More on the Vision Demonstration...
Text by Ann Randolph (2003)
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What is the Vision Demonstration?
The vision demonstration is a specifically made box that will show the human eye's sensitivity to different colors of the visible spectrum.
How the Eye Works
http://www.photo.net/photo/edscott/vis00010.htm , 8/3/01
To begin to understand how the vision box works, it is important to understand a little about how the eyes work. They are part of the central nervous system, the only part, in fact, that is open to the outside of the body. The human eye consists of three distinct layers of tissues: the sclera, the choroid, and the retina. The sclera is the inflexible white outer layer of the eye. In the front of the sclera is where the light first enters the eye through the cornea. The cornea is the bulge in the eye; it slows down light and bends it toward the center of the eye without scattering any of the light. The cornea is transparent and must remain so and therefore, unlike other parts of the body, the cornea does not get its nutrients from blood but from a transparent liquid called the aqueous humor. The aqueous humor is produced in the choroid and is replenished once each. The aqueous humor also has to keep a particular volume and pressure to ensure that the cornea's bulge is kept constant so the cornea's ability to bend light is is also conserved. The cornea bends light more at the center and less so where it meets up with the sclera. It therefore creates a distortion that is known as an aberration, to compensate for this aberration, the cornea flattens out as it meets the sclera.1
The inner surface of the sclera is known as the choroid, which supplies nutrients to the rest of the eye. The sclera also contains melanin. Melanin is the pigment which gives the skin and hair color. It also traps stray light that enters the eye. If melanin did not trap the stray light, then the image that our eyes produce would fade like a television picture does in the light of day. Right behind the aqueous humor is the lens that is surrounded by the iris. It is part of the choroid layer. The iris has the ability to make the pupil as large as one-third of an inch and as small as six-one-hundredths of an inch. Although the iris can come in many different colors, only one pigment is found here, melanin. When a baby is born, the melanin lies deep within the iris, thus giving the baby blue eyes, within a couple of months, the melanin will come up to the surface and give the iris a different color.1
As stated before, the iris surrounds the lens. The darkened surface of the lens is known as the pupil. The lens has the ability to change its thickness and shape. This ability is called accommodation and the ability to do this decreases with age. The lens is a layer of cells but it does not scatter light. The lens is held in place by the ciliary zonule which is attached to the choroid coat. The zonule stretches the lens and thus flattens the lens. The normal resting position of the lens is so that the eye is focused on objects that are further than twenty feet away. To be able to focus on an object that is closer than twenty feet, the zonule relaxes and then the lens bulges out. The lens grows with age with the older layers settling in the middle of the lens where they harden. The lens is also slightly yellow tinted that filters out ultraviolet light. As the lens gets older, the lens darkens, which should mean that geriatrics should see less blue and violet that red in this exhibit. After the lens is the the vitreous humor, which is the transparent liquid of the eye that hold the eyes shape.1
At last the light finally falls on the retina. The area in the retina that contains the color sensing photoreceptors is the fovea. In the fovea can be found the cones that give color vision and work during the day; the rest of the retina contains light sensing rods that are used for night vision. Rods only require one photon, particle of light, to make it send an electrical signal to the brain, while the cones need more light to fire a signal. Because the cones are only found in the fovea while the rods are found on the rest of the retina, there are about eighteen times more rods than cones. The only part of the retina that is not composed of photoreceptors is where the optic nerve leaves the eye and heads towards the brain. The optic nerve is responsible for the the blind spot in vision. If a person is trying to focus on an image whose image is projected onto the optic nerve, the image will not be seen.1
Before more is learned about how an image is seen, it is important to learn how the rods and cones function and thus create an image. There are three types on cones in the eyes: red (r), green (g), blue (b). The red cones, that make up about 64% of the cones2, pickup light with a wavelength between 475nm and 700nm1, peaking about 580nm3. The green cones, that make up about 32% of the cones2, pickup light with a wavelength between 435nm and 635nm1, peaking about 540nm3. Blue cones, that make up only 2% of the cones2, pickup light with a wavelength between 400nm and 550nm1, peaking about 450nm3. These peaks can be seen in the following graph is a representation of the different cones sensitivities to different wavelengths of light.
The color spectrum for cones only.
http://www.photo.net/photo/edscott/vis00010.htm , 8/3/01
The name of the pigments in the red, green, and blue cones are respectively erythrolabe, chlorolabe, and cyanolabe. Each one of these pigments is a different variety of the protein opsin. In the rods and cones, the different varieties of opsin bind to vitamin A creating erythrolabe, chlorolabe, cyanolabe, and rhodopsin in the rods. Vitamin A enters the body through food that is eaten. It then is sent to the choroid layer where it is bound to the four different types of opsins. Before it binds to the opsins, vitamin A is a straight chain. When vitamin A binds to the opsins, it is forced to bend around the proteins. When a photon hits the pigments in the rods and cones, it snaps back into a straight chain, thus disrupting the electrical signals in the photoreceptors, thus sending an impulse to the brain.1
Once the rods and cones have been stimulated, the signal is sent to the bipolar cells and then sent to the ganglion cells before the optic nerve is signaled. Once the optic nerve has been stimulated, the impulse travels through the optic chiasm and then to the visual cortex where the optic nerves from both eyes split into two pieces. Each eye sees both a left field of view and a right field of view. From each eye, the information from the left field of view from both eyes goes to the right side of the brain, and visa versa. This semi-crisscrossing of the optical nerve is what gives humans the ability to see in 3D. Then the signals are sent to the lateral geniculte nuclei and then the striate cortex where spatial organization, shapes, brightness and shading are processed. From there signals go to several different places including the temporal lobes, superior colliculus, and the cerebral cortex.1
http://www.photo.net/photo/edscott/vis00010.htm , 8/3/01
There are several other things about the eye that are interesting about that should be known. Each cone has its own bipolar and ganglion cells while each rod has to share the bipolar and ganglion cells with four other rods. This means that the for the bipolar and ganglion cells to send a signal to the optic nerve, five rods right next to each other have to fire simultaneously. The cones, as stated previously, are used during the day for photopic vision4, while the rods are used for night vision which is known as scotopic vision4. Going from photopic to scotopic vision is called adaption. Within the first minuet of adaption, the eye is ten times more sensitive to light, more willing to have rods fire. At the twenty minuet mark, the eye is six thousands times more sensitive to light, and at the forty minuet mark, the eye peaks in sensitivity at thirty thousand times more sensitive than it was in light. The pupil, however, only has the ability to increase the eyes sensitivity by thirty times from going from its minimum diameter to its maximum.1
The eyes also have seven distinct types of movements. The first type of movement is due to the three pairs of eye muscles competing for eye-movement thus causing the eye to tremble and the eye movement called tremors. The second type of eye movement is called drift because it cause an image to drift off center so that all the pigments in the rods or cones that are being used is not used up. The third type of movement is used to correct the drift movement; this third movement is called flick because it flicks the image back to the center of the fovea. The fourth movement is smooth pursuit which is used when someone sees and tracks a moving object. The next eye movement is called saccadic and is used when the eye darts from one place to another such as reading a paragraph. Saccadic movement is also used during REM sleep. Another type of eye movement is called vergence and it gives humans the ability to turn the eyes inward and focus an image on the foveas that are really close to the face. The last type of eye movement is called vestibulo and is is used when something comes into the peripheral vision and it keeps the image on the foveas while the head and the body catches up with the eyes.1
Colorblindness
In some cases, the cones in the do not function properly and therefore, the person has some sort of color deficiency; in most cases though, the viewer is not color blind. Color vision problems are caused by a few things. Two of problems can be either the cones have something wrong with them (either the photopigments are not produced in the correct cones, the photopigments are not produced at all) or the cones are missing completely1. The reason that something is wrong with the color vision is due to the person's genes. The gene for rhodopsin can be found on the third chromosome. If you are looking for the gene for the blue cones it can be found on the seventh chromosome. The red and green cone information can be found the the X chromosome; one can find one gene for the erythrolabe pigment and several for the chlorolabe pigment. The red and green genes are about 96% identical which means that they are relatively new genes.5
This is important to know because it means that the red/green cones are somewhat gender related. What is meant by this is that because the defective gene is recessive, males are more likely to be red/green color deficient because their Y chromosome cannot carry a dominate gene to override a color deficient gene that their mother has passed on to them. About 8% of the male population in the United States has some type of color deficiency while only about 0.64% of the female population has color vision problems.1
The different types of color blindness are protanopia, deuteranopia, tritanopia, anomalous trichromacy, and monochromacy. The first three are due to when the red, green, or blue photopigments are missing. Protanopes, deuteranopes, and tritanopes are usually referred to as dichromates meaning that they see two colors. Monochromacy is present when an individual has no working cones or only one of them has photopigment. This individual will not see colors, he is truly color blind. The anomalous trichromate has all three photopigments but one of them is not working properly. The anomalous trichromate will see colors slightly differently than the normal viewer.5
Conclusion
We were very satisfied with the working of the vision box. There are still some slight modifications that we would like to add. One of the things that we would like to accomplish is to be able to have someone look through an eye piece and be able to see various wavelength scaling of the spectrum. We would also like to be able to make an eyepiece that would separate the individual colors and that would contain a scale (1-10) so that the viewer can measure the height of each color that he sees relative to each other.
Simulated picture of sensitivity of visible spectrum: http://www.photo.net/photo/edscott/vis00010.htm , 8/3/01
Works Cited
1. Vertenbaker, Lael. "The Human Body: The Window to the World." US News and World Report, Inc. Washington DC. 1981.
2. http://hyperphysics.phy-astr.gsu.edu/ hbase/vision/colcon.html 7/20/01
3. http://www.photo.net/phot/edscott/vis /vis.00010htm 7/20/01
4. http://www.arce.ku.edu/book/eye/ sensitiv/htm 7/20/01
5. McIwain, James T. "An Introduction to the Biology of Vision." Cambridge University Press. UK. 1996.