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W.W. Dawson, E.C. Ogle, B.E. Cunningham, J.C. Dawson, J. Gonzalez–Matinez; Macular Drusen Are Associated With Rod Cell Disfunction in Monkeys . Invest. Ophthalmol. Vis. Sci. 2005;46(13):5281.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: To evaluate rod cell electrical response kinetics in monkeys with macular drusen. Because early AMD related changes in human dark–adaptation rod function have been reported by Eisner, etal. (IOVS, 1987) and Owsley etal. (Ophthal. 2001) using psychophysical methods. Methods: Rhesus macaques from the Florida AMD colony exhibit macular drusen loads which were rated for severity. Very early (6.5 ms) potentials were measured in response to the probe flash of a test–probe pair. Stimulus pair timing of 12,000 td s, short wavelength (<480 nm) flashes was adjusted to produce a pure cone signal (600–1800 ms) and a derived rod signal (2000–5000 ms) by subtraction (ie. Friedburg etal. (J. Physiol., 2001). Kinetics of the cone and rod components were estimated by calculation of slope constants (Ks) during these test–probe pair delay periods for four eyes with varied drusen loads and four clinically normal eyes of the same age range. Results: There was a reliable shift in 6.5 ms probe response properties at about 1000–1200 ms after the test flash. Responses declined and then rose in the rod phase. For the normal eyes and drusen eyes there was no significant Ks difference or relationship between Ks results relating to age or drusen load during the cone response delay period sampled at 600–1800 ms. Rod recovery Ks values for drusen eyes were significantly reduced during 2000–5000 ms (Mann–Whitney U. p=0.028. F=43.1, p= 0.0058). The distributions did not overlap. For rod response kinetics age and drusen load variables produced no significant results. Conclusions: Drusen in aging monkeys produce rod cell disfunctions similar to those in humans which may be quantified and detected by test–probe flash stimulus manipulation of rod receptor saturation.
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