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W. W. Dawson, E. C. Ogle; The Macular Drusen Environment Depresses Rod Cell Recovery in Aging Inbred Monkeys. Invest. Ophthalmol. Vis. Sci. 2007;48(13):20.
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Previous human clinical experiments (Eisner etal. IOVS, 1991; Owsley etal. Ophthalmol. 2001) have demonstrated consistant, large delays in the onset of scotopic vision in drusen bearing eyes. Very early measurement of rod cell recovery (dark adaptation) from a saturating flash of light ("two flash". Dawson and Hope, Brain Resch, 1979; "test-probe", Friedberg; Thomas and Lamb, J. Physiol., 2001) can, with varied interflash periods, be achieved electrophysiologically from the late receptor potential. This enables a quantitative measure of function and rod-cell influence of the drusen environment in our drusen bearing monkeys and further tests their model value.
Seven rhesus (Macaca mulatta) monkeys from the Florida macular drusen-bearing colony were matched for age range with seven normal-fundus rhesus. Under Midazolam- N2O anesthesia ERG signals were recorded in response to 10,000 td, short wavelength saturating flashes. The 85 degree flashes (spectrally <480 nm) had interflash periods ranged from 500-2000 msec. Two-flash cycles were 2 min. Amplitudes of the response (at 6.5 msec) to the saturating flash (R1) and delayed flash (R2) produced recovery-response ratios (R2/R1) which form complex cone and rod recovery functions against recovery time (interflash period) as described for normal humans by Friedberg etal (2001).
There was an early rod recovery phase at 500-1100 msec and late rod phase 1200-2100 msec. The very early cone phase (10-500 msec) was not used. For the early rod phase the slope constant for R2/R1 vs recovery time of the drusen group was relatively reduced by almost 50 per cent (p<0.005). Differences between groups for later rod phase recovery slopes were not significant. There was a significant negative correlation between estimates of drusen load and the rod-recovery slope constant (r2 = 0.62, p=0.02).
Nonhuman drusen-bearing primates show dark adaptation changes as demonstrated by early AMD humans. These originate in the receptor cells. Factors controlling rod cell function recovery are modulated by the early pathophysiology relating to macular drusen load.
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