title: Biphasic photoreceptor degeneration induced by light in a T17M rhodopsin mouse model of cone bystander damage.
abstract: OBJECTIVE
  To evaluate light-induced retinal damage in transgenic T17M rhodopsin mice as a novel model for bystander cone damage during retinal degeneration.
  
  
  METHODS
  Mouse eyes were exposed to bright white light (15,000 lux, 2.5 minutes). After exposure, electroretinography was performed on mice dark adapted for 12 or more hours at 0 to 5 days to test photoreceptor response or for 0 to 12 hours to test response recovery. Retinal cryosections were examined by TUNEL staining and outer nuclear layer thickness measurements. Cone morphology was assessed by peanut agglutinin staining in retinal flatmounts and cryosections.
  
  
  RESULTS
  T17M retinal function and morphology changed rapidly after exposure to light. Scotopic and photopic electroretinogram responses declined progressively from 0.5 to 3 days. Scotopic response recovery peaked at 50% to 60% of the unilluminated response in 3 hours, indicating an early, rapid decline in scotopic signaling. Photopic responses were near normal or supernormal from 0 to 6 hours. Cell death peaked at 1 day, and outer nuclear layer thickness declined from 1 to 5 days. Disorganized cones were observed at 6 hours, intact and damaged cones were observed at 12 hours and 1 day, but only cone remnants were observed at 3 and 5 days. Light exposure had little to no effect on ERG responses in nontransgenic littermates and other retinal degeneration models.
  
  
  CONCLUSIONS
  The time course of light-induced T17M retinal damage is biphasic, with an initial decline in rod function within hours followed by bystander cone and rod deterioration within days. The rapid and synchronous induction of damage in this model is attractive for characterizing bystander effects in retinal degeneration.
authors.affiliation: Department of Ophthalmology and the Charlie Mack Overstreet Laboratories for Retinal Degeneration, University of Florida, Gainesville, Florida, USA.
authors.forename: Mark P
authors.initials: MP
authors.lastname: Krebs
authors.forename: D Alan
authors.initials: DA
authors.lastname: White
authors.forename: Shalesh
authors.initials: S
authors.lastname: Kaushal
mesh_terms: D000818:Animals; D024201:Bystander Effect; D016923:Cell Death; D003623:Dark Adaptation; D004195:Disease Models, Animal; D004596:Electroretinography; D020287:In Situ Nick-End Labeling; D008027:Light / Q000009:adverse effects; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D008822:Mice, Transgenic; D009154:Mutation; D016133:Polymerase Chain Reaction; D011833:Radiation Injuries, Experimental / Q000235:genetics / Q000503:physiopathology*; D017949:Retinal Cone Photoreceptor Cells / Q000473:pathology / Q000502:physiology / Q000528:radiation effects*; D012162:Retinal Degeneration / Q000235:genetics / Q000503:physiopathology*; D017948:Retinal Rod Photoreceptor Cells / Q000473:pathology / Q000502:physiology / Q000528:radiation effects*; D012243:Rhodopsin / Q000235:genetics*
chemical_list: D012243:Rhodopsin