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Ohlendorf A.,University of Tubingen | Tabernero J.,Laboratorio Of Optica | Schaeffel F.,University of Tubingen | Schaeffel F.,Institute for Ophthalmic Research
Optometry and Vision Science

Purpose. To compare the effects of "simulated" and "real" spherical and astigmatic defocus on visual acuity (VA). Methods. VA was determined with letter charts that were blurred by calculated spherical or astigmatic defocus (simulated defocus) or were seen through spherical or astigmatic trial lenses (real defocus). Defocus was simulated using ZEMAX and the Liou-Brennan eye model. Nine subjects participated [mean age, 27.2 ± 1.8 years; logarithm of the minimum angle of resolution (logMAR), -0.1]. Three different experiments were conducted in which VA was reduced by 20% (logMAR 0.0), 50% (logMAR 0.2), or 75% (logMAR 0.5) by either (1) imposing positive spherical defocus, (2) imposing positive and negative astigmatic defocus in three axes (0, 45, and 90°), and (3) imposing cross-cylinder defocus in the same three axes as in (2). Results. Experiment (1): there were only minor differences in VA with simulated and real positive spherical defocus. Experiment (2): simulated astigmatic defocus reduced VA twice as much as real astigmatic defocus in all tested axes (p < 0.01 in all cases). Experiment (3): simulated cross-cylinder defocus reduced VA much more than real cross-cylinder defocus (p < 0.01 in all cases), similarly for all three tested axes. Conclusions. The visual system appears more tolerant against "real" spherical, astigmatic, and cross-cylinder defocus than against "simulated" blur. Possible reasons could be (1) limitations in the modeling procedures to simulate defocus, (2) higher ocular aberrations, and (3) fluctuations of accommodation. However, the two optical explanations (2) and (3) cannot account for the magnitude of the effect, and (1) was carefully analyzed. It is proposed that something may be special about the visual processing of real astigmatic and cross-cylinder defocus-because they have less effect on VA than simulations predict. © 2011 American Academy of Optometry. Source

Julien S.,Institute for Ophthalmic Research | Biesemeier A.,Institute for Ophthalmic Research | Kokkinou D.,Institute for Ophthalmic Research | Eibl O.,University of Tubingen | Schraermeyer U.,Institute for Ophthalmic Research

Background: Age-related macular degeneration (AMD) is associated with lipofuscin accumulation whereas the content of melanosomes decreases. Melanosomes are the main storage of zinc in the pigmented tissues. Since the elderly population, as the most affected group for AMD, is prone to zinc deficit, we investigated the chemical and ultrastructural effects of zinc deficiency in pigmented rat eyes after a six-month zinc penury diet. Methodology/Principal Findings: Adult Long Evans (LE) rats were investigated. The control animals were fed with a normal alimentation whereas the zinc-deficiency rats (ZD-LE) were fed with a zinc deficient diet for six months. Quantitative Energy Dispersive X-ray (EDX) microanalysis yielded the zinc mole fractions of melanosomes in the retinal pigment epithelium (RPE). The lateral resolution of the analysis was 100 nm. The zinc mole fractions of melanosomes were significantly smaller in the RPE of ZD-LE rats as compared to the LE control rats. Light, fluorescence and electron microscopy, as well as immunohistochemistry were performed. The numbers of lipofuscin granules in the RPE and of infiltrated cells (Ø>3 μm) found in the choroid were quantified. The number of lipofuscin granules significantly increased in ZD-LE as compared to control rats. Infiltrated cells bigger than 3 μm were only detected in the choroid of ZD-LE animals. Moreover, the thickness of the Bruch's membrane of ZD-LE rats varied between 0.4-3 μm and thin, rangy ED1 positive macrophages were found attached at these sites of Bruch's membrane or even inside it. Conclusions/Significance: In pigmented rats, zinc deficiency yielded an accumulation of lipofuscin in the RPE and of large pigmented macrophages in the choroids as well as the appearance of thin, rangy macrophages at Bruch's membrane. Moreover, we showed that a zinc diet reduced the zinc mole fraction of melanosomes in the RPE and modulated the thickness of the Bruch's membrane. © 2011 Julien et al. Source

Seeliger M.W.,Institute for Ophthalmic Research | Brombas A.,Julich Research Center | Weiler R.,Carl von Ossietzky University | Humphries P.,Trinity College Dublin | And 3 more authors.
Nature Communications

Retinal photoreceptors permit visual perception over a wide range of lighting conditions. Rods work best in dim, and cones in bright environments, with considerable functional overlap at intermediate (mesopic) light levels. At many sites in the outer and inner retina where rod and cone signals interact, gap junctions, particularly those containing Connexin36, have been identified. However, little is known about the dynamic processes associated with the convergence of rod and cone system signals into ON- and OFF-pathways. Here we show that proper cone vision under mesopic conditions requires rapid adaptational feedback modulation of rod output via hyperpolarization-activated and cyclic nucleotide-gated channels 1. When these channels are absent, sustained rod responses following bright light exposure saturate the retinal network, resulting in a loss of downstream cone signalling. By specific genetic and pharmacological ablation of key signal processing components, regular cone signalling can be restored, thereby identifying the sites involved in functional rodĝ€"cone interactions. © 2011 Macmillan Publishers Limited. All rights reserved. Source

Schnichels S.,University of Tubingen | Heiduschka P.,Institute for Ophthalmic Research | Heiduschka P.,University of Munster | Julien S.,Institute for Ophthalmic Research
Graefe's Archive for Clinical and Experimental Ophthalmology

Background The death and the failure of neurons to regenerate their axons after lesion of the central nervous system in mammals, as in the case of spinal cord injury and optic nerve trauma, remain a challenge. In this study, we focused on the repulsive guidance molecule A (RGMA) and its receptor neogenin. Since it was reported that RGMA+ cells accumulate in lesioned areas after spinal cord injury, brain trauma, and optic nerve crush, and curiously, anti-apoptotic effects of RGMA were also described, we investigated the role of RGMA and neogenin in the retina after optic nerve crush (ONC). Methods We evaluated the spatial and temporal protein pattern of RGMA and neogenin in the rat retina without (non-regenerating model) or with (regenerating model) lens injury (LI). We investigated the presence of RGMA, neogenin and other proteins at up to nine time points (6 h-20 days post-surgery) by performing immunohistochemistry and Western blots. Results Independent of the treatment, RGMA protein was present in the nuclear layers (NLs), plexiform layers (PLs), nerve fiber layer (NFL), and in retinal ganglion cells (RGCs) of the rat retina. RGC and nerve fibers were always RGMA+. Further RGMA+ cells in the retina were blood vessel endothelial cells, astrocytes, Müller cells, and some microglial cells. The RGMA pattern for the specific retinal cells resembled those of previously published data. The neogenin pattern was congruent to the RGMA pattern. Western blots of retinal tissue showed further RGMA+ products only in LI animals. Furthermore, a higher amount of RGMA was found in the retinae of ONC + LI rats compared to ONC rats. Conclusions Although a difference in the localization of RGMA is not obvious, the difference in the amount of RGMA is striking, the higher amount of RGMA in the retinae of ONC + LI rats compared to ONC rats indicates a role for RGMA during degeneration/regeneration processes. Our results are consistent with several reported neuroprotective effects of RGMA. Our new data showing the upregulation of RGMA after ONC in our regenerating model (plus LI) confirm these findings conducted in different settings. © Springer-Verlag 2011. Source

Heiduschka P.,Institute for Ophthalmic Research | Julien S.,Institute for Ophthalmic Research | Schuettauf F.,University of Tubingen | Schnichels S.,University of Tubingen
Experimental Eye Research

The DBA/2J mouse is a common animal model of glaucoma. The intraocular pressure increases with age, and retinal ganglion cells (RGC) degenerate, usually starting at an age of approximately six months. In this study, we used two-year-old DBA/2J mice presuming an end-point of RGC degeneration. We investigated visual function in these animals using electroretinography (ERG) and visual evoked potentials (VEP), and we checked the number of remaining RGC by retrograde staining. Almost no RGC were left in the retina, and VEP were hardly recordable. Surprisingly, also ERG amplitudes of scotopic a-waves and b-waves, photopic b-waves and oscillatory potentials were decreased significantly by approximately 40% compared to amplitudes measured in age-matched C57BL/6J mice. The latencies were not changed in DBA/2J mice compared to C57BL/6J mice, and so were the ratios between amplitudes of a-waves, b-waves and oscillatory potentials. Our results indicate that, in addition to degeneration of RGC, also photoreceptors are affected by pathological processes in the eye caused by the mutations present in DBA/2J mice. © 2010 Elsevier Ltd. Source

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