title: Long-term characterization of retinal degeneration in rd1 and rd10 mice using spectral domain optical coherence tomography.
abstract: OBJECTIVE
  We characterize the in vivo changes over time in the retinal structure of wild-type mice alongside two lines of mice deficient in the β-subunit of phosphodiesterase (rd1 and rd10 mice) using spectral domain optical coherence tomography (SD-OCT).
  
  
  METHODS
  SD-OCT images were obtained using the Bioptigen spectral domain ophthalmic imaging system (SDOIS). Wild-type C57BL/6J, rd1 and rd10 mice ranging in age from P14 to P206 were sedated with 1% isoflurane. Horizontal and vertical linear scans through the optic nerve, and annular scans around the optic nerve were obtained.
  
  
  RESULTS
  SD-OCT imaging of wild-type mice demonstrated visibility of the inner segment/outer segment (IS/OS) junction, external limiting membrane (ELM), outer nuclear layer (ONL), and outer plexiform layer (OPL). At P14, most rd10 mice exhibited normal SD-OCT profiles, but some displayed changes in the IS/OS junction. At the same time point, rd1 mice had severe outer retinal degeneration. In rd10 mice, imaging revealed loss of the IS/OS junction by P18, hyperreflective changes in the ONL at P20, hyperreflective vitreous opacities, and shallow separation of the neural retina from the RPE. Retinal separations were not observed in rd1 mice. Segmentation analysis in wild-type mice demonstrated relatively little variability between animals, while in rd10 and rd1 mice there was a steady decline in outer retinal thickness. Histologic studies demonstrated correlation of retinal features with those seen on SD-OCT scans. Segmentation analysis provides a quantitative and reproducible method for measuring in vivo retinal changes in mice.
  
  
  CONCLUSIONS
  SD-OCT provides a non-invasive method of following long-term retinal changes in mice in vivo. Although rd10 and rd1 mice have mutations in the same gene, they demonstrate significantly different features on SD-OCT.
authors.affiliation: Casey Eye Institute, Oregon Health & Science University, Portland, OR 97239, USA. pennesim@ohsu.edu
authors.forename: Mark E
authors.initials: ME
authors.lastname: Pennesi
authors.forename: Keith V
authors.initials: KV
authors.lastname: Michaels
authors.forename: Sienna S
authors.initials: SS
authors.lastname: Magee
authors.forename: Anastasiya
authors.initials: A
authors.lastname: Maricle
authors.forename: Sean P
authors.initials: SP
authors.lastname: Davin
authors.forename: Anupam K
authors.initials: AK
authors.lastname: Garg
authors.forename: Michael J
authors.initials: MJ
authors.lastname: Gale
authors.forename: Daniel C
authors.initials: DC
authors.lastname: Tu
authors.forename: Yuquan
authors.initials: Y
authors.lastname: Wen
authors.forename: Laura R
authors.initials: LR
authors.lastname: Erker
authors.forename: Peter J
authors.initials: PJ
authors.lastname: Francis
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D010727:Phosphoric Diester Hydrolases / Q000172:deficiency* / Q000235:genetics; D012162:Retinal Degeneration / Q000201:enzymology / Q000473:pathology*; D055213:Retinal Pigment Epithelium; D041623:Tomography, Optical Coherence / Q000379:methods*
chemical_list: D010727:Phosphoric Diester Hydrolases