Celia Sánchez-Ramos

Mesopic contrast sensitivity in the presence or absence of glare in a large driver population

BackgroundTo evaluate mesopic contrast sensitivity in conditions of glare and no glare in a vehicle driver population, and to explore the effects of age, habitual spectacle correction, photopic visual acuity and driving exposure.MethodsA cross-sectional study was performed on 297 drivers stratified by age into six groups. The mesopic contrast sensitivity was measured in the absence or presence of glare using the Mesotest II (Oculus, Germany) in each subject both with habitual and best spectacle correction. A questionnaire on the subject’s driving habits was completed.ResultsThere were no significant differences between contrast sensitivity measured with habitual or best spectacle correction. In conditions of no glare, the mesopic contrast sensitivity gradually got worse from 51 to 60 years onwards, and from 41 to 50 years onwards in the presence of glare. In both conditions, the total decrease in contrast sensitivity was 0.3 log units. The with-glare and without-glare mesopic contrast sensitivity improved as photopic visual acuity increased. Forty-five per cent of drivers who reported difficulties in driving at night were unable to perform any of the tests with glare, compared to 20% without glare. However, the effect of driving habits on contrast sensitivity was only significant in the oldest age group.ConclusionsThe mesopic contrast sensitivity and glare sensitivity seem to be stable until the age of 50 years, from which point they start to decline at a rate of 0.1 log contrast sensitivity loss per decade. Drivers with poor visual acuity and/or older drivers who avoided night driving presented worse mesopic contrast sensitivity and greater glare sensitivity.

Normal values for photopic and mesopic letter contrast sensitivity.

PURPOSE The exponential increase of patients having refractive surgery has increased the number of patients with night vision disturbances, such as decreased contrast sensitivity. However, there are no standard contrast sensitivity scales in normal persons in the mesopic range. We describe Pelli-Robson contrast sensitivity under photopic and mesopic luminance conditions in a large Spanish population over a wide range of age groups to provide normal values. A further aim was to evaluate the effect of photopic visual acuity on photopic and mesopic contrast sensitivity. METHODS A cross-sectional study was performed on 292 participants stratified by age into six groups. Binocular contrast sensitivity was determined with best spectacle correction using the Pelli-Robson letter chart at 1 m under photopic (85 cd/m2) and mesopic (0.15 cd/m2) luminance conditions. RESULTS Phototopic letter contrast sensitivity began to decrease gradually from the 61 to 70-year-old age group onward, and for mesopic conditions, from the 51 to 60-year-old age group onward. The reduction in mean contrast sensitivity between the oldest and the youngest age groups was 0.20 log units (photopic) and 0.33 log units (mesopic). Loss in contrast sensitivity due to luminance (two successive triplets) increased slightly with age. Both photopic and mesopic letter contrast sensitivity significantly improved as photopic visual acuity increased. CONCLUSIONS Under mesopic conditions, Pelli-Robson contrast sensitivity began to decline 1 decade earlier than under photopic conditions and was affected by visual acuity. Normal values for mesopic contrast sensitivity could be of help in deciding whether mesopic function is normal or a decrease in contrast sensitivity is pathologic in nature.

Effects of Light‐emitting Diode Radiations on Human Retinal Pigment Epithelial Cells In Vitro

Human visual system is exposed to high levels of natural and artificial lights of different spectra and intensities along lifetime. Light‐emitting diodes (LEDs) are the basic lighting components in screens of PCs, phones and TV sets; hence it is so important to know the implications of LED radiations on the human visual system. The aim of this study was to investigate the effect of LEDs radiations on human retinal pigment epithelial cells (HRPEpiC). They were exposed to three light–darkness (12 h/12 h) cycles, using blue‐468 nm, green‐525 nm, red‐616 nm and white light. Cellular viability of HRPEpiC was evaluated by labeling all nuclei with DAPI; Production of reactive oxygen species (ROS) was determined by H2DCFDA staining; mitochondrial membrane potential was quantified by TMRM staining; DNA damage was determined by H2AX histone activation, and apoptosis was evaluated by caspases‐3,‐7 activation. It is shown that LED radiations decrease 75–99% cellular viability, and increase 66–89% cellular apoptosis. They also increase ROS production and DNA damage. Fluorescence intensity of apoptosis was 3.7% in nonirradiated cells and 88.8%, 86.1%, 83.9% and 65.5% in cells exposed to white, blue, green or red light, respectively. This study indicates three light–darkness (12 h/12 h) cycles of exposure to LED lighting affect in vitro HRPEpiC.

Effect of a yellow filter on contrast sensitivity and disability glare after laser in situ keratomileusis under mesopic and photopic conditions.

PURPOSE To analyze the effect of a yellow filter on contrast sensitivity and disability glare under mesopic and photopic luminance conditions in laser in situ keratomileusis (LASIK) patients and control subjects. METHODS Contrast sensitivity with and without glare was determined in 27 patients who had undergone LASIK at least 1 year previously and in 30 control subjects. Tests were performed with and without a coated yellow filter (X-482 nm cut-off) using the Mesotest II or Mesoptometer II (Oculus, Wetzlar, Germany) under mesopic conditions, and the Contrast Glaretester 1000 (Takagi, Seiko Co Ltd, Nagano, Japan) under photopic conditions. RESULTS Under mesopic conditions, log contrast sensitivity without glare decreased by 0.14 log units in the LASIK group. When the yellow filter was used, this variable showed a significant increase of 0.04 log units and the proportion of patients able to discriminate the mesopic contrast limit of 1:5 rose from 70% to 78%. With glare, the yellow filter also improved contrast sensitivity in LASIK patients, but not significantly. Under photopic conditions, no statistical differences were observed between results obtained with and without the yellow filter in the LASIK group or between the LASIK and control group without glare. CONCLUSIONS Mesopic contrast sensitivity without glare was worse in LASIK patients and increased significantly with the yellow filter. The filter had no effect under photopic conditions. No disability glare differences were noted between the LASIK and control groups or between the LASIK without and with filter groups under mesopic and photopic conditions.

Expression and cell localization of brain‐derived neurotrophic factor and TrkB during zebrafish retinal development

Brain‐derived neurotrophic factor (BDNF) signaling through TrkB regulates different aspects of neuronal development, including survival, axonal and dendritic growth, and synapse formation. Despite recent advances in our understanding of the functional significance of BDNF and TrkB in the retina, the cell types in the retina that express BDNF and TrkB, and the variations in their levels of expression during development, remain poorly defined. The goal of the present study is to determine the age‐dependent changes in the levels of expression and localization of BDNF and TrkB in the zebrafish retina. Zebrafish retinas from 10 days post‐fertilization (dpf) to 180 dpf were used to perform PCR, Western blot and immunohistochemistry. Both BDNF and TrkB mRNAs, and BDNF and full‐length TrkB proteins were detected at all ages sampled. The localization of these proteins in the retina was very similar at all time points studied. BDNF immunoreactivity was found in the outer nuclear layer, the outer plexiform layer and the inner plexiform layer, whereas TrkB immunoreactivity was observed in the inner plexiform layer and, to a lesser extent, in the ganglion cell layer. These results demonstrate that the pattern of expression of BDNF and TrkB in the retina of zebrafish remains unchanged during postembryonic development and adult life. Because TrkB expression in retina did not change with age, cells expressing TrkB may potentially be able to respond during the entire lifespan of zebrafish to BDNF either exogenously administered or endogenously produced, acting through paracrine mechanisms.

Light regulates the expression of the BDNF/TrkB system in the adult Zebrafish retina

The retina of the adult zebrafish express brain‐derived neurotrophic factor (BDNF) and its signaling receptor TrkB. This functional system is involved in the biology of the vertebrate retina and its expression is regulated by light. This study was designed to investigate the effects of cyclic (12 h light/12 h darkness) or continuous (24 h) exposure during 10 days to white light, white‐blue light, and blue light, as well as of darkness, on the expression of BDNF and TrkB in the retina. BDNF and TrkB were assessed in the retina of adult zebrafish using quantitative real‐time polymerase chain reaction and immunohistochemistry. Exposure to white, white‐blue, and blue light causes a decrease of BDNF mRNA and of BDNF immunostaining, independently of the pattern of light exposition. Conversely, in the same experimental conditions, the expression of TrkB mRNA was upregulated and TrkB immunostaining increased. Exposition to darkness diminished BDNF and TrkB mRNAs, and abolished the immunostaining for BDNF but not modified that for TrkB. These results demonstrate the regulation of BDNF and TrkB by light in the retina of adult zebrafish and might contribute to explain some aspects of the complex pathophysiology of light‐induced retinopathies. Microsc. Res. Tech., 2013.

Expression of TRPV4 in the zebrafish retina during development.

The transient receptor potential (TRP) channels are involved in sensing mechanical/physical stimuli such as temperature, light, pressure, as well as chemical stimuli. Some TRP channels are present in the vertebrate retina, and the occurrence of the multifunctional channel TRP vanilloid 4 (TRPV4) has been reported in adult zebrafish. Here, we investigate the expression and distribution of TRPV4 in the retina of zebrafish during development using polymerase chain reaction (PCR), Western blot, and immunohistochemistry from 3 days post fertilization (dpf) until 100 dpf. TRPV4 was detected at the mRNA and protein levels in the eye of zebrafish at all ages sampled. Immunohistochemistry revealed the presence of TRPV4 in a population of the retinal cells identified as amacrine cells on the basis of their morphology and localization within the retina, as well as the co‐localization of TRPV4 with calretinin. TRPV4 was first (3 dpf) found in the soma of cells localized in the inner nuclear and ganglion cell layers, and thereafter (10 dpf) also in the inner plexiform layer. The adult pattern of TRPV4 expression was achieved by 40 dpf the expression being restricted to the soma of some cells in the inner nuclear layer and ganglion cell layers. These data demonstrate the occurrence and developmental changes in the expression and localization of TRPV4 in the retina of zebrafish, and suggest a role of TRPV4 in the visual processing. Microsc. Res. Tech. 75:743–748, 2012.

Acid-sensing ion channels (ASICs) 2 and 4.2 are expressed in the retina of the adult zebrafish

Acid-sensing ion channels (ASICs) are H+-gated, voltage-insensitive cation channels involved in synaptic transmission, mechanosensation and nociception. Different ASICs have been detected in the retina of mammals but it is not known whether they are expressed in adult zebrafish, a commonly used animal model to study the retina in both normal and pathological conditions. We study the expression and distribution of ASIC2 and ASIC4 in the retina of adult zebrafish and its regulation by light using PCR, in situ hybridization, western blot and immunohistochemistry. We detected mRNA encoding zASIC2 and zASIC4.2 but not zASIC4.1. ASIC2, at the mRNA or protein level, was detected in the outer nuclear layer, the outer plexiform layer, the inner plexiform layer, the retinal ganglion cell layer and the optic nerve. ASIC4 was expressed in the photoreceptors layer and to a lesser extent in the retinal ganglion cell layer. Furthermore, the expression of both ASIC2 and ASIC4.2 was down-regulated by light and darkness. These results are the first demonstration that ASIC2 and ASIC4 are expressed in the adult zebrafish retina and suggest that zebrafish could be used as a model organism for studying retinal pathologies involving ASICs.

Photoprotective Effects of Blue Light Absorbing Filter against LED Light Exposure on Human Retinal Pigment Epithelial Cells In Vitro

Abstract Background: Over the recent years, several researches have speculated about the effects of Light Emitting Diodes (LEDs) radiation on retinal epithelium cells (RPE). Worldwide, most people live exposed to LEDs irradiation incorporated in screens of PCs, phones and TV sets. These lights give rise to the formation of reactive oxygen species and induce mutagenic mechanisms which lead to apoptosis and consequently to degenerative eye diseases, such as age-related macular degeneration (AMD). Thus, it is a priority interest to develop appropriate solutions for the growing industry field of LED light phototoxicity. The aim of this study was to investigate the protective effects of blue light absorbing filters in order to decrease induced apoptosis on human retinal pigment epithelial cells. Methods: Human retinal pigment epithelial cells were exposed to 3 light-darkness (12 hours/12 hours) cycles of white (Ta5400°K), blue (468 nm), green (525 nm) and red (616 nm) LED light. Light irradiance was 5 mW/cm2. Oxidative stress was evaluated by H2DCFDA staining, mitochondrial membrane potential by TMRM staining, DNA damage by H2AX histone activation, apoptosis by caspase-3 activation, and cell viability by DAPI. Results: Our results have shown that the use of a blue light absorbing filter decreased cellular apoptosis by 56-89% and DNA damage by 57-81%. A decrease in ROS level production and an increase in cellular viability was also obtained. Conclusion: This study suggests that blue light absorbing filters may protect against LED lighting photo toxicity and, consequently, provides a photo protector effect.

Removal of the blue component of light significantly decreases retinal damage after high intensity exposure

Light causes damage to the retina (phototoxicity) and decreases photoreceptor responses to light. The most harmful component of visible light is the blue wavelength (400–500 nm). Different filters have been tested, but so far all of them allow passing a lot of this wavelength (70%). The aim of this work has been to prove that a filter that removes 94% of the blue component may protect the function and morphology of the retina significantly. Three experimental groups were designed. The first group was unexposed to light, the second one was exposed and the third one was exposed and protected by a blue-blocking filter. Light damage was induced in young albino mice (p30) by exposing them to white light of high intensity (5,000 lux) continuously for 7 days. Short wavelength light filters were used for light protection. The blue component was removed (94%) from the light source by our filter. Electroretinographical recordings were performed before and after light damage. Changes in retinal structure were studied using immunohistochemistry, and TUNEL labeling. Also, cells in the outer nuclear layer were counted and compared among the three different groups. Functional visual responses were significantly more conserved in protected animals (with the blue-blocking filter) than in unprotected animals. Also, retinal structure was better kept and photoreceptor survival was greater in protected animals, these differences were significant in central areas of the retina. Still, functional and morphological responses were significantly lower in protected than in unexposed groups. In conclusion, this blue-blocking filter decreases significantly photoreceptor damage after exposure to high intensity light. Actually, our eyes are exposed for a very long time to high levels of blue light (screens, artificial light LED, neons…). The potential damage caused by blue light can be palliated.