoma.

Purpose: To establish the identity of a prominent protein, approximately 70 kDa, that is markedly increased in the retina of monkeys with experimental glaucoma compared with the fellow control retina, the relationship to glaucoma severity, and its localization in the retina.

Methods: Retinal extracts were subjected to 2-D gel electrophoresis to identify differentially expressed proteins. Purified peptides from the abundant 70 kDa protein were analyzed and identified by liquid chromatography/mass spectrometry/mass spectrometry (LC/MS/MS) separation, and collision-induced dissociation sequencing.

Scaling the structure--function relationship for clinical perimetry.

Purpose: The full ranges of glaucomatous visual field defects and retinal ganglion cell losses extend over several orders of magnitude and therefore an interpretation of the structure-function relationship for clinical perimetry requires scaling of both variables. However, the most appropriate scale has not been determined. The present study was undertaken to compare linear and logarithmic transformations, which have been proposed for correlating the perimetric defects and neural losses of glaucoma.

Neural losses correlated with visual losses in clinical perimetry.

Purpose: The validity of clinical perimetry for evaluation of the pathology of glaucoma is based on correlated losses in retinal ganglion cells and visual sensitivity, but procedures to quantify neural losses from visual field defects have not been developed. The purpose of the present study was to investigate the neural and sensitivity losses from experimental glaucoma to establish the framework for a quantitative model for the structure-function relationships of standard clinical perimetry.

Methods: Perimetry, by behavioral testing, and retinal histology data were obtained from rhesus monkeys with significant visual field defects caused by experimental glaucoma.

Glutathione content is altered in Müller cells of monkey eyes with experimental glaucoma.

Extracellular levels of glutamate are thought to be increased in glaucoma and thus contribute to retinal damage. An increase in glutamate concentration or duration in the extracellular retinal space is expected to impact glutathione content in Müller cells since glutamate is the rate-limiting constituent in glutathione synthesis. We have investigated whether glutathione content is changed in retinal Müller cells of monkeys with experimental glaucoma using immunocytochemistry and image analysis.

Activation of protein kinase C reduces GLAST in the plasma membrane of rat Müller cells in primary culture.

In this study, a Müller cell culture preparation from young rats was used to investigate the regulation of GLAST transport activity in native cells. Immunohistochemical analysis confirmed GLAST to be the predominant glutamate transporter expressed by the cells through five passages. [3H]-glutamate uptake assays showed the typical Na+-dependent glutamate transport which was blocked by L-(-)-threo-3-hydroxyaspartate (L-THA), a competitive inhibitor.

Vitreal glutamate concentration in monkeys with experimental glaucoma.

Purpose: To investigate the hypothesis that the pathophysiology for the death of retinal ganglion cells in glaucoma involves excitotoxic effects from elevated concentrations of vitreal glutamate.

Methods: Experimental glaucoma was induced in the right eyes of 18 rhesus monkeys by argon laser treatments to the trabecular meshwork. After significant visual field defects and/or typical clinical glaucomatous changes had developed (1.

Visual field defects and neural losses from experimental glaucoma.

Glaucoma is a relatively common disease in which the death of retinal ganglion cells causes a progressive loss of sight, often leading to blindness. Typically, the degree of a patient's visual dysfunction is assessed by clinical perimetry, involving subjective measurements of light-sense thresholds across the visual field, but the relationship between visual and neural losses is inexact. Therefore, to better understand of the effects of glaucoma on the visual system, a series of investigations involving psychophysics, electrophysiology, anatomy, and histochemistry were conducted on experimental glaucoma in monkeys.