title: Establishment of monocular-limited photoreceptor degeneration models in rabbits.
abstract: BACKGROUND
  Numerous rodent models of photoreceptor degeneration have been developed for the study of visual function. However, no viable model has been established in a species that is more closely related to Homo sapiens. Here, we present a rabbit model of monocular photoreceptor degeneration.
  
  
  METHODS
  We tested 2 chemicals, verteporfin and sodium nitroprusside (SNP), for developing a 1-eye limited photoreceptor degeneration model in pigmented rabbits. After the intravenous injection of verteporfin, the retina was exposed to light from a halogen lamp for 0, 10, 30, or 60 min. Alternately, 100 μL of various concentrations of sodium nitroprusside (0.1 mM, 0.5 mM, and 1 mM) were intravitreously injected into the rabbit eye. Retinal degeneration was evaluated by fundus photography, electroretinogram (ERG), and histological examinations.
  
  
  RESULTS
  Fundus photographs of animals in the verteporfin- or SNP-treated groups showed evidence of retinal degeneration. The severity of this degradation depended on the duration of light exposure and the concentration of SNP administered. The degeneration was clearly limited to the light-exposed areas in the verteporfin-treated groups. Extensive retinal atrophy was observed in the SNP-treated groups. The a- and b-wave amplitudes were dramatically decreased on the ERGs from SNP-treated groups. Histological examination revealed that either verteporfin or SNP induced severe photoreceptor degeneration. High-dose SNP treatment (1 mM) was also associated with inner retinal layer degeneration.
  
  
  CONCLUSIONS
  Both SNP and verteporfin clearly caused photoreceptor degeneration without any effect on the contralateral eye. These compounds therefore represent valuable tools for the empirical investigation of visual function recovery. The findings will inform guidelines for clinical applications such as retinal prostheses, cell-based therapy, and gene therapy.
authors.affiliation: Laboratory of Visual Neuroscience, Department of Chemistry and Bioengineering, Iwate University Graduate School of Engineering, 4-3-5 Ueda Morioka, Iwate 020-8551, Japan.
authors.forename: Hitomi
authors.initials: H
authors.lastname: Isago
authors.forename: Eriko
authors.initials: E
authors.lastname: Sugano
authors.forename: Namie
authors.initials: N
authors.lastname: Murayama
authors.forename: Makoto
authors.initials: M
authors.lastname: Tamai
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Tomita
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D004596:Electroretinography; D007275:Injections, Intravenous; D008027:Light; D009599:Nitroprusside; D010781:Photography; D020419:Photoreceptor Cells, Vertebrate / Q000187:drug effects / Q000528:radiation effects; D017319:Photosensitizing Agents / Q000494:pharmacology; D011166:Porphyrins; D011817:Rabbits; D012162:Retinal Degeneration / Q000139:chemically induced* / Q000473:pathology; D014665:Vasodilator Agents / Q000494:pharmacology; D000077362:Verteporfin
chemical_list: D017319:Photosensitizing Agents; D011166:Porphyrins; D014665:Vasodilator Agents; D000077362:Verteporfin; D009599:Nitroprusside