Retinal degeneration in rcs rats raised under ambient light levels

doi:10.1016/0042-6989(79)90124-X

Vision Research

Volume 19, Issue 1, 1979, Pages 79-81

https://doi.org/10.1016/0042-6989(79)90124-X Get rights and content

Abstract

RCS rats have an inherited, light sensitive retinal degeneration. In the present experiment, this decline was measured as a decline in ERG amplitude and is shown to be dependent on the illumination levels in the animals' living quarters. Regardless of rearing conditions the decline in ERG amplitude was nonlinear and may reflect the earlier degeneration of rods followed by the slower deterioration of the more resistant cones.

References (12)

A.J. Dewar et al.
The effect of light deprivation on the progress of retinal degeneration in two strains of dystrophic rat
Expl. Eye Res.
(1975)
M. Kaitz
The effect of light on brightness perception in rats with retinal dystrophy
Vision Res.
(1976)
M.M. La Vail et al.
Influence of eye pigmentation and light deprivation on inherited retinal dystrophy in the rat
Expl Eye Res.
(1975)
E.L. Pautler et al.
The slow ERG potentials in hereditary retinal dystrophy of albino and pigmented rats
Expl Eye Res.
(1976)
C.M. Yates et al.
Histological and biochemical studies on the retina of a new strain of dystrophic rat
Expl Eye Res.
(1974)
C.M. Cicerone
Cones survive rods in the light-dominated eye of the albino rat
Science
(1976)

There are more references available in the full text version of this article.

Cited by (13)

Optimising the structure and function of the adult P23H-3 retina by light management in the juvenile and adult
2009, Experimental Eye Research
Citation Excerpt :
In humans suffering retinal degeneration, however, results of light restriction have been mixed; Berson (Berson, 1971) reporting no effect, while Pe'er and Meron (Stone et al., 1999) reported slowing of visual field loss in 10 of 14 patients. Light restriction has been shown to slow retinal degeneration robustly in the RCS rat (Dowling and Sidman, 1962; Kaitz and Auerbach, 1978, 1979), the P23H-3 transgenic mouse (Naash et al., 1996) and rat (Bicknell et al., 2002), and in the rhodopsin-mutant dog (Cideciyan et al., 2005). A recent review noted evidence that light restriction slowed degenerations in 15 of 20 rodent strains surveyed (Paskowitz et al., 2006).
This study tests the potential of light restriction to optimise retinal structure and function in adulthood, using the P23H-3 rhodopsin-mutant transgenic rat as a model. P23H-3 rats were reared in scotopic (5 lux) or mesopic (40–60 lux) cyclic (12 h/12 h light/dark) light. A further 2 groups were reared in one of these light conditions to P(postnatal day)30, and then were transferred to the other condition. Retinae were examined at P30-365. Rod and cone function were assessed by the dark-adapted flash electroretinogram. The rate of photoreceptor death was assessed with the TUNEL technique, and photoreceptor survival by the thickness of the outer nuclear layer (ONL). Photoreceptor structural changes were assessed by immunohistochemistry. Mesopic rearing severely reduced the number, function and outer segment (OS) length of photoreceptors. Light restriction in the adult (achieved by moving mesopic-reared animals to scotopic conditions at P30) slowed photoreceptor death, induced recovery of the ERG and of OS length in survivors, resulting in an adult retina that matched the scotopic-reared in function, photoreceptor survival (stability) and structure. Conversely, light exposure in the adult (achieved by moving scotopic-reared animals to mesopic conditions at P30) accelerated photoreceptor death, shortened OSs and reduced the ERG, resulting in a retina that was as damaged and dysfunctional as a mesopic-reared retina, and showed greater photoreceptor instability. Present observations suggest, that the stability and function of adult photoreceptors are determined by both early and adult ambient light experience. Light restriction in the adult was effective in inducing the self-repair of photoreceptors, and the recovery of their function and stability. Light restriction in the juvenile (before P30) improved early photoreceptor survival but made adult photoreceptors vulnerable to brighter light experienced in adulthood. For comparable human dystrophies, these results suggest that light restriction begun after retinal maturation may be effective in optimising the structure, function and stability of the adult retina.
Genetically induced retinal degeneration leads to changes in metabotropic glutamate receptor expression
2006, Neuroscience Letters
In the retina, neurotransmission from photoreceptors to ON-cone and rod bipolar cells is sign reversing and mediated by the metabotropic glutamate receptor mGluR6, which converts the light-evoked hyperpolarization of the photoreceptors into depolarization of ON bipolar cells. The Royal College of Surgeons (RCS) rat retina undergoes progressive photoreceptor loss due to a genetic defect in the pigment epithelium cells. The consequences of photoreceptor loss and the concomitant loss of glutamatergic input to second-order retinal neurons on the expression of the metabotropic glutamate receptor was investigated in the RCS rat retina from early stages of photoreceptor degeneration (P17) up to several months after complete rod and cone degeneration (P120). The expression of the gene encoding mGluR6 was studied by in situ hybridization in the retina, using an [³⁵S]dATP-labeled oligonucleotide probe. In congenic control and RCS retina, we found mRNA expression of mGluR6 receptor only in the outer half of the inner nuclear layer (INL) on emulsion-coated retinal sections. Quantitative analysis of the hybridization signal obtained from the autoradiographic films revealed decreased expression levels of the mGluR6 mRNA at early stages of photoreceptor degeneration (P17). On the contrary, increased expression levels were observed at late stages of degeneration (P60 and P120) in RCS compared to congenic control retina. In conclusion, our data demonstrate that the metabotropic glutamate receptor-6 mRNA levels are altered in the young and adult RCS rat retina and suggest that the genetically induced degeneration of photoreceptors affects the expression of this receptor by the INL retinal neurons.
Developmentally regulated postsynaptic localization of a metabotropic glutamate receptor in rat rod bipolar cells
1994, Cell
The retinal bipolar cell receiving glutamate transmission from photoreceptors mediates a key process in segregating visual signals into ON center and OFF center pathways. This transmission involves a G protein-coupled metabotropic glutamate receptor (mGluR). Immunocytochemical and immunoelectron microscopic studies indicate the restricted localization of a specific mGluR subtype, mGluR6, at the postsynaptic site of the rat rod bipolar cell. This specialization is developmentally regulated: mGluR6 is initially distributed in both the soma and dendrites and is finally concentrated on the postsynaptic site. The mGluR6 localization is reversed when photoreceptors degenerate in the mutant rat with retinal dystrophy. Evidence is thus presented indicating specialized, developmentally regulated receptor distribution in the central nervous system and the crucial role of mGluR6 in photoreceptor-bipolar cell synaptic transmission.
Development and degeneration of retina in rds mutant mice: Effects of light on the rate of degeneration in albino and pigmented homozygous and heterozygous mutant and normal mice
1986, Vision Research
The effect of light on the rate of visual cell loss in mice afflicted by therds (retinal degeneration slow) gene was analyzed by comparing the changes in the thickness of the outer nuclear layer. Visual cell loss in the pigmented, homozygous mutant mice, maintained in cyclic light, is slightly slower than in the albino mutant mice. In the pigmented mutant mice, exposed to constant light, and in the albino mutant mice, reared in darkness, rate of cell loss is not significantly altered. In the albino animals exposed to constant light, the rate of cell loss is faster in the homozygous mutant than in the normal, and intermediate in the heterozygous mutant retina. The accelerated cell loss in the mutant retina progresses from the centre to the periphery, and affects the rods earlier than the cones. This resembles the photic lesion in the normal retina but is unlike the genetic lesion in the mutant retina which appears to progress from the periphery to the centre and affects both rods and cones. It is concluded that the visual cells in the retina ofrds mutant mice are more vulnerable to photic damage than those in the retina of normal mice.
Action spectrum for light-induced retinal degeneration in dystrophic rats
1979, Vision Research
Rats with an inherited retinal dystrophy were reared under red. green or blue lights and the time course of their retinal degeneration was followed electroretinographically. When light intensities were matched for total energy flux, the retinal degeneration in rats reared under red light was far slower than in those raised under the green and blue light conditions. When the colored lights were matched for equal energy absorbed by rhodopsin, the retinal degeneration of all rats followed an identical time course. The action spectrum for the damaging effect of light therefore follows the rhodopsin absorption curve.
The interplay of environmental luminance and genetics in the retinal dystrophy induced by the dominant RPE65 mutation
2022, Proceedings of the National Academy of Sciences of the United States of America

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Retinal degeneration in rcs rats raised under ambient light levels

Abstract

Expl. Eye Res.

Vision Res.

Expl Eye Res.

Expl Eye Res.

Expl Eye Res.

Cones survive rods in the light-dominated eye of the albino rat

Science