November 1998
Volume 39, Issue 12
Free
Articles  |   November 1998
Photoreceptor dystrophy in the RCS rat: roles of oxygen, debris, and bFGF.
Author Affiliations
  • K Valter
    NSW Retinal Dystrophy Research Centre, Department of Anatomy and Histology, University of Sydney, Australia.
  • J Maslim
    NSW Retinal Dystrophy Research Centre, Department of Anatomy and Histology, University of Sydney, Australia.
  • F Bowers
    NSW Retinal Dystrophy Research Centre, Department of Anatomy and Histology, University of Sydney, Australia.
  • J Stone
    NSW Retinal Dystrophy Research Centre, Department of Anatomy and Histology, University of Sydney, Australia.
Investigative Ophthalmology & Visual Science November 1998, Vol.39, 2427-2442. doi:
  • Views
  • PDF
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      K Valter, J Maslim, F Bowers, J Stone; Photoreceptor dystrophy in the RCS rat: roles of oxygen, debris, and bFGF.. Invest. Ophthalmol. Vis. Sci. 1998;39(12):2427-2442.

      Download citation file:


      © ARVO (1962-2015); The Authors (2016-present)

      ×
  • Supplements
Abstract

PURPOSE: To examine the roles of oxygen, basic fibroblast growth factor (bFGF), and photoreceptor debris in the photoreceptor dystrophy of the Royal College of Surgeons (RCS) rat. METHODS: Pups were exposed during the critical period of their development (postnatal day [P] 16-24) and for some days thereafter to hypoxia and hyperoxia. The effects of these exposures on photoreceptor death, debris accumulation in the subretinal space, and the expression of bFGF protein and mRNA by surviving cells were studied. RESULTS: During the critical period hyperoxia slowed photoreceptor death in a dose-related fashion and decreased bFGF protein levels, whereas hypoxia accelerated death and increased bFGF levels. At the edges of the retina, where photoreceptors survive longest in normoxia, hypoxia had little effect on either photoreceptor death or bFGF protein levels. Oxygen-induced modulation of rates of death could not be related to the accumulation of debris in the subretinal space. After P27, the relationship between oxygen and photoreceptor death changed markedly, hyperoxia no longer delaying and hypoxia no longer accelerating death. CONCLUSIONS: The death of RCS rat photoreceptors in the period P16 to P27 is precipitated by hypoxia that may result from the accumulation of photoreceptor debris in the subretinal space. This debris, the result of the phagocytotic failure of the retinal pigment epithelium in this strain, lies in the normal pathway of oxygen diffusing to the photoreceptors from the choriocapillaris. During this period the retina responds to hypoxia by increasing expression of a potentially protective protein (bFGF), but hypoxia-induced damage overwhelms any protection provided by this or other mechanisms. Later stages of the dystrophy may not be hypoxia-induced.

×
×

This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.

×