title: Photic history modifies susceptibility to retinal damage in albino trout.
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.
authors.affiliation: The University of Michigan, Department of Molecular, Cellular, and Developmental Biology, Ann Arbor, Michigan, USA.
authors.forename: W Ted
authors.initials: WT
authors.lastname: Allison
authors.forename: Ted E
authors.initials: TE
authors.lastname: Hallows
authors.forename: Trudi
authors.initials: T
authors.lastname: Johnson
authors.forename: Craig W
authors.initials: CW
authors.lastname: Hawryshyn
authors.forename: Donald M
authors.initials: DM
authors.lastname: Allen
mesh_terms: D016117:Albinism, Ocular / Q000473:pathology / Q000503:physiopathology*; D000818:Animals; D002352:Carrier Proteins / Q000378:metabolism; D002452:Cell Count / Q000379:methods; D016923:Cell Death / Q000528:radiation effects; D049109:Cell Proliferation / Q000528:radiation effects; D005786:Gene Expression Regulation / Q000528:radiation effects; D007150:Immunohistochemistry / Q000379:methods; D020287:In Situ Nick-End Labeling / Q000379:methods; D066298:In Vitro Techniques; D008027:Light / Q000009:adverse effects*; D018809:Proliferating Cell Nuclear Antigen / Q000378:metabolism; D012162:Retinal Degeneration / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*; D012243:Rhodopsin / Q000378:metabolism; D012374:Rod Cell Outer Segment / Q000473:pathology / Q000528:radiation effects*; D017299:Rod Opsins / Q000378:metabolism; D013997:Time Factors; D014337:Trout / Q000502:physiology*
chemical_list: D002352:Carrier Proteins; D018809:Proliferating Cell Nuclear Antigen; D017299:Rod Opsins; D012243:Rhodopsin