title: The status of cones in the rhodopsin mutant P23H-3 retina: light-regulated damage and repair in parallel with rods.
abstract: OBJECTIVE
  This study tests whether cones in the rhodopsin-mutant transgenic P23H-3 retina are damaged by ambient light and whether subsequent light restriction allows repair of damaged cones.
  
  
  METHODS
  P23H-3 rats were raised in scotopic cyclic (12 hours of 5 lux, 12 hours of dark) ambient light. At postnatal day 90 to 130, some were transferred to photopic conditions (12 hours of 300 lux, 12 hours of dark) for 1 week and then returned to scotopic conditions for up to 5 weeks. Photoreceptor function was assessed by the dark-adapted flash-evoked electroretinogram, using a two-flash paradigm to isolate the cone response. Outer-segment structure was demonstrated by immunohistochemistry for cone and rod opsins and by electron microscopy.
  
  
  RESULTS
  Exposure for 1 week to photopic ambient light reduced the cone b-wave, the rod b-wave, and the rod a-wave by 40% to 60% and caused shortening and disorganization of cone and rod outer segments. Restoration of scotopic conditions for 2 to 5 weeks allowed partial recovery of the cone b-wave and the rod a- and b-waves, and regrowth of outer segments.
  
  
  CONCLUSIONS
  Modest increases in ambient light cause rapid and significantly reversible loss of cone and rod function in the P23H-3 retina. The reduction and recovery of cone function are associated with shortening and regrowth of outer segments. Because the P23H mutation affects a protein expressed specifically in rods, this study emphasizes the close dependence of cones on rod function. It also demonstrates the capacity of cones and rods to repair their structure and regain function.
authors.affiliation: CNS Stability and Degeneration Group and the ARC Centre of Excellence in Vision Science, Research School of Biological Sciences, The Australian National University, Canberra, Australia.
authors.forename: Vicki
authors.initials: V
authors.lastname: Chrysostomou
authors.forename: Jonathan
authors.initials: J
authors.lastname: Stone
authors.forename: Sally
authors.initials: S
authors.lastname: Stowe
authors.forename: Nigel L
authors.initials: NL
authors.lastname: Barnett
authors.forename: Krisztina
authors.initials: K
authors.lastname: Valter
mesh_terms: D000818:Animals; D030801:Animals, Genetically Modified; D000831:Animals, Newborn; D016923:Cell Death / Q000502:physiology; D002470:Cell Survival / Q000502:physiology; D003623:Dark Adaptation; D004596:Electroretinography; D019084:Fluorescent Antibody Technique, Indirect; D008027:Light / Q000009:adverse effects; D009154:Mutation; D010775:Photic Stimulation; D011833:Radiation Injuries, Experimental / Q000235:genetics / Q000503:physiopathology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012160:Retina / Q000528:radiation effects; D017949:Retinal Cone Photoreceptor Cells / Q000503:physiopathology* / Q000528:radiation effects / Q000648:ultrastructure; D012162:Retinal Degeneration / Q000235:genetics / Q000503:physiopathology*; D017948:Retinal Rod Photoreceptor Cells / Q000503:physiopathology* / Q000528:radiation effects / Q000648:ultrastructure; D012243:Rhodopsin / Q000235:genetics*; D017299:Rod Opsins / Q000378:metabolism
chemical_list: D017299:Rod Opsins; D012243:Rhodopsin