1. Vision – 4 Color Vision
Dr. Salah Elmalik

2. Objectives
Define color vision Identify and describe the mechanism of color vision and the three types of cones, including the range of spectral sensitivity and color blindness
Identify color vision theory
Describe the items needed for any color perception Compare different types of color blindness

4. Color Vision It the ability to discriminate between different colors.
1- there are 3 primary colors( blue- red- green) sensed by cones in fovea & appreciated within photopic vision.
2- sensation of extraspectral colors as white, yellow, orange, purple, can be produced by mixing properties of the blue &red & green in different combinations.
3- black means absence of light ( not darkness because in dark we do not see black only)

5. Color (Photopic) Vision
‘Young - Helmholtz theory’
‘The Trichromatic theory’

6. Color vision theory :_( Young- Helmholtz theory )
1- we have 3 kinds of cones each has a specific photopigment (iodopsin)& is sensitive to one of the 3 primary colors
a- Blue cone system:- has S pigment ( blue sensation pigment) which respond to short wave length ( 440 nm senses the blue color)
b- Green cone system:- has M pigment ( green sensation pigment) which respond to middle wave length ( 535 nm senses the green color & less to yellow) & absorb light at the green portion.

7. Red cone system:- has L pigment ( red sensation pigment) which respond to large wave length at or > 535 nm so senses the red & yellow color & absorb light at the red portion.

10. History of color vision
Newton (1704) used a prism to show that sunlight was composed of light with all colors in the rainbow. He defined it as the spectrum.

11. Mixing colors

12. Photopic vision (CONES)
Helmholtz :
The three primary colors are perceived by three photoreceptor pigments (with broad absorption curves)
White light is produced by mixing three colours

13. Cone wavelength rangesM L
Relative absorption
400
500
600
700
Wavelength (nm)

14. Photopic vision (CONES)
Cone pigments: three kinds
565
535
440

15. Cone wavelength rangesM L
Relative absorption
400
500
600
700
Wavelength (nm)

16. Photopic vision Sensation of any color determined by:
a-wavelength of light
b-amount of light absorbed by each type of cones
c-frequency of impulses from each cone system to ganglion cells which is determined by wave length of light.

17. (white is a combination of all wave lengths)
Photopic vision
perception of white is due to:
equal stimulation of
blue & red & green cones.
(white is a combination of all wave lengths)

19. Color vision is coded by :-
different responses in ganglion cells that depends upon the wave length of stimulus which determine frequency of impulses in ganglion cells
the color perception in the brain depends on the amount of activity in each of the 3 cone systems as mentioned above.

20. Color Perception
Perception of orange is due to stimulation of 99% of red cones & 42% of green cones & 0% of blue cones( so ratio is 99:42: 0)
For perception of yellow the ratio is 83:83: 0.
Perception of blue is due to stimulation of 0% of red cones & 0% of green cones & 97% of blue cones( so ratio is 0:0: 97 )

22. Ishihara Charts

23. Color Blindness
Weakness or total blindness in detecting a primary color:
Definitions:
Trichromats: see the 3 1ry colors
Dichromats: blind to one 1ry color
Monochromats: have only one color pigment

24. Color Blindness –cont.
Prot …… Red
Deuter …. Green
Trit …… Blue
Anamoly …weakness
Protanamoly
Deuteranamoly Trichromats
Tritanamoly

25. Color Blindness –cont.
Anamoly …weakness
Anopia …. Total loss
Protanopia
Deuteranopia Dichromats
Tritanopia

26. COLOR BLINDNESS Red – Green Blindness:-
Green & red cones see different colors between wave length nm & distinguish them.
If either of these cones are absent, the person can not distinguish 4 colors ( red – green- yellow- orange)& he can not distinguish red from green (primary colors) so called ( red – green blindness).

27. Trichromatic/dichromatic color vision
In its most severe forms, colorblindness is caused by the absence of one of the cone visual pigments. Shown here, the spectral sensitivities of the cone pigments in color normal trichromats are compared with those of a color blind person. Also compare the spectrum as it appears to a color normal person with the illustration of how it might look to a red-green color blind person.
Red-green color blindness is common--about 4-5% of the population (8-10% men red-green colorblind).
Dichromats – missing one whole group of photopigments (cat and dogs – dichromats)
a. Missing M pigments = deuteranopes
b. Missing L pigments = protanopes
Monochromats – missing two groups of photopigments
Moderate colorblindness – anomolous trichromats; 3 different color pigments but from only 2 of the photopigment groups
a. 2 different L-type pigments = deuteranomalous
b. 2 different M photopigments = protanomalous
More information on this topic can be found elsewhere (Nathans et al., 1992; Sharpe et al., 1998; Sharpe et al., 1999; Stockman et al., 2000).
Here, we provide a brief summary of those areas that are relevant to cone spectral sensitivity measurements made in dichromats in order to determine the
"normal" M- and L-cone spectral sensitivities.
Persons with red-green defects have difficulty distinguishing between reds, greens and yellows but can discriminate between blues and yellows. Protanopes often can name red and green correctly because green looks lighter to them than red.
The M- and L-cone photopigment genes lie in a head to tail tandem array on the q-arm of the X-chromosome. Each gene consists of six coding
regions, called exons, which are transcribed to produce the opsin. Because the M- and L-cone photopigment genes are highly homologous and adjacent
to one another, intragenic recombination between them is common and can lead to the production of hybrid or fusion genes, some of which code for
anomalous pigments. Each hybrid gene can be identified by the site, usually between exons, at which the fusion occurs. For example, L3M4 indicates a
hybrid gene in which exons 1 to 3 derive from an L-cone pigment gene and exons 4 to 6 from an M-cone pigment gene. Because exons 1 and 6 in the L-
and M-cone pigment genes are identical, a L1M2 hybrid pigment gene encodes a de facto M-cone photopigment.
The classification of hybrid genes, and genes in general, is complicated by polymorphisms in the normal population, the most common of which is the
frequent substitution of alanine by serine at codon 180 in exon 3. Of 304 genotyped Caucasian males, we estimate that 56% have the serine variant
[identified as L(S180)] and 44% the alanine variant [identified as L(A180)] for their L-cone gene (see Table 1, which summarizes data from Winderickx
et al., 1993; Neitz & Neitz, 1998; Sharpe et al., 1998; and from Schmidt, Sharpe, Knau & Wissinger, personal communication).
The L-cone polymorphism, and its distribution in the normal population, must be considered when estimating the "normal" L-cone spectral sensitivities.
In contrast, the M(A180) versus M(S180) polymorphism for the M-cone pigment is much less frequent: 94% (Winderickx et al., 1993) or 93% (Neitz
& Neitz, 1998) of males have the M(A180) variant.
The spectral sensitivity of the photopigment that is encoded by the L2M3(A180) hybrid gene is practically indistinguishable from the photopigment
encoded by the normal M(A180) [(or L1M2(A180)] cone pigment gene, its lmax being only 0.2 nm (Merbs & Nathans, 1992) or 0.0 nm (Asenjo, Rim
& Oprian, 1994) or insignificantly different (Sharpe et al., 1998) from that of the M(180) cone pigment. Thus, spectral sensitivities from protanopes
carrying either L1M2(A180) or L2M3(A180) genes in their opsin gene array can be reasonably combined to estimate the normal M-cone spectral
sensitivities, as was done by Stockman and Sharpe (2000).
Dichromats with single photopigment genes in the M- and L-cone pigment gene array [e.g., L(A180), L(S180), L1M2(A180) or L2M3(A180)] are
especially useful for measuring normal cone spectral sensitivities, since they should possess only a single longer wavelength photopigment. Dichromats
with multiple photopigment genes are less useful, unless the multiple genes produce photopigments with the same or nearly the same spectral sensitivities:
for example, L1M2(A180)+M(A180) or L2M3(A180)+M(A180).
Trichromatic/dichromatic color vision

28. Color Blindness –cont.
It is x- linked disease transmitted from females to their male sons, never occure in females as they have 2 x chromosomes –
Males have one x & one y chromosome so if this one x chromosome miss the gene for color vision , he will get red-green color blindness(their gene is on x chromosome). –
Females show the disease only if both x chromosomes lack the gene –
Females from color blind fathers are carriers transmit the disease to ½ of their sons.