Purpose: The growth factor, bFGF, slows the rate of photoreceptor cell (PRC) degeneration in the RCS rat, a model with defective RPE phagocytosis. The purpose of the present study was to determine whether bFGF could retard the rate of PRC loss in the vitiligo mouse, a model in which PRCs are lost slowly over many months. The cause of vitiligo PRC death is not known, but we have evidence that the RPE is the primary cellular site of the retinal defect: RPE microvillous processes are malformed in the optic nerve head region and phagocytosis of outer segment disks is reduced. Methods: bFGF [0.5μg/eye] was injected intravitreally into vitiligo mice at ages 2, 4, 6, 8 and 13 weeks; the contralateral eye served as vehicle control. Scotopic ERG's were performed on one group of mice prior to killing. Mice were killed 4, 6 or 10 weeks following the injection. Eyes were processed for histology and analyzed. Results: ERGs: the amplitude of the b-wave was significantly smaller (p<0.01) in mice injected with bFGF than in PBS-injected and non-injected eyes regardless of the time of injection or duration after injection. Histologic examination revealed no rescue of dying PRCs. The number of rows of PRCs did not differ significantly between bFGF-injected, vehicle- or non-injected mice. There were significantly more PRCs displaced to subretinal space (p<0.01) and the attachment of outer segments to RPE was disturbed. Conclusions: bFGF did not improve the electrophysiological functioning of the retina nor rescue the dying PRCs in the vitiligo mouse. Although the vitiligo mouse may have a defect in the RPE that triggers PRC loss, bFGF is not effective in retarding degeneration of PRCs as it is in the RCS rat.
|Original language||English (US)|
|Journal||Investigative Ophthalmology and Visual Science|
|State||Published - Feb 15 1996|
ASJC Scopus subject areas
- Sensory Systems
- Cellular and Molecular Neuroscience