December 2002
Volume 43, Issue 13
Free
ARVO Annual Meeting Abstract  |   December 2002
Cone Photoreceptor Death Preceding Light-Induced Retinal Damage
Author Affiliations & Notes
  • WC Gordon
    Neuroscience/Ophthalmology LSUHSC New Orleans LA
  • NG Bazan
    Neuroscience/Ophthalmology LSUHSC New Orleans LA
  • Footnotes
    Commercial Relationships   W.C. Gordon, None; N.G. Bazan, None. Grant Identification: Support: The Marilyn Rosenson Fund
Investigative Ophthalmology & Visual Science December 2002, Vol.43, 3735. doi:
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      WC Gordon, NG Bazan; Cone Photoreceptor Death Preceding Light-Induced Retinal Damage . Invest. Ophthalmol. Vis. Sci. 2002;43(13):3735.

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Abstract

Abstract: : Purpose:To understand cone photoreceptor survival, which is critical for the development of therapies for macular degeneration, new experimental approaches are needed. We have studied very early changes within the outer nuclear layer (ONL) of the rat during the first 60 h after light, focusing on rod and cone cellular integrity. Methods:After 3 days dark adaptation, albino rats were exposed for 5 h to circular fluorescent bulbs and retinas were sampled at 6-h intervals (0-60 h). Cell count profiles of the ONL were constructed from sections cut from the superior to the inferior retinal margin through the optic nerve. Photoreceptor cell damage and loss were observed at both the light- and electron-microscope level; EM sections were obtained from the region of highest light sensitivity, centered 33% from the superior margin. Results:Within the retinal area of highest damage, cones display marked sensitivity at 6 h after light onset, with swelling around the nucleus, while nuclear disorganization occurs from 12-18 h. This time course is unlike that seen in rods. The first indication of rod damage, peripheral nuclear condensation, occurs around 18 h with no evidence of swelling. In regions adjacent to the photodamaged area, cones appear normal. By 60 h 48% of photoreceptor nuclei are gone; no photoreceptor nuclei remain within the subretinal space in the area of highest damage. Conclusion:Light damage in cones appears earlier and is morphologically different from that observed in rods, suggesting a different mechanism. Counts of damaged cones (10/600 undamaged rods) suggest that these are green-sensitive cones containing an opsin similar to that of rods. Therefore, the wavelengths triggering cone degeneration would be the same as those for rods. Because the rat retina is predominately rod, until now it has been difficult to apply what is known about cell degeneration to cones of the human macula. However, our observations that cones are selectively affected at a very early time suggest that rat retina can be used to understand mechanisms of cone degeneration.

Keywords: 341 cell death/apoptosis • 537 radiation damage: light/UV • 517 photoreceptors 
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