320 research outputs found

    Effect of eccentricity on luminance-pedestal flicker thresholds

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    AbstractWe investigated the effect that spatially coincident luminance increments (luminance pedestals) have on flicker thresholds at several eccentricities and target sizes. Luminance pedestals elevated flicker amplitude-thresholds more when stimuli were presented eccentrically, both at low (4 Hz) and high (20 Hz) temporal frequencies. Altering the size of the eccentric stimulus failed to equate central and eccentric thresholds at all pedestal amplitudes. Comparisons with flicker thresholds at various background luminances suggests that the increase in luminance-pedestal flicker thresholds peripherally is due to increased suppressive rod–cone interactions, increased effectiveness of luminous contrast on edge-sensitive flicker mechanisms, as well as increased gain in the light adaptation response

    Multiple processes mediate flicker sensitivity

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    AbstractBy systematically manipulating the luminance of a flickering spot and the area immediately surrounding it, we investigated why thresholds from flickering stimuli that cause a change in average luminance are elevated relative to those from stimuli with no luminance change. Threshold elevation resulted from local light adaptation and from temporal-frequency-specific interactions between the spot and its surround: at low frequencies, the contrast between the spot and the surround elevated thresholds, whereas at high frequencies, dark adaptation within the surround elevated thresholds. Our findings suggest that two common ways of determining temporal sensitivity may give markedly different outcomes

    Susceptibility of streptozotocin-induced diabetic rat retinal function and ocular blood flow to acute intraocular pressure challenge.

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    PURPOSE. To consider the hypothesis that streptozotocin (STZ)-induced hyperglycemia renders rat retinal function and ocular blood flow more susceptible to acute IOP challenge. METHODS. Retinal function (electroretinogram [ERG]) was measured during acute IOP challenge (10-100 mm Hg, increments of 5 mm Hg, 3 minutes per step, vitreal cannulation) in adult Long-Evans rats (6 weeks old; citrate: n ¼ 6, STZ: n ¼ 10) 4 weeks after citrate buffer or STZ (65 mg/kg, blood glucose >15 mM) injection. At each IOP, dim and bright flash (À4.56, À1.72 log cd.s.m À2 ) ERG responses were recorded to measure inner retinal and ON-bipolar cell function, respectively. Ocular blood flow (laser Doppler flowmetry; citrate: n ¼ 6, STZ: n ¼ 10) was also measured during acute IOP challenge. Retinas were isolated for quantitative PCR analysis of nitric oxide synthase mRNA expression (endothelial, eNos; inducible, iNos; neuronal, nNos). CONCLUSIONS. STZ-induced diabetes increased functional susceptibility during acute IOP challenge. This functional vulnerability is associated with a reduced capacity for diabetic eyes to upregulate eNos expression and to autoregulate blood flow in response to stress. (Invest Ophthalmol Vis Sci. RESULTS. STZ-induced diabetes increase

    Identifying cell class specific losses from serially generated electroretinogram components

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    Purpose. Processing of information through the cellular layers of the retina occurs in a serial manner. In the electroretinogram (ERG), this complicates interpretation of inner retinal changes as dysfunction may arise from “upstream” neurons or may indicate a direct loss to that neural generator. We propose an approach that addresses this issue by defining ERG gain relationships. Methods. Regression analyses between two serial ERG parameters in a control cohort of rats are used to define gain relationships. These gains are then applied to two models of retinal disease. Results. The to gain is unity whereas the to and to gains are greater than unity, indicating “amplification” (). Timing relationships show amplification between to and compression for to and to , (). Application of these gains to -3-deficiency indicates that all timing changes are downstream of photoreceptor changes, but a direct pSTR amplitude loss occurs (). Application to diabetes indicates widespread inner retinal dysfunction which cannot be attributed to outer retinal changes (). Conclusions. This simple approach aids in the interpretation of inner retinal ERG changes by taking into account gain characteristics found between successive ERG components of normal animals

    Blood Pressure Modifies Retinal Susceptibility to Intraocular Pressure Elevation

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    Primary open angle glaucoma affects more than 67 million people. Elevated intraocular pressure (IOP) is a risk factor for glaucoma and may reduce nutrient availability by decreasing ocular perfusion pressure (OPP). An interaction between arterial blood pressure and IOP determines OPP; but the exact contribution that these factors have for retinal function is not fully understood. Here we sought to determine how acute modifications of arterial pressure will affect the susceptibility of neuronal function and blood flow to IOP challenge. Anaesthetized (ketamine:xylazine) Long-Evan rats with low (∼60 mmHg, sodium nitroprusside infusion), moderate (∼100 mmHg, saline), or high levels (∼160 mmHg, angiotensin II) of mean arterial pressure (MAP, n = 5–10 per group) were subjected to IOP challenge (10–120 mmHg, 5 mmHg steps every 3 minutes). Electroretinograms were measured at each IOP step to assess bipolar cell (b-wave) and inner retinal function (scotopic threshold response or STR). Ocular blood flow was measured using laser-Doppler flowmetry in groups with similar MAP level and the same IOP challenge protocol. Both b-wave and STR amplitudes decreased with IOP elevation. Retinal function was less susceptible to IOP challenge when MAP was high, whereas the converse was true for low MAP. Consistent with the effects on retinal function, higher IOP was needed to attenuated ocular blood flow in animals with higher MAP. The susceptibility of retinal function to IOP challenge can be ameliorated by acute high BP, and exacerbated by low BP. This is partially mediated by modifications in ocular blood flow

    A quantitative scoring technique for panel tests of color vision

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    Panel tests of color vision (eg FMIOO-Hue test) lack a common quantitative method for the scoring of cap arrangements. We describe a scoring method applicable to all panel tests that makes use of a novel technique to analyze test cap data, namely the calculation of a moment of inertia from the Color Difference Vectors (CDVs) of any arrangement pattern. Using the Farnsworth D-15 panel, as an example, we specify how to determine CDVs and demonstrate the benefits of calculating a moment of inertia for the analysis of these vectors. Moment of inertia analysis yields three factors which quantify cap arrangements: the first is the confusion angle which identifies the type of color defect; the second is the Confusion index (C-index) which quantifies the degree of color loss relative to a perfect arrangement of caps; and the third is the Selectivity index (S-index) which quantifies the amount of polarity or lack of randomness in a cap arrangement. A retrospective study on the results of 53 normal and 66 congenitally color defective observers is reported and provides normative data. We show that the technique differentiates between different types of color defect and provides useful clinical information regarding a loss of color vision. Likewise, a similar observation is made on a smaller sample of FMIOO-Hue results. A BASIC computer program is provided for anyone wishing to use the technique

    Using the electroretinogram to understand how intraocular pressure elevation affects the rat retina

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    Intraocular pressure (IOP) elevation is a key risk factor for glaucoma. Our understanding of the effect that IOP elevation has on the eye has been greatly enhanced by the application of the electroretinogram (ERG). In this paper, we describe how the ERG in the rodent eye is affected by changes in IOP magnitude, duration, and number of spikes. We consider how the variables of blood pressure and age can modify the effect of IOP elevation on the ERG. Finally, we contrast the effects that acute and chronic IOP elevation can have on the rodent ERG

    Gene Therapy with Endogenous Inhibitors of Angiogenesis for Neovascular Age-Related Macular Degeneration: Beyond Anti-VEGF Therapy

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    Age-related macular degeneration (AMD) is the leading cause of substantial and irreversible vision loss amongst elderly populations in industrialized countries. The advanced neovascular (or “wet”) form of the disease is responsible for severe and aggressive loss of central vision. Current treatments aim to seal off leaky blood vessels via laser therapy or to suppress vessel leakage and neovascular growth through intraocular injections of antibodies that target vascular endothelial growth factor (VEGF). However, the long-term success of anti-VEGF therapy can be hampered by limitations such as low or variable efficacy, high frequency of administration (usually monthly), potentially serious side effects, and, most importantly, loss of efficacy with prolonged treatment. Gene transfer of endogenous antiangiogenic proteins is an alternative approach that has the potential to provide long-term suppression of neovascularization and/or excessive vascular leakage in the eye. Preclinical studies of gene transfer in a large animal model have provided impressive preliminary results with a number of transgenes. In addition, a clinical trial in patients suffering from advanced neovascular AMD has provided proof-of-concept for successful gene transfer. In this mini review, we summarize current theories pertaining to the application of gene therapy for neovascular AMD and the potential benefits when used in conjunction with endogenous antiangiogenic proteins
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