Abstract
EXPOSURE of rats to continuous illumination leads to cellular deterioration within the retina and a concurrent reduction of electroretinogram (ERG) responses1,2. Grignolo et al.3 showed that at early stages, this ‘damage’ due to light is hypertrophic in that tubules and vesciculae appear in receptor cell outer segments. They surmised that losses in retinal functioning are initially due to disorganisation rather than degeneration. But, experiments on recovery from light damage2 indicate that ERG sensitivity returns as the rhodopsin-containing disks of the outer segments are regenerated even though their original lamellar structure is not restored. It is thereby implied that as long as visual pigment is present at functional sites, the normal structure of the outer segments may not be crucial to ERG responsivity. Here we describe an experiment which quantitatively examines the role of visual pigment remaining in the albino rat retina which has been exposed to continuous low-intensity light. The ERG sensitivity, rhodopsin content and morphological state of the retina were assessed for various exposure durations. Our findings indicate that reductions in visual pigment levels due to constant light persist indefinitely in the dark. Furthermore, the log ERG (b wave) sensitivity varied directly with the rhodopsin content of exposed retinas even as progressive deterioration was apparent. With respect to this log–lienar relationship, light damage resembles ‘normal’ light adaptation due to short term bleaching exposure.
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RAPP, L., WILLIAMS, T. Rhodopsin content and electroretinographic sensitivity in light-damaged rat retina. Nature 267, 835–836 (1977). https://doi.org/10.1038/267835a0
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DOI: https://doi.org/10.1038/267835a0
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