Monochromacy

Monochromacy
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.
SpecialtyOphthalmology

Monochromacy (from Greek mono, meaning "one" and chromo, meaning "color") is the ability of organisms or machines to perceive only light intensity, without respect to spectral composition (color). Organisms with monochromacy are called monochromats.

For example, about 1 in 30,000 people have monochromatic vision because the color-sensitive cone cells in their eyes do not function. Affected people can distinguish light, dark, and shades of gray but not color.

Many species, such as marine mammals, the owl monkey and the Australian sea lion (pictured at right) are monochromats under normal conditions. In humans, absence of color discrimination or poor color discrimination is one among several other symptoms of severe inherited or acquired diseases, as for example inherited achromatopsia, acquired achromatopsia or inherited blue cone monochromacy.

Humans

Vision in humans is due to a system that includes rod and cone photoreceptors, retinal ganglion cells and the visual cortex in the brain. Color vision is primarily achieved through cone cells. Cone cells are more concentrated in the fovea centralis, which is the central portion of the retina. This allows greater spatial resolution and color discrimination.

Rod cells are concentrated in the periphery of the human retina. Rod cells are more light sensitive than cone cells, and are mainly responsible for scotopic (night) vision. Cones in most humans have three types of opsins with different spectral sensitivities which allow for trichromatic color discrimination, whereas rods all have a similar, broad spectral response which does not allow for color discrimination. 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).[1]

These types of color blindness can be inherited, resulting from alterations in cone pigments or in other proteins needed for the process of phototransduction:[2]

  1. Anomalous trichromacy, when one of the three cone pigments is altered in its spectral sensitivity but trichromacy (distinguishing color by both the green-red and blue-yellow distinctions) is not fully impaired.
  2. Dichromacy, when one of the cone pigments is missing and colour is reduced to the green-red distinction only or the blue-yellow distinction only.
  3. Monochromacy, when two of the cones are not functional. Vision reduced to blacks, whites, and greys.
  4. Rod monochromacy (achromatopsia), when all three of the cones are non functional and light perception is achieved only with rod cells. Color vision is heavily or completely impaired, vision reduced to seeing only the level of light coming from an object. Dyschromatopsia is a less severe type of achromatopsia.

Monochromacy is one of the symptoms of diseases that occur when only one kind of light receptor in the human retina is functional at a particular level of illumination. It is one of the symptoms of either acquired or inherited disease as for example acquired achromatopsia, inherited autosomal recessive achromatopsia and recessive X-linked blue cone monochromacy.[3][4][5][6]

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]

  • Rod monochromacy (RM), also called congenital complete achromatopsia or total color blindness, is a rare and extremely severe form of an autosomal recessively inherited retinal disorder resulting in severe visual handicap. People with RM have a reduced visual acuity, (usually about 0.1 or 20/200), have total color blindness, photo-aversion and nystagmus. The nystagmus and photo-aversion usually are present during the first months of life, and the prevalence of the disease is estimated to be 1 in 30,000 worldwide.[10] Additionally, since patients with RM have no cone function and normal rod function,[10] a rod monochromat cannot see any color but only shades of grey.
  • Cone monochromacy (CM) is the condition of having both rods and cones, but only having one functioning type of cone. A cone monochromat can have good pattern vision at normal daylight levels, but will not be able to distinguish hues.

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[11] have three differing forms of cone monochromacy, named according to the single functioning cone class:

  1. Blue cone monochromacy (BCM), also known as S-cone monochromacy,[3][4] is an X-linked cone disease.[12] It is a rare congenital stationary cone dysfunction syndrome, affecting less than 1 in 100,000 individuals, and is characterized by the absence of L- and M-cone function.[13] BCM results from mutations in a single red or red–green hybrid opsin gene, mutations in both the red and the green opsin genes or deletions within the adjacent LCR (locus control region) on the X chromosome.[3][4][10]
  2. Green cone monochromacy (GCM), also known as M-cone monochromacy, is a condition where the blue and red cones are absent in the fovea. The prevalence of this type of monochromacy is less than 1 in 1 million.
  3. Red cone monochromacy (RCM), also known as L-cone monochromacy, is a condition where the blue and green cones are absent in the fovea. Like GCM, RCM is also present in less than 1 in 1 million people. Animal research studies have shown that the nocturnal wolf and ferret have lower densities of L-cone receptors.[14]
  • Cone monochromacy, type II, if its existence were established, would be the case in which the retina contains no rods, and only a single type of cone. Such an animal would be unable to see at all at lower levels of illumination, and of course would be unable to distinguish hues. In practice, it is hard to produce an example of such a retina, at least as the normal condition for a species.

Animals that are monochromats

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 marine 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. The same is true of the owl monkeys, genus Aotus.

A recent study using through PCR analysis of genes OPN1SW, OPN1LW, and PDE6C determined that all mammals in the order Xenarthra (representing sloths, anteaters and armadillos) developed rod monochromacy through a stem ancestor.[15]

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.[14] 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.)" [14] Therefore, the variety of visible availability in some animals resulted in them losing their S-cone opsins.

Monochromat capability

According to Jay Neitz, a color vision researcher at the University of Washington, each of the three standard color-detecting cones in the retina of trichromats can detect approximately 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.[16] Therefore, a monochromat would be able to distinguish about 100 colors.[17]

See also

References

  1. ↑ Kalat, James (2013). Biological Psychology. Jon-David Hague. p. 158. ISBN 978-1-111-83100-4.
  2. ↑ Neitz, J; Neitz, M (2011). "The genetics of normal and defective color vision". Vision Res. 51 (7): 633–651. doi:10.1016/j.visres.2010.12.002. PMC 3075382. PMID 21167193.
  3. 1 2 3 Nathans, J; Davenport, C M; Maumenee, I H; Lewis, R A; Hejtmancik, J F; Litt, M; Lovrien, E; Weleber, R; Bachynski, B; Zwas, F; Klingaman, R; Fishman, G (1989). "Molecular genetics of human blue cone monochromacy". Science. 245 (4920): 831–838. doi:10.1126/science.2788922. PMID 2788922.
  4. 1 2 3 Nathans, J; Maumenee, I H; Zrenner, E; Sadowski, B; Sharpe, L T; Lewis, R A; Hansen, E; Rosenberg, T; Schwartz, M; Heckenlively, J R; Trabulsi, E; Klingaman, R; Bech-Hansen, N T; LaRoche, G R; Pagon, R A; Murphey, W H; Weleber, R G (1993). "Genetic heterogeneity among blue-cone monochromats". Am. J. Hum. Genet. 53 (5): 987–1000. PMC 1682301. PMID 8213841.
  5. ↑ Lewis, R A; Holcomb, J D; Bromley, W C; Wilson, M C; Roderick, T H; Hejtmancik, J F (1987). "Mapping X-linked ophthalmic diseases: III. Provisional assignment of the locus for blue cone monochromacy to Xq28". Arch. Ophthalmol. 105 (8): 1055–1059. doi:10.1001/archopht.1987.01060080057028. PMID 2888453.
  6. ↑ Spivey, B E (1965). "The X-linked recessive inheritance of atypical monochromatism". Arch. Ophthalmol. 74 (3): 327–333. doi:10.1001/archopht.1965.00970040329007. PMID 14338644.
  7. ↑ Alpern M (Sep 1974). "What is it that confines in a world without color?" (PDF). Invest Ophthalmol. 13 (9): 648–74. PMID 4605446.
  8. ↑ Hansen E (Apr 1979). "Typical and atypical monochromacy studied by specific quantitative perimetry". Acta Ophthalmol (Copenh). 57 (2): 211–24. doi:10.1111/j.1755-3768.1979.tb00485.x. PMID 313135. S2CID 40750790.
  9. ↑ Ali, Mohamed Ather; Klyne, M.A. (1985). Vision in Vertebrates. New York: Plenum Press. p. 162. ISBN 978-0-306-42065-8.
  10. 1 2 3 Eksandh L, Kohl S, Wissinger B (June 2002). "Clinical features of achromatopsia in Swedish patients with defined genotypes". Ophthalmic Genet. 23 (2): 109–20. doi:10.1076/opge.23.2.109.2210. PMID 12187429. S2CID 25718360.
  11. ↑ Nathans, J; Thomas, D; Hogness, D S (1986). "Molecular genetics of human color vision: the genes encoding blue, green, and red pigments". Science. 232 (4747): 193–202. CiteSeerX 10.1.1.461.5915. doi:10.1126/science.2937147. PMID 2937147.
  12. ↑ Weleber RG (June 2002). "Infantile and childhood retinal blindness: a molecular perspective (The Franceschetti Lecture)". Ophthalmic Genet. 23 (2): 71–97. doi:10.1076/opge.23.2.71.2214. PMID 12187427. S2CID 30741530.
  13. ↑ Michaelides M, Johnson S, Simunovic MP, Bradshaw K, Holder G, Mollon JD, Moore AT, Hunt DM (January 2005). "Blue cone monochromatism: a phenotype and genotype assessment with evidence of progressive loss of cone function in older individuals". Eye (Lond). 19 (1): 2–10. doi:10.1038/sj.eye.6701391. PMID 15094734.
  14. 1 2 3 Peichl, Leo; Behrmann, Gunther; Kroger, Ronald H. H. (April 2001). "For whales and seals the ocean is not blue: a visual pigment loss in marine mammals". European Journal of Neuroscience. 13 (8): 1520–1528. CiteSeerX 10.1.1.486.616. doi:10.1046/j.0953-816x.2001.01533.x. PMID 11328346. S2CID 16062564.
  15. ↑ Emerling, Christopher A.; Springer, Mark S. (2015-02-07). "Genomic evidence for rod monochromacy in sloths and armadillos suggests early subterranean history for Xenarthra". Proceedings of the Royal Society B: Biological Sciences. 282 (1800): 20142192. doi:10.1098/rspb.2014.2192. ISSN 0962-8452. PMC 4298209. PMID 25540280.
  16. ↑ Mark Roth (September 13, 2006). "Some women who are tetrachromats may see 100,000,000 colors, thanks to their genes". Pittsburgh Post-Gazette.
  17. ↑ Neitz J, Carroll J, Neitz M (2001). "Color Vision: Almost Reason Enough for Having Eyes". Optics and Photonics News. 12 (1): 26. doi:10.1364/OPN.12.1.000026. ISSN 1047-6938.
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