[Leica] Re: Trichromatic vision

[LRZeitlin@aol.com]

In a senior moment, I don't recall if I sent this post. If it a duplicate, I 
apologize for the wasted bandwidth.

Larry Z
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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, sensory 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.
Thus some people with a normal complement of color vision genes, 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 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 addition to teasing out the exact mechanism of color vision, work for 
sensory psychologists and physiologists also involves 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 sensation to perception 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. I suspect that this 
area is of greater interest to photographers than understanding the specific 
mechanism of color vision. In short, each of us sees color slightly differently 
and there are some colors that humans can see which cannot be duplicated by any 
trichromatic process using fixed primary colors.

Larry Z
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