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M.E. Pennesi, M.T. Matthes, D. Yasumura, M.M. La Vail; Relationship of Retinal Vasculature Development and Photoreceptor Degeneration in Mutant Rhodopsin Transgenic Rats . Invest. Ophthalmol. Vis. Sci. 2006;47(13):5783.
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© ARVO (1962-2015); The Authors (2016-present)
The deep capillary plexus (DCP) that supplies the inner nuclear layer of the retina fails to develop in rd1/rd1 mice that lose most photoreceptor (PR) nuclei during the developmental period of the DCP. To characterize better the relationship between retinal vascular development and PR degeneration, we have examined the formation of the DCP in 8 lines of transgenic rats with different ages of onset and rates of PR cell loss.
Capillary profiles in plastic–embedded sections of retinas from 3 lines of P23H (P–1, P–2 and P–3) and 5 lines of S334ter (S–3, S–4, S–5, S–7 and S–9) transgenic rats were counted and compared to age matched Sprague–Dawley rats. All of the profiles in a single section along the vertical meridian were counted in each of 3 rats of each line at postnatal day (P) 15 and P30. The DCP develops between P10–P15 in the rat. Blood vessel profiles in the ganglion cell layer and inner plexiform layer made up the inner (superficial) capillary plexus, and those in the inner nuclear layer and innermost border of the outer plexiform layer comprise the DCP.
In the inner plexus, there was no significant difference in number of vascular profiles among any of the lines at either age. By contrast, the DCP is missing at P15 and P30 in two lines with an early and rapid PR loss, S–7 and S–3. In these lines, about 90% and 75%, respectively, of the PRs are already lost by P15. In lines where almost all PRs are still present at P15 (S–4, S–9, P–2 and P–3), the number of profiles in the DCP is the same as that in wild–type controls. In two lines with an intermediate rate of degeneration (S–5 and P–1), where only about 25% of the PRs are lost by P15, there is an intermediate number of vascular profiles in the DCP at P15 and P30.
There is a close relationship between the number of PRs and vessel profiles in the DCP during its development, and the absence of PR nuclei correlates with the failure of the DCP to develop. Several mechanisms may explain this relationship including changes in the level of physiological hypoxia or release of angiogenic factors that normally drive vessel development.
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