December 2002
Volume 43, Issue 13
Free
ARVO Annual Meeting Abstract  |   December 2002
Evolving Neurovascular Relationships in the RCS Rat with Age
Author Affiliations & Notes
  • R Lund
    Moran Eye Center University of Utah Salt Lake City UT
  • S Wang
    Moran Eye Center University of Utah Salt Lake City UT
  • T Holmes
    Moran Eye Center University of Utah Salt Lake City UT
  • JM Lawrence
    Institute of Ophthalmology University College London London United Kingdom
  • M Vidal-Sanz
    Laboratorio de Oftalmologia Experimental Facultad de Medicina Universidad de Murcia Espinardo Murcia Spain
  • N Hurtado-Montalbán
    Laboratorio de Oftalmologia Experimental Facultad de Medicina Universidad de Murcia Espinardo Murcia Spain
  • MP Villegas-Pérez
    Laboratorio de Oftalmologia Experimental Facultad de Medicina Universidad de Murcia Espinardo Murcia Spain
  • Footnotes
    Commercial Relationships   R. Lund, None; S. Wang, None; T. Holmes, None; J.M. Lawrence, None; M. Vidal-Sanz, None; N. Hurtado-Montalbán, None; M.P. Villegas-Pérez, None. Grant Identification: Action Research, UK, Foundation Fighting Blindness, European Union CT 96-0976, FIS 98/0341, FIS 99/1
Investigative Ophthalmology & Visual Science December 2002, Vol.43, 2719. doi:
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      R Lund, S Wang, T Holmes, JM Lawrence, M Vidal-Sanz, N Hurtado-Montalbán, MP Villegas-Pérez; Evolving Neurovascular Relationships in the RCS Rat with Age . Invest. Ophthalmol. Vis. Sci. 2002;43(13):2719.

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

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Abstract

Abstract: : Purpose: We have found previously that the progressive loss of photoreceptors that occurs in the Royal College of Surgeons (RCS) rat leads in time to axonal dystrophy in the optic fiber layer and to subsequent retinal ganglion cell loss. It appears that changes in the retinal vascular are responsible for the neuronal changes; here we examine how they develop and suggest mechanisms whereby the axonal loss occurs. Methods: Both dystrophic and congenic RCS rats (2-24month old) were used in this study. Animals were anesthetized and perfused intracardially. Whole-mount retinae were first stained for neurofilament protein (RT97), and then were transferred to an incubation medium for NADPH-diaphorase staining. A separate group of dystrophic rats were injected with Type II Peroxidase into the femoral vein; the whole-mount retinae were processed for HRP histochemistry. Results: The first changes are seen in the deep vascular plexus, as the photoreceptors are lost, this plexus comes into close proximity to the retinal pigment epithelial (RPE) cell layer. RPE cells are attracted to vessels of the plexus by an as yet unknown mechanism and this leads to a series of progressive changes in which the vessels form focal complexes including dilated or convoluted vessels associated with RPE cells. These complexes become more elaborate with many small vessels radiating from them. Vessels arising from the inner retinal circulation that supply the complexes must cross nerve fiber bundles before they plunge into the retina. With time, they appear to come under tension, pulling the optic axons that they cross into the retina. At these tension points, axons are ligated, and this leads to retinal ganglion cell (RGC) loss by retrograde degeneration. The vascular events begin in the ventral retina around the optic nerve head at around 3 months eventually extending into the dorsal retina. Axonal dystrophy similarly begins ventrally at between 5 and 6 months and spreads over much of the retinal area with age. Conclusions: These observations show a complex series of events whereby vascular changes can have secondary repercussions for neurons distant from the primary lesion.

Keywords: 566 retinal neovascularization • 385 degenerations/dystrophies • 480 mutations 
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