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Photic history modifies susceptibility to retinal damage in albino trout

Published online by Cambridge University Press:  09 March 2006

W. TED ALLISON
Affiliation:
The University of Michigan, Department of Molecular, Cellular, and Developmental Biology, Ann Arbor, Michigan Department of Biology, University of Victoria, Victoria, British Columbia, Canada
TED E. HALLOWS
Affiliation:
Utah Division of Wildlife Resources, Kamas State Hatchery, Kamas, Utah
TRUDI JOHNSON
Affiliation:
Department of Biology, University of Victoria, Victoria, British Columbia, Canada
CRAIG W. HAWRYSHYN
Affiliation:
Department of Biology, University of Victoria, Victoria, British Columbia, Canada Current address, Professor and Canada Research Chair in Visual Neuroscience and Behavior, Department of Biology, Queens University, Kingston, ON K7L 3N6 Canada.
DONALD M. ALLEN
Affiliation:
Department of Science & Mathematics, University of Texas of the Permian Basin, Odessa, Texas

Abstract

Albino vertebrates exposed to intense light typically lose photoreceptors via apoptosis, and thus serve as useful models of retinal degeneration. In contrast, albino rainbow trout exposed to intense light maintain populations of rod and cone nuclei despite substantial damage to rod outer segments (ROS). The aim of this study was to differentiate between two hypotheses that could account for this divergent result: (1) trout rod nuclei remain intact during light damage, or (2) rod nuclei die but are replaced by cell proliferation. A further aim was to examine whether photic history modulates retinal damage, as in rodents. Albino and normally pigmented trout were moved from defined photic regimes into full daylight, while some were not moved to serve as protected controls. ROS were always maintained in pigmented fish and in albinos protected from full daylight. In albinos exposed to full daylight, ROS were removed over most of the central retina, whereas rod nuclei were maintained in the outer nuclear layer over 10 days. Pyknotic and TUNEL-labeled rod nuclei were abundant in affected albinos at all time-points tested. Rod death occurred without a decrease in the number of rod nuclei, confirming that proliferation must be replacing cells. Indeed a transient increase in proliferation was observed in retinal progenitors of albinos receiving 5 days of damaging light. This proliferative response was decreased with further damage. Cones remained intact even in areas where rod nuclei had degenerated. Pretreatment with light of moderate versus low intensity light affected the cell death and proliferative responses, and the ectopic localization of rod opsin. We conclude that apoptotic demise of rods, but not cones, occurred during light damage in retinas of albino trout and proliferative responses have a limited a capacity to replace lost rods.

Type
Research Article
Copyright
2006 Cambridge University Press

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