Teacher Information
Commonly Asked Questions
on
Vision and Color Perception
Lynda Jones and Linda K. Ellis
Overview
Students commonly ask questions about vision and color perception which may be difficult to answer without taking the time to look them up. This module contains a list of questions which often arise when biology students are studying the nervous system. They have been researched and are presented as a quick reference for teachers when teaching this unit.
Biological Concept
The synthesis, structure and function of rhodopsin.
The relationship between the different wavelengths of visible light and color.
Color vision and color blindness.
How molecules change color.
Night vision and night blindness.
Background Information
Q. How is reflected light converted into a visual image?
A. Photons of light which enter the eye strike photoreceptor cells in the retina. Rod cells are a type of photoreceptor cell which responds to dim light. These cells contain molecules of rhodopsin, which have two major components. One of these components is a protein called opsin and the other is an aldehyde derivative of Vitamin A, retinal. Retinal exists in several conformational forms, two of which are important in vision. The 11-cis retinal is a bent molecule. When rhodopsin absorbs a photon with just the right amount of energy, 11-cis retinal is isomerized to the all-trans form, which has a straight carbon chain. This all-trans form dissociates from the opsin, triggering a change in the permeability of the membrane which ultimately leads to depolarization of neurons in the retina. The resulting signal is carried to the brain via the optic nerve. This signal is passed along several circuits in the brain where its integration and interpretation occur. The result is what we know as a visual image.
Q. How do we see color?
A. Color perception can occur in several ways. A sample may absorb all visible wavelengths (from 400 to 700 nm on the electromagnetic spectrum) and appear black since no color reaches the eye. A sample may absorb no visible wavelengths so the eye sees the sample as white. A sample may absorb all visible wavelengths but one and that wavelength is the color seen as it is reflected back (as in green plants or red apples). On the other hand, a sample may absorb only one wavelength (say orange-red) and the sample would be perceived as blue, its complementary color (as in blueberries).
Violet, 400-420 nm (410-pure color), is the complement of Yellow, 580-590 nm (580 nm).
Blue, 420-490 nm (470 nm), is the complement of Orange, 590-650 nm (600 nm).
Green, 490-580 nm (520 nm), is the complement of Red, 650-700 nm (650 nm).
In order to stimulate a photoreceptor cell, light must be absorbed and the light-absorbing group must change shape after it absorbs the photon. Rods and cones contain 11-cis-retinal, a form of vitamin A. In the various cells, the retinal is associated with different proteins that, in turn, determine which wavelength of light is absorbed. In rods, retinal is attached to an opsin protein to form rhodopsin; this complex absorbs light at a peak of 500 nm, reflecting light in the 400 nm range (blue) and 600 nm range (red). It is referred to as "visual purple". Cones contain retinal attached to slightly different opsin-related proteins; one complex absorbs at a peak of 455 nm, one at 530 nm, and one at 625 nm, appearing blue, green, and red (orange-red), respectively. They are referred to as SW, MW, and LW opsin, for short, medium, and long wavelengths. These molecules are, themselves, pigmented, as are all molecules which absorb only certain wavelengths of visible light.
Q. How does one perceive colors other than red, blue, and green?
A. "All a single cone can do is capture light and tell you something about its intensity; it tells you nothing about color". (Jeffrey Nathans, Johns Hopkins University School of Medicine) To see different colors, the brain compares input from other kinds of cones. The color of an object isn't determined in isolation, but is derived from a comparison of wavelengths from the object and its surroundings. Like the screen on a television set, these colors can combine to create all of the colors we see.
Q. Why do our eyes have to adjust when we go from a brightly lighted area to a dim area?
A. In the presence of bright light, a great many of the rhodopsin molecules are dissociated and it takes a little time for them to be regenerated. In the reduced light, there are fewer photons and with fewer rhodopsin molecules, the probability of a photon-rhodopsin interaction is greatly reduced. After a minute or so, enough rhodopsin is regenerated to make normal vision possible. Under average conditions, the amount of light striking the retina is regulated by opening and closing the pupil. In very bright light, the system can be overwhelmed. This is quite obvious when one tries to read outside in bright sunlight; sun glasses can help solve this problem.
Q. Does everyone see color the same way?
A. Most people do, but there are exceptions. The best known exception is color-blindness. People with normal color vision are said to be trichromatic; that is, their cone cells are sensitive to the light of three colors - red, green, and blue. The genes which code for the red and green colors are found on the X chromosome. The gene for the blue opsin is found on chromosome #7 and rhodopsin is found coded on chromosome #3. The variation in color vision that is commonly referred to as colorblindness arises from the loss of either the red or the green cone pigment (dichromacy) or from the production of a pigment with a slightly altered absorption peak (anomalous trichromacy). These red-green pigment genes are organized in a head-to-tail tandem arrangement with 98% homology. This predisposes them to homologous but unequal recombination. The hybrid proteins which result have considerable variation in absorption properties.The relatively high frequency of these defects in males (approximately 2% for dicromacy and 6% for anomalous trichromacy) is not surprising considering the X chromosome location of these genes. It is apparently very rare for anyone to be colorblind for blue.
Q. Is it possible for a person to be totally colorblind?
A. The complete absence of color vision is very rare, affecting only about l person in 30,000. If both the red and green cone sensitivities are lacking, blue cone monochromacy results. Defects in the blue cone pigment gene are inherited as an autosomal dominant trait, with incomplete penetrance.
Q. How did color vision evolve?
A. Recent studies indicate that there was probably one gene for photopigment protein in the earliest ancestors of primates. This ancestral rhodopsin gene may have undergone duplications resulting in multiple copies of the gene. This is seen today in many of our genes, including the red/green photopigment genes on the X chromosomes. Over time, changes in the DNA could result in the production of molecules with different absorption properties. Additional duplications and divergence (resulting from the splitting of large chromosomes or the union of small ones) would disperse these new genes resulting in their present locations.
Q. Do all animals see in color?
A. Much is known about color vision in various animals from studies of the microanatomy of their retinas. Color vision is found in all vertebrate classes, but not in all species. Nocturnal animals have many rods which function well in low light, but do not perceive color. More light is required to stimulate cones which explains why these receptors do not function at night. While many mammals can see colors, they may not rely on it as much as humans and other primates. Most are nocturnal; therefore, maximizing the number of rods is an important adaptation. Cats have limited color vision, although only at close range. Scientists seem to disagree about the perception of color in dogs. Fishes, amphibians, reptiles, and birds have well-developed color vision. In many animals, the ability to detect small movements is far more important to them than color. In others, such as butterflies, photosensitive pigments absorb in the ultraviolet ranges, causing them to see flowers as brightly glowing objects where we see only a light pinkish-purple color. Desert rattlesnakes have specialized organs which receive infrared signals, converting these to images. This is very handy when one has to find prey in the dark.
Q. What causes a substance to change color? For example, why does blood change from a bluish-red to a crimson-red when it picks up oxygen?
A. When oxygen binds to the Fe+2 in the hemoglobin molecule, changes in the d orbitals of this transition metal occur. This change alters the absorption properties of the molecule very slightly, resulting in the reflection of light of a slightly different color. Another very useful example of color change is found in acid/base indicators. In these molecules, the addition or removal of hydrogen ions result in a molecule which has different color properties. In the presence of acids (excess H+1), the phenolphthalein molecule is colorless, as all the light which strikes it passes through. However, when the pH increases, it loses H+1 and the resulting molecule is a bright magenta color. In most cases, changes in color indicate chemical changes, as a new substance with different properties has formed.
Q. What is meant by "night blindness"?
A. With plenty of light available, a person's vision in daylight might be normal, but at night, when light is scarce, that same person might have difficulty. This is because a person's ability to see at night depends on both the number of rod cells and the availability of rhodopsin. The retinal part of the rhodopsin molecule is synthesized from Vitamin A. Either a diminished amount of rods which occurs in certain diseases, such as retinitis pigmentosa, or a deficiency of Vitamin A can lead to night blindness. An early symptom of inherited retinitis pigmentosa is impaired night vision and eventually the affected person will go totally blind by age 40. The defect was mapped by Peter Humphries at Trinity College in Dublin, Ireland, and was found to be in the same region of chromosome #3 as the rhodopsin.
Q. How do the night vision instruments work?
A. These "night scopes" work by intensifying light and converting it to an electronic image on a screen. They are very sensitive to minute amounts of ambient light from visible through infrared. They can gather light, such as starlight, which is focused on an image intensifier, converting the light energy of the photons to the electrical energy of electrons. Each photon can be converted into between 1000 and 30,000 electrons. These electrons strike an electron multiplier and ultimately strike a phospor screen where we see the image.
Q. How do nocturnal animals see at night?
A. In addition to having a large number of rod cells, nocturnal animals have eyes which are very good at collecting every photon. In owls, this includes having a huge retina (their eyes are very large, relative to the skull). Many animals have a special reflecting membrane behind the retina which reflects photons that have missed hitting a rod cell. This membrane, called the tapedum lucidum, is responsible for the glow you see in an animal's eyes when bright light, such as from automobile headlights, shines on them.
Q. Why was the tail of the recent comet (Kahoutek) much more visible when one viewed it out of the corner of the eye?
A. Rods and cones form an uneven mosaic within the retina and, except for the center of the retina, the rods outnumber the cones by 10 to 1. Although the fovea is essential for sharp vision, it is less sensitive to light than the surrounding retina because rods are completely absent. Rods are found in the greatest density at the lateral regions of the retina. In order to detect the faint tail of the comet at night, a side glance at it projected the image onto the more sensitive rods since the light reflected from the comet was insufficient to trigger cones into action. This is true for any dimly lighted object viewed in the dark.
Extensions/Variations
Many of the discussions with students about their questions will generate additional questions which can be researched by students and added to this list.
Resources
Atkins, P. W., Molecules, Scientific American Library, 1987.
Brown, Theodore L., & LeMay, H. Eugene, Chemistry, The Central Science, 4th Edition, Prentice Hall, 1988.
Campbell, Neil A., Biology, 2nd Edition, The Benjamin/Cummings Publishing Co., Inc., 1990.
Kandel, E.R., Schwartz, J.H., Principles of Neural Science, Elsevier/North-Holland 1982.
Matthews, E. R., "Night Vision and Birding", 1996 Optics for Birding Home Page, http://www.aib.com:~edm/optics/night.html.
Montgomery, Geoffrey, "Breaking the Code of Color" and "A Narrow Tunnel of Light", from "Seeing, Hearing, and Smelling the World", A Report from the Howard Hughes Medical Institute, 1995.
Nathans, J. ,"In the Eye of the Beholder:Visual Pigments and Inherited Variation in Human Vision", Cell, 1994, Aug 12 78 (3): 357-60.
Office of Public Affairs, The University of Texas-Houston Health Science Center, "UT-Houston Scientists Discover How Color Vision Evolved", http://www.uth.tmc.edu/uth_orgs/pub_affairs/news/releases/li.html.
Sieving, P. A., et al., "Dark-Light: Model for Nightblindness from the Human Rhodopsin Gly-90 --> Asp Mutation", Proceedings of the National Academy of Science, USA, 1995, Jan 31 92 (3): 880-4.
Stryer, Lubert, Biochemistry, 3rd Edition, W. H. Freeman & Co., 1988.
Tovee, M. J., "Colour Vision. Dalton's Eyes and Monkey Genes", Current Biology, 1995, Jun 1; 5 (6): 583-6.
About the Authors
Lynda Jones is a science teacher at Catlin Gabel School in Portland, Oregon. Lynda can be contacted at Catlin Gabel School, 8825 S.W. Barnes Road, Portland, Oregon 97225 or by e-mail at jones@catseq.catlin.edu.
Linda K. Ellis is the Director of the Secondary Programme at the International School of Grenada in Grenada, West Indies. Linda can be reached at the International School of Grenada, P.O. Box 744, St. George's, Grenada, West Indies or by e-mail at bmcs@caribsurf.com.