出典(authority):フリー百科事典『ウィキペディア(Wikipedia)』「2015/08/21 23:27:50」(JST)
It has been suggested that this article be merged with achromatopsia. (Discuss) Proposed since January 2014. |
Monochromacy | |
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Monochromacy is a disease state in human vision, but is normal in pinnipeds (such as Neophoca cinerea shown here), cetaceans, owl monkeys and some other animals
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Classification and external resources |
Monochromacy (mono meaning one and chromo color) is, among animals, the condition of possessing only one type of cone cell for color vision, which results in a monochromatic-like (in most cases black and white) vision.[1][clarification needed]
Organisms with monochromacy are called monochromats. The perceptual effect of any arbitrarily chosen light from the visible spectrum can be matched by any pure spectral light.
Many species, such as all marine mammals, the owl monkey, and the Australian sea lion (pictured at right) are monochromats under normal conditions. However, in other mammal species, including humans, individuals having such vision are considered carriers of full color blindness disease. In humans that disease is called achromatopsia.[2]
There are two kinds of visual receptors in humans:
Rods outnumber cones by about 20 to 1 in the human retina, but cones provide about 90% of the brain's input.[3] Cones respond faster than rods, and have three types of pigments with different color sensitivities, where rods only have one and so are achromatic (colorless).[3] Because of the distribution of rods and cones in the human eye, people have good color vision near the fovea (where cones are) but not in the periphery (where the rods are).[3]
These types of color blindness can be inherited, resulting from alterations in cone pigments:[2]
Monochromacy can either be acquired or inherited:
Monochromacy is when the organism's retina contains only a single kind of light receptor cell, or that only one kind of light receptor is active at any particular level of illumination. Therefore, monochromacy is caused by either a defect or complete absence of the retinal cones.[2] As for humans who suffer from blue-cone monochromacy, or (BCM), research has shown through examining different families that BCM is inherited as an X-linked recessive trait.[4] Researchers also concluded through multiple studies in the human eye, that there are various pathways to mutation resulting in BCM. People who have red- or green-cone monochromacy,[clarification needed] which is a term used to encompass protanomaly, deuteranomaly, protanopia, and deuteranopia, both are X-linked recessive traits.[5]
Author J. W. Baird, also argues in his article "The Problems of Color Blindness" that color deficiency in the eyes is in fact transmitted by heredity. He also illustrates that color blindness can "result from certain traumatic conditions, disease, and from the action of chemical agents." [6] An injury or wound to the eye near the retina for example, where the rods and cones are located, could potentially cause color blindness even if that individuals' vision appears to be normal and images/objects still look "sharp". Finally, he concludes that color blindness can also be caused by "doses of santonin and of other drugs produce typical disturbances of color vision.[6] And it may be mentioned in this connection that a continuous chromatic stimulation, as when one sits in a colored illumination, reduces the sensitivity to that color, and hence produces an abnormal condition of color vision.[6]
Another way a form of color blindness can be acquired is through aging. As an individual becomes older, the pigment in the cones and rods weakens over time and it is possible to acquire a form of color blindness.
Since all monochromacy types are caused by the x-linked recessive trait including the most common type of color deficiency, the red–green color deficiency, caused by the gene deficiency on the X chromosome,[3] it explains why more men than women inherit one of the forms of monochromacy. Since boys are born with the chromosome makeup XY and girls with XX, it is much less likely for a girl to have a defect the same cone gene in both her X chromosomes than for a boy to have that gene defect in his lone X chromosome. However, it is also shown in research that women with one normal gene and one color-deficient gene (and that includes all women with a red-green color deficient father) are slightly less sensitive to red and green than the average for other people.[3]
Another important fact author J. W. Baird addresses about color blindness "is that color-blindness is a defect of color-sensing, not of color-naming." [6] In other words, individuals who have a form of color blindness mentally know what the names of the colors are but can not visually "sense" which colors are which depending on what form of color blindness he/she possesses. Baird explains an example of this in his article when he says, "The circumstance that one individual describes a certain spectral region as green or greenish, while another calls it blue or bluish, indicates nothing more than that, in the vocabularies of these two individuals, the same significance does not attach to these two color-names." [6]
Some individuals have diseases or injuries that lead to nyctalopia, or night blindness, where rod cells stop responding properly to light.
There are two basic types of monochromacy.[7][8] "Animals with monochromatic vision may be either rod monochromats or cone monochromats. These monochromats contain photoreceptors which have a single spectral sensitivity curve."[9]
In humans, who have three types of cones, the short (S or blue) wavelength sensitive, middle (M or green) wavelength sensitive and long (L or red) wavelength sensitive cones,[4] have three differing forms of cone monochromacy,[1] named according to the single functioning cone class:
Regardless of whether an individual has blue-, green-, or red-cone monochromacy, many patients with these forms of monochromacy have similar signs and symptoms: profoundly impaired color vision, poor visual acuity (about 6/60), nystagmus, photophobia, profoundly reduced sensitivity to long wavelength light and abnormal photopic electroretinographic responses.[5]
Another type of color vision deficiency that is the most common in humans is the red–green color deficiency. People with this deficiency have trouble distinguishing between the colors red and green because their long- and medium- wavelength cones have the same photopigment instead of different ones.[3] About 8% of men are red–green colorblind compared with less than 1% of women.[3]
According to author Baird, he identified a different stage of color blindness that forms before the complete transformation of Color Blindness. He calls this pre-stage color weakness which is "consisted in nothing more serious than a slight but uniform blunting of sensitivity to all colors."[6] He also adds that "the individual who suffers from 'color-weakness' is unable to pass even the least searching tests of color-blindness; and his abnormality is most strikingly revealed in the presence of reds and greens.[6]
It used to be confidently claimed that most mammals other than primates were monochromats. In the last half-century, however, evidence of at least dichromatic color vision in a number of mammalian orders has accumulated. While typical mammals are dichromats, with S and L cones, two of the orders of sea mammals, the pinnipeds (which includes the seal, sea lion, and walrus) and cetaceans (which includes dolphins and whales) clearly are cone monochromats, since the short-wavelength sensitive cone system is genetically disabled in these animals.[dubious – discuss] The same is true of the owl monkeys, genus Aotus.
Researchers Leo Peichl, Guenther Behrmann, and Ronald H. H. Kroeger report that of the many animal species studied, there are three carnivores that are cone monochromats: raccoon, crab-eating raccoon and kinkajou and a few rodents are cone monochromats because they are lacking the S-cone.[12] These researchers also report that the animal's living environment also plays a significant role in the animals' eyesight. They use the example of water depth and the smaller amount of sunlight that is visible as one continues to go down. They explain it as follows, "Depending on the type of water, the wavelengths penetrating deepest may be short (clear, blue ocean water) or long (turbid, brownish coastal or estuarine water.)" [12] Therefore, the variety of visible availability in some animals resulted in them losing their S-cone opsins.
Both rod and cone monochromacy occur as very rare forms of color blindness in humans. Rod monochromacy, or maskun, is the more common of the two. The majority of people described as color blind, however, are either dichromats or anomalous trichromats.
According to Jay Neitz, a renowned color vision researcher at the University of Washington, each of the three standard color-detecting cones in the retina of trichromats can pick up about 100 gradations of color. The brain can process the combinations of these three values so that the average human can distinguish about one million colors.[13] Therefore, a monochromat would be able to distinguish about 100 colors.[14]
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(help)For Further Reading:
Rossi, Ethan (February 2013). "Visual Function and Cortical Organization in Carriers of Blue Cone Monochromacy". PLoS ONE 8 (2): 1–17. doi:10.1371/journal.pone.0057956.
Weleber, Richard (June 2002). "Infantile and childhood retinal blindness: A molecular perspective (TheFranceschetti Lecture).". Ophthalmic Genetics 23 (2): 71–98. doi:10.1076/opge.23.2.71.2214. PMID 12187427.
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リンク元 | 「一色覚」「monochromatopsia」「1色覚」「全色盲」「単色性色覚」 |
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