May 2003
Volume 44, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2003
Differential Fate of Rods and Cones in Light-induced Retinal Damage
Author Affiliations & Notes
  • W.C. Gordon
    Ophthalmology/Neuroscience, LSUHSC, New Orleans, LA, United States
  • M.S. Cortina
    Ophthalmology/Neuroscience, LSUHSC, New Orleans, LA, United States
  • S.T. Ragbir
    Neuroscience, LSUHSC, New Orleans, LA, United States
  • N.G. Bazan
    Neuroscience, LSUHSC, New Orleans, LA, United States
  • Footnotes
    Commercial Relationships  W.C. Gordon, None; M.S. Cortina, None; S.T. Ragbir, None; N.G. Bazan, None.
  • Footnotes
    Support  NEI EY05121; The EENT Foundation
Investigative Ophthalmology & Visual Science May 2003, Vol.44, 5133. doi:
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      W.C. Gordon, M.S. Cortina, S.T. Ragbir, N.G. Bazan; Differential Fate of Rods and Cones in Light-induced Retinal Damage . Invest. Ophthalmol. Vis. Sci. 2003;44(13):5133.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Abstract: : Purpose: Stimulation by bright fluorescent light triggers rat photoreceptor cell death in rods and cones by two different mechanisms. Rods undergo apoptosis 48h after light treatment; cones display necrosis-like process terminating after 12 h (ARVO 2002). The distribution of rod dropout after light treatment is concentrated in the superior central retina, 1.2 mm from the optic nerve. However, we do not understand how light damage affects cones or the retinal region of subsequent loss. Thus, we decided to define the various light protocols to trigger cone loss and to determine the extent of damage across the retina. Methods: Sprague-Dawley rats (dark adapted 2d), light treated for 2-5h with bright fluorescent light, and returned to dark (ARVO 2002). Eyes were collected from dark controls and at 0-6 and 12h after stimulation, and examined with EM or in retinal whole-mounts in which cones were labeled with biotinylated peanut agglutinin (PNA). Rod and cone morphology was observed and the distribution of cone dropout plotted. Results: Electron micrographically, inner segment mitochondria indicate first that rods and cones have been damaged by shortening, rounding, and swelling. This occurs immediately after 5h of light but only after 6h following 3h of light. Rod and cone nuclei have different responses. After 3h of light, rod nuclei begin to show condensation, slowly increasing until blebbing and cell dropout occurs; cone nuclei maintain their morphology. Only with 4h of light are cones markedly affected, displaying swollen perinuclear cytoplasm and necrosis-like death by 12h. Distribution maps of PNA-labeled cones demonstrate cone dropout concentrated around a region in the superior central retina, 1.2 mm from the optic nerve, and corresponds to the rod loss region described by Noell. Conclusions: 5h light triggers early rapid necrosis-like cone loss by 12h, but triggers slow rod loss through DNA fragnentation and apoptosis by 48h. Therefore, once the light stimulus induces cell death, two different mechanisms are triggered within these photoreceptors. Cone death is initiated by a longer light duration (4h) than that of rods (3h) and occurs very rapidly, but does not resemble apoptosis. However, the two events are linked in that they both occur within the same retinal region, suggesting some common signaling. Thus, these two different events provide an opportunity to pharmacologically investigate rod and cone death and rescue within the same retina.

Keywords: apoptosis/cell death • photoreceptors • retinal degenerations: cell biology 
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