Retinal damage after prolonged exposure to visible light. A light and electron microscopic study

O'Steen, W. Keith; Shear, Charles R.; Anderson, Kenneth V.

doi:10.1002/aja.1001340103

Cited by 99 publications

(28 citation statements)

References 11 publications

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“…3D). Our results are thus in agreement with previous studies that showed a significant impairment in retinal structure [5,7] and function [33][34][35] following chronic light exposure. Persistence of a residual photopic b-wave (in responses evoked to the brightest stimuli; Table 1) indicates that cones were more resistant than rods, a claim also previously advanced by others [36][37][38].…”

Section: Discussionsupporting

confidence: 96%

“…For example, as little as one hour of light exposure is sufficient to yield ultrastructural changes at the photoreceptors as documented with electron microscopy [7,8]. Extending the exposure to 24 h will cause severe and irreversible functional and structural (histological) damages to the retina of adult rats such as a complete extinction of the ERG as well as a concomitant marked reduction in the thickness of the ONL [9][10][11][12].…”

Section: Introductionmentioning

confidence: 98%

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Structural and functional consequences of bright light exposure on the retina of neonatal rats

et al. 2006

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In a previous study we showed that juvenile rats exposed, for various durations of time, to a bright luminous environment between P14 (eye opening) and P34 developed a light-induced retinopathy (LIR), the severity of which depending on the duration of exposure as well as the age of the rat at the onset of exposure. Our study also revealed that the severity of the LIR increased as the time elapsed between the cessation of exposure and the structural/functional evaluation increased, suggesting that the LIR degenerative process proceeded in two distinct steps namely, an initial (rapid) acute phase that was followed by a (slower) chronic phase. In view of the above, the purpose of the present study was to reinvestigate previous claims suggesting that exposure to bright light prior to eyelid opening had no measurable consequences on the retinal structure and function; the claim being that despite a non-detectable acute phase, bright light exposure prior to eyelid opening could nonetheless yield a significant retinopathy during the chronic phase of development of LIR. In order to test our hypothesis, neonatal rats were raised in a bright luminous environment from birth to P14. At P30, analysis of the results obtained from rats exposed between P0-P14 did not reveal, as previously acknowledged by others, significant LIR damages. However, results obtained at P60 disclosed significant functional anomalies with relative sparing of the retinal ultrastructure. Our results confirm that, in spite of closed eyelids, postnatal exposure to bright environment did trigger a slow degenerative process.

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Section: Discussionsupporting

confidence: 96%

Section: Introductionmentioning

confidence: 98%

Structural and functional consequences of bright light exposure on the retina of neonatal rats

et al. 2006

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“…Our data are in agreement with those reported by Noell et al (1966), O'Steen (1970), O'Steen et al (1972), and Rapp and Williams (1980). Since the Brown Norway rats received the same light treatment and were exposed to the same ambient temperature as the Sprague-Dawley rats, we suggest that all changes in tissue levels observed in Sprague-Dawley rats are most likely due to the damaged retina in the albino rats.…”

supporting

confidence: 95%

Effects of bright artificial light on monoamines and neuropeptides in eight different brain regions compared in a pigmented and nonpigmented rat strain

Humpel

Neudorfer

Philipp

et al. 1992

J of Neuroscience Research

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Seasonal affective disorder is a form of depression which recurs at the same time of the year. Exposure to bright artificial light at a dose of 2,500 lux is used to treat seasonal affective disorders. We exposed a pigmented (Brown Norway) and a nonpigmented (Sprague-Dawley) rat strain with bright artificial light for 21 days at two doses (2,500 and 6,100 lux) and analyzed dopamine, dihydroxyphenyl-acetic acid, 5-hydroxytryptamine (5-HT), and 5-hydroxyindole-acetic acid (5-HIAA) by high performance liquid chromatography (HPLC) and electrochemical detection in eight different brain regions. Furthermore, we measured tissue levels of substance P (SP), neurokinins (NK), vasoactive intestinal polypeptide (VIP), calcitonin gene-related peptide (CGRP), and neuropeptide Y (NPY) with radioimmunoassay. Our data obtained with light microscopy show that bright artificial light at both doses induced a massive destruction of photoreceptors in the retina of albino rats but not of the pigmented rat strain. Retinal lesion of photoreceptors resulted in increased tissue levels of all measured neuropeptides except SP in the hypothalamus and increased VIP in the ventral tegmental area/substantia nigra. Furthermore, increased 5-HT and 5-HIAA tissue levels were found in the ventral tegmental area/substantia nigra. In contrast, in the frontal cortex there was a significant reduction in 5-HIAA tissue levels and a decreased 5-HIAA/5-HT ratio, indicating decreased 5-HT metabolism. Light exposure of the pigmented rat strain revealed no changes in the measured biogenic amines and neuropeptides in any investigated brain region. Our data suggest that retinal lesion but not direct visual neurotransmission induced changes in neurotransmitters in some brain regions. We conclude that Brown Norway rats but not Sprague-Dawley rats are useful to study neurochemical effects of bright artificial light. However, Sprague-Dawley rats may be a useful tool to study biochemical mechanisms of photoreceptor damage by bright light.

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“…The 24:0 light cycle was attained by keeping the animals in ventilated cabinets with overhead cool white fluorescent light sources producing an irradiance of 750 ± 150 gW/cm2; this irradiance of constant light has been shown to induce photorecep tor atrophy [3,7,8,13]. On the night of the experiment, groups of 6 or 7 rats each, weighing approximately 250 g, from both the 14:10 and the 24:0 cycles, were killed in the dark, or after exposure to cool white fluorescent light irradiances of 0.0005,0.175 or 3.33 gW/ cm2 for 15 or 30 min.…”

Section: Experiments Imentioning

confidence: 99%

“…Light influences the gland by means of a multisynaptic neural pathway which connects the retinas to the pineal [12], Previous studies indicate that the sensitivity of the pineal to light may vary according to the animals' previ ous lighting history [14]. In comparative studies, pineal serotonin N-acetyltransferase (NAT) activity and melat onin levels in diurnally active animals, such as the Richard son's ground squirrel [18] and the Eastern chipmunk [16], are much less sensitive to light inhibition than are those of nocturnally active rodents such as the Syrian hamster [4] and the cotton rat [22], Long-term light exposure causes severe photoreceptor damage and degeneration in the retinas of albino rats [7,8,13]. These animals still, however, are sensitive to light-in duced pineal inhibition when exposed to alternating light…”

mentioning

confidence: 99%

Photoreceptor Damage and Eye Pigmentation: Influence on the Sensitivity of Rat Pineal N-Acetyltransferase Activity and Melatonin Levels to Light at Night

et al. 1985

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The threshold of light irradiance capable of inhibiting nighttime pineal serotonin N-acetyltransferase (NAT) activity and melatonin content, and the importance of intact photoreceptors and eye pigmentation on these changes, were investigated in the rat. Groups of intact albino and black-eyed rats and albino animals with light-induced photoreceptor damage were studied in the dark period before, and after 15 and 30 min of exposure to either 0.0005, 0.175 or 3.33 µW/cm² irradiance of light. In animals with photoreceptor damage, the sensitivity of the pineal gland to light decreased so that only the highest irradiance tested (3.33 µW/cm²) was capable of totally inhibiting pineal NAT activity and melatonin levels. In one study, pineal NAT and melatonin levels in intact albino rats were inhibited by all three irradiances studied. In a second experiment, albino and black-eyed animals behaved identically, only responding with a depression in pineal NAT and melatonin after exposure to light irradiances of either 0.175 or 3.33 µW/cm². In conclusion, the lowest irradiance of cool white light capable of inhibiting pineal NAT and melatonin in albino rats is around 0.0005 µW/cm². At the irradiances studied, photoreceptor damage influences the response of pineal NAT and melatonin to acute light exposure at night. On the other hand, eye pigmentation does not seem to have a major effect on the nighttime inhibition of the pineal by light.

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Retinal damage after prolonged exposure to visible light. A light and electron microscopic study

Cited by 99 publications

References 11 publications

Structural and functional consequences of bright light exposure on the retina of neonatal rats

Structural and functional consequences of bright light exposure on the retina of neonatal rats

Effects of bright artificial light on monoamines and neuropeptides in eight different brain regions compared in a pigmented and nonpigmented rat strain

Photoreceptor Damage and Eye Pigmentation: Influence on the Sensitivity of Rat Pineal N-Acetyltransferase Activity and Melatonin Levels to Light at Night

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