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John C. Saari, Maria Nawrot, Gregory G. Garwin, Matthew J. Kennedy, James B. Hurley, Norbert B. Ghyselinck, Pierre Chambon; Analysis of the Visual Cycle in Cellular Retinol-Binding Protein Type I (CRBPI) Knockout Mice. Invest. Ophthalmol. Vis. Sci. 2002;43(6):1730-1735.
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purpose. To determine whether the visual cycle is affected in mice without a functional gene for cellular retinol-binding protein type I (CRBPI −/− mice).
methods. Visual-cycle retinoids and rhodopsin levels were analyzed in eyes of dark adapted (DA) CRBPI −/− and wild-type (wt) mice before and during recovery from a flash. The rate of dark adaptation was analyzed using electroretinography (ERG).
results. all-trans-Retinyl esters were reduced to approximately 33% of wt levels in DA CRBPI −/− mice. Recovery from a flash in wt mice produced transient accumulations of all-trans-retinal and all-trans-retinyl ester, as the pulse of retinoid produced by the flash traversed the visual cycle. In CRBPI −/− mice, all-trans-retinal accumulated transiently, as in wt mice. However, all-trans-retinol also accumulated transiently in the neural retina, and the transient increase in all-trans-retinyl ester of the wt was reduced. Rates of 11-cis-retinal and rhodopsin formation were comparable in wt and CRBPI −/− mice. Dark adaptation was delayed by a factor of approximately two.
conclusions. The accumulation of all-trans-retinol in neural retina, in the absence of CRBPI and the reduced amount of retinyl esters in the RPE suggest that the binding protein participates in a process that drives diffusion of all-trans-retinol from photoreceptor cells to RPE, perhaps by delivering vitamin A to lecithin-retinol acyltransferase (LRAT) for esterification. Because the perturbation occurred upstream of a slow step of the visual cycle, there was no major impairment of the rate of visual pigment regeneration.
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