Foveal cone detection statistics in color-normals and dichromats

Wesner, Michael F.; Pokorny, Joel; Shevell, Steven K.; Smith, Vivianne C.

doi:10.1016/0042-6989(91)90207-l

Cited by 68 publications

(46 citation statements)

References 22 publications

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“…According to our experience, however, the parameters provided by Ingling and Tsou's model produce better results. Moreover, Müller's theory explanation for the occurrence of deuteranopia [14] does not seem to be in accordance with evidence reported in the literature [2,6,27,31].…”

Section: Simulating Color Vision Deficiencycontrasting

confidence: 53%

“…Currently, researchers work with three possible alternatives for explaining the lack of one kind of cone photopigment [2]: (i) the empty spaces model, which states that a given class of cones and its corresponding photopigment are lost, producing empty spaces in the cone mosaic. This hypothesis, however, is not supported by the findings of Wesner et al [31] who verified that the foveal cone photoreceptor mosaics of dichromats are similar in structure to the ones normal trichromats.…”

Section: Simulating Dichromacymentioning

confidence: 82%

“…Finally, (iii) the empty cones model suggests that a given class of cones contains no photopigment. While the work of Vos and Walraven [29] may support models (i) or (iii), evidence supporting the replacement model can be found in the results of several researchers [2,6,31]. This makes the photopigment substitution the most accepted model for explaining dichromacy, with genetic arguments for protanopia and deuteranopia.…”

Section: Simulating Dichromacymentioning

confidence: 98%

“…The replacement model seems to be the most plausible hypothesis for explaining dichromacy [2,6,31]. The occurrence of a given photopigment in a "wrong" type of cone seems more plausible between the L and M cones, and less plausible when it involves the S cones.…”

Section: The Replacement Modelmentioning

confidence: 99%

See 3 more Smart Citations

A Physiologically-based Model for Simulation of Color Vision Deficiency

Machado

Oliveira

Fernandes

2009

IEEE Trans. Visual. Comput. Graphics

153

126

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ReferenceProtanomaly (6 nm) Protanomaly (14 nm) Protanopia We present a physiologically-based model for simulating color perception. Our model is based on the stage theory of human color vision and is derived from data reported in electrophysiological studies. It is the first model to consistently handle normal color vision, anomalous trichromacy, and dichromacy in a unified way. We have validated the proposed model through an experimental evaluation involving groups of color vision deficient individuals and normal color vision ones. Our model can provide insights and feedback on how to improve visualization experiences for individuals with CVD. It also provides a framework for testing hypotheses about some aspects of the retinal photoreceptors in color vision deficient individuals.

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Section: Simulating Color Vision Deficiencycontrasting

confidence: 53%

Section: Simulating Dichromacymentioning

confidence: 82%

Section: Simulating Dichromacymentioning

confidence: 98%

Section: The Replacement Modelmentioning

confidence: 99%

See 2 more Smart Citations

A Physiologically-based Model for Simulation of Color Vision Deficiency

Machado

Oliveira

Fernandes

2009

IEEE Trans. Visual. Comput. Graphics

153

126

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show abstract

“…Psychophysical experiments, based on frequency of seeing curves, have also provided evidence that the packing of foveal cones in dichromats is comparable to that in trichromats (2,3). Most recently, in comparing mean contrast gains derived from the electroretinogram (ERG) for dichromats to those of trichromats, Kremers et al (4) concluded that complete replacement occurs in dichromacy.…”

mentioning

confidence: 99%

Functional photoreceptor loss revealed with adaptive optics: An alternate cause of color blindness

Carroll

Neitz

Hofer

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

236

216

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There is enormous variation in the X-linked L͞M (long͞middle wavelength sensitive) gene array underlying ''normal'' color vision in humans. This variability has been shown to underlie individual variation in color matching behavior. Recently, red-green color blindness has also been shown to be associated with distinctly different genotypes. This has opened the possibility that there may be important phenotypic differences within classically defined groups of color blind individuals. Here, adaptive optics retinal imaging has revealed a mechanism for producing dichromatic color vision in which the expression of a mutant cone photopigment gene leads to the loss of the entire corresponding class of cone photoreceptor cells. Previously, the theory that common forms of inherited color blindness could be caused by the loss of photoreceptor cells had been discounted. We confirm that remarkably, this loss of one-third of the cones does not impair any aspect of vision other than color.cone mosaic ͉ dichromacy ͉ retinal imaging H uman trichromacy relies on three different cone types in the retina; long-(L), middle-(M), and short-(S) wavelengthsensitive. Dichromatic color vision results from the functional loss of one cone class; however, one of the central questions has been whether individuals with this form of red-green colorblindness have lost one population of cones or whether they have normal numbers of cones filled with either of two instead of three pigments. Evidence has accumulated favoring the latter view, in which the photopigment in one class of cone is replaced, but the issue has not been resolved directly. Berendschot et al.(1) measured optical reflectance spectra of the fovea for normals and dichromats, and their analysis favored a replacement model. Psychophysical experiments, based on frequency of seeing curves, have also provided evidence that the packing of foveal cones in dichromats is comparable to that in trichromats (2, 3). Most recently, in comparing mean contrast gains derived from the electroretinogram (ERG) for dichromats to those of trichromats, Kremers et al. (4) concluded that complete replacement occurs in dichromacy.The L-and M-cone photopigments are encoded by genes that reside in a head-to-tail tandem array on the X chromosome (5). Two categories of mutations of these genes have been found to be associated with dichromacy. In one category of mutations, the gene(s) for a spectral class of pigment have been deleted or replaced with a functional gene for a different spectral class (6-10). In the other genetic category, a normal gene is replaced by a mutant one encoding a photopigment that does not function properly (11,12). The most frequently reported example of this latter cause is a mutation that substitutes the amino acid arginine for a cysteine at position 203 (C203R) of the pigment molecule. This cysteine is highly conserved among all G protein-coupled receptors, and is involved in forming an essential disulfide bond in the photopigment molecule (13). The mutation was originally discov...

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Color Vision

and¹,

Abramov²

2008

Blackwell Handbook of Sensation and Perception

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Foveal cone detection statistics in color-normals and dichromats

Cited by 68 publications

References 22 publications

A Physiologically-based Model for Simulation of Color Vision Deficiency

A Physiologically-based Model for Simulation of Color Vision Deficiency

Functional photoreceptor loss revealed with adaptive optics: An alternate cause of color blindness

Color Vision

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