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Invest Ophthalmol Vis Sci
2009 Sep 01;509:4477-86. doi: 10.1167/iovs.08-3186.
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Light responses in rods of vitamin A-deprived Xenopus.
Solessio E
,
Umino Y
,
Cameron DA
,
Loew E
,
Engbretson GA
,
Knox BE
,
Barlow RB
.
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Accumulation of free opsin by mutations in rhodopsin or insufficiencies in the visual cycle can lead to retinal degeneration. Free opsin activates phototransduction; however, the link between constitutive activation and retinal degeneration is unclear. In this study, the photoresponses of Xenopus rods rendered constitutively active by vitamin A deprivation were examined. Unlike their mammalian counterparts, Xenopus rods do not degenerate. Contrasting phototransduction in vitamin A-deprived Xenopus rods with phototransduction in constitutively active mammalian rods may provide new understanding of the mechanisms that lead to retinal degeneration. The photocurrents of Xenopus tadpole rods were measured with suction electrode recordings, and guanylate cyclase activity was measured with the IBMX (3-isobutyl-1-methylxanthine) jump technique. The amount of rhodopsin in rods was determined by microspectrophotometry. The vitamin A-deprived rod outer segments were 60% to 70% the length and diameter of the rods in age-matched animals. Approximately 90% of its opsin content was in the free or unbound form. Analogous to bleaching adaptation, the photoresponses were desensitized (10- to 20-fold) and faster. Unlike bleaching adaptation, the vitamin A-deprived rods maintained near normal saturating (dark) current densities by developing abnormally high rates of cGMP synthesis. Their rate of cGMP synthesis in the dark (15 seconds(-1)) was twofold greater than the maximum levels attainable by control rods ( approximately 7 seconds(-1)). Preserving circulating current density and response range appears to be an important goal for rod homeostasis. However, the compensatory changes associated with vitamin A deprivation in Xenopus rods come at the high metabolic cost of a 15-fold increase in basal ATP consumption.
Ames,
Energy metabolism of rabbit retina as related to function: high cost of Na+ transport.
1992, Pubmed
Ames,
Energy metabolism of rabbit retina as related to function: high cost of Na+ transport.
1992,
Pubmed
Baylor,
Responses of retinal rods to single photons.
1979,
Pubmed
Bridges,
Spectroscopic properties of porphyropsins.
1967,
Pubmed
Burns,
Dynamics of cyclic GMP synthesis in retinal rods.
2002,
Pubmed
Cornwall,
Bleached pigment activates transduction in isolated rods of the salamander retina.
1994,
Pubmed
Cornwall,
Electrophysiological methods for measurement of activation of phototransduction by bleached visual pigment in salamander photoreceptors.
2000,
Pubmed
Dizhoor,
The human photoreceptor membrane guanylyl cyclase, RetGC, is present in outer segments and is regulated by calcium and a soluble activator.
1994,
Pubmed
Dowling,
THE BIOLOGICAL FUNCTION OF VITAMIN A ACID.
1960,
Pubmed
Dowling,
VITAMIN A DEFICIENCY AND NIGHT BLINDNESS.
1958,
Pubmed
Engbretson,
Rod sensitivity and visual pigment concentration in Xenopus.
1978,
Pubmed
,
Xenbase
Fain,
Photoreceptor degeneration in vitamin A deprivation and retinitis pigmentosa: the equivalent light hypothesis.
1993,
Pubmed
Fan,
Opsin activation of transduction in the rods of dark-reared Rpe65 knockout mice.
2005,
Pubmed
Gorczyca,
Purification and physiological evaluation of a guanylate cyclase activating protein from retinal rods.
1994,
Pubmed
Hodgkin,
Control of light-sensitive current in salamander rods.
1988,
Pubmed
Hsu,
Glucose metabolism in photoreceptor outer segments. Its role in phototransduction and in NADPH-requiring reactions.
1994,
Pubmed
Jin,
Rpe65 is the retinoid isomerase in bovine retinal pigment epithelium.
2005,
Pubmed
Jin,
Opsin activation as a cause of congenital night blindness.
2003,
Pubmed
,
Xenbase
Krispel,
RGS expression rate-limits recovery of rod photoresponses.
2006,
Pubmed
Lem,
Constitutive opsin signaling: night blindness or retinal degeneration?
2004,
Pubmed
Loew,
A third, ultraviolet-sensitive, visual pigment in the Tokay gecko (Gekko gekko).
1994,
Pubmed
MacNichol,
A unifying presentation of photopigment spectra.
1986,
Pubmed
Marlhens,
Mutations in RPE65 cause Leber's congenital amaurosis.
1997,
Pubmed
Melia,
A comparison of the efficiency of G protein activation by ligand-free and light-activated forms of rhodopsin.
1997,
Pubmed
Molday,
Monoclonal antibodies to rhodopsin: characterization, cross-reactivity, and application as structural probes.
1983,
Pubmed
,
Xenbase
Naash,
Retinal abnormalities associated with the G90D mutation in opsin.
2004,
Pubmed
Nikonov,
Kinetics of recovery of the dark-adapted salamander rod photoresponse.
1998,
Pubmed
Nikonov,
The role of steady phosphodiesterase activity in the kinetics and sensitivity of the light-adapted salamander rod photoresponse.
2000,
Pubmed
Okawa,
ATP consumption by mammalian rod photoreceptors in darkness and in light.
2008,
Pubmed
Pepperberg,
Light-dependent delay in the falling phase of the retinal rod photoresponse.
1992,
Pubmed
Pugh,
Amplification and kinetics of the activation steps in phototransduction.
1993,
Pubmed
Pugh,
Molecular mechanisms of vertebrate photoreceptor light adaptation.
1999,
Pubmed
Redmond,
Mutation of key residues of RPE65 abolishes its enzymatic role as isomerohydrolase in the visual cycle.
2005,
Pubmed
Sampath,
Bleached pigment produces a maintained decrease in outer segment Ca2+ in salamander rods.
1998,
Pubmed
Sieving,
Dark-light: model for nightblindness from the human rhodopsin Gly-90-->Asp mutation.
1995,
Pubmed
Sieving,
Constitutive "light" adaptation in rods from G90D rhodopsin: a mechanism for human congenital nightblindness without rod cell loss.
2001,
Pubmed
Solessio,
Developmental regulation of calcium-dependent feedback in Xenopus rods.
2004,
Pubmed
,
Xenbase
Torre,
Role of calcium in regulating the cyclic GMP cascade of phototransduction in retinal rods.
1986,
Pubmed
Van Hooser,
Recovery of visual functions in a mouse model of Leber congenital amaurosis.
2002,
Pubmed
Wald,
The molecular basis of visual excitation.
1968,
Pubmed
Witkovsky,
Photoreceptor thresholds and visual pigment levels in normal and vitamin A-deprived Xenopus tadpoles.
1976,
Pubmed
,
Xenbase
Woodruff,
Constitutive excitation by Gly90Asp rhodopsin rescues rods from degeneration caused by elevated production of cGMP in the dark.
2007,
Pubmed
Woodruff,
Spontaneous activity of opsin apoprotein is a cause of Leber congenital amaurosis.
2003,
Pubmed
