[Leica] Human color vision and the cone photoreceptors.

[LRZeitlin@aol.com]

To continue to beat a horse of a different color, this is a long post, 
extracted from current research literature, explaining the assertion that there are 
more than three types of color receptors in the human eye. The trichromatic 
theory of color vision is not invalidated, as such, but it has been 
significantly modified. It helps explain why we can see colors that we cannot normally 
photograph and why people disagree on the exact color match of pieces of fabric. 
(This is my problem when my wife takes me shopping with her.)
      
A long accepted fundamental property of human vision is trichromacy. The 
trichromatic theory helps to explain our color perceptions and color 
discriminations. The anatomical basis of trichromacy begins with the complement of cone 
photoreceptors in the retina. For over one hundred years researchers thought that 
the color-normal eye contained three cone types, designated as S, M, and L, 
whose photopigments were later psychophysically estimated to have peak spectral 
sensitivities near 440, 540, and 560 nanometers. There is considerable 
overlap in sensitivity of the middle wavelength sensitive and long wavelength 
sensitive cone types.

Over the years, however, psychologists questioned whether subtle variations 
may exist in normal color vision based on small individual differences in the 
spectral sensitivities of the photopigments (Alpern & Wake, 1977; Neitz & 
Jacobs, 1986). The findings of the early studies were viewed with some skepticism, 
however, because of the difficulty in ruling out measurement error and 
confounding factors. As the psychophysical evidence grew, researchers began to 
investigate this possibility from many angles.
 
Today, psychophysical (Neitz & Jacobs, 1990; Mollon, 1992), 
microspectrophotometric (Dartnall, Bowmaker, & Mollon, 1983), and molecular genetic studies 
(Nathans, Piantanida, Eddy, Shows, & Hogness, 1986; Winderickx et al., 1992) 
provide evidence of substantial variation in the number and spectral sensitivity 
of the cone types in the color-normal eye (also see Mollon, Cavonius, and 
Zrenner, 1998). The evidence now suggests the presence of three broad families of 
normally occurring cone photopigments. There is thought to be only one 
photopigment with a peak spectral sensitivity in the short wavelengths (blue), but 
there is now evidence that there are multiple middle wavelength (green) 
photopigments and multiple long wavelength (red) photopigments. The difference in 
spectral sensitivity among the middle wavelength pigments or among the long 
wavelength pigments has been estimated to be approximately 5-7nm(Neitz, Neitz, & 
Jacobs, 1995). In fact there may be as many as 9 different cone types with various 
peaks in photosensitivity among the middle and long wavelength families. 

Molecular genetic analyses show that individuals may inherit a surprisingly 
large number of different X-linked, recessive genes that encode the production 
of these photopigments (Neitz, Neitz, & Grishok, 1995). An obvious question is 
why do we have so many color vision genes? The genes that encode the middle 
and long wavelength sensitive pigments reside near the end of one of the arms 
of the X chromosome and they have very similar DNA sequences. In fact, the 
substitution of one amino acid in the DNA of a photopigment gene is sufficient to 
cause a change in the spectral sensitivity of that photopigment and in our 
color perceptions. The location and similarity of these genes makes them 
susceptible to the kinds of genetic errors that produce multiple gene copies, as well 
as hybrid genes that are genetic composites of the original ones (Nathans, et 
al., 1986).  

At present, it appears that normal color vision results from inheriting at 
least one cone type from each cone class (short, middle, and long). It is 
unclear, however, which complement of genes and cone types result in specific types 
of color vision deficiency. There is a great deal of genetic variation among 
individuals with the same type of color defect, making this work difficult. 
However, it appears that both the type and severity of a color vision defect can 
be linked to the complement of different cone types in the retina. Hybrid 
genes, which have been associated with small differences in the spectral 
sensitivity of the photopigments, are thought to be involved.
 
These findings lead to an interesting question: if humans possess more than 
three cone types in their retina, do they still have trichromatic vision? The 
answer appears to be yes, presumably because the outputs of the different 
middle or longwavelength cone photoreceptors are summed together before leaving the 
retina. The resulting signals differ to a small but significant degree across 
individuals, though, because they affect color perception in some situations. 
Individuals with different complements of cone pigments will not accept each 
other's color matches in the long wavelength end of the spectrum and they will 
disagree on color names for certain wavelengths of light (Neitz, Neitz, & 
Jacobs, 1993). For example, a particular mixture of red and green light might 
appear a perfect yellow to your eye, but appear a greenish-yellow or slightly 
orange to someone else. This type of color vision assessment, called the Rayleigh 
Match, is the most accurate method for measuring color discrimination and 
diagnosing the congenital color vision defects.

The distribution of photoreceptors in the retina appears to be nearly random. 
The ratio of R / G / B cone types varies, but the long wavelength cones are 
the most prevalent; short wavelength cones the least prevalent in the retina.
Women who are heterozygous for the normal complement of color vision genes, th
erefore, may have a mosaic retina: a patchwork of color-normal and 
color-deficient regions (Cohn, Emmerich, & Carlson, 1989). The nature of this mosaic 
depends on the inherited complement of color vision genes and on the point in 
development that X-chromosome inactivation occurred. That is, some women 
heterozygous for these genes may develop a color vision deficiency while others may 
develop normal color vision (Miyahara, Pokorny, Smith, Baron, & Baron, 1998). 
And, in fact, there are reports in the literature of identical (monozygotic) 
twins where one twin has normal color vision and the second is color-deficient 
(Jorgenson, et al., 1992).
 
In light of these current findings, sensory psychologists and other 
perception researchers are designing psychophysical tasks to try to tease apart the 
nature of color processing in the eyes of individuals with different complements 
of cone photoreceptors. The challenge will then fall to neuroscientists, 
molecular biologists, and others to support or refute these findings at the 
cellular level.
 
Future work for sensory psychologists will also involve investigating the 
extent to which these individual differences in color vision affect interactions 
with the world. Society uses color to code information in a variety of 
settings, including art. photography, education and transportation. In many 
occupations color discrimination is critical, for example, in discriminating electrical 
wiring and colored signal lights or in medical research. While these 
individual differences are small, they may prove to be problematic in some settings.
 
In contrast to the research directed at the earliest stages of sensory 
processing, today there is also substantial exciting research interest at the other 
end of the S&P continuum: This research is directed at higher level perceptual 
processes and phenomena in the gray area where perception and cognition meld. 
Culture, desire, expectation, and learning are as important in determining 
what we see as the sensation itself. 

Larry Z
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