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Physiology, Color Perception

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Last Update: September 12, 2022.


In humans, the perception and ability to distinguish different colors are mediated by various mechanisms in the retina and the brain. Understanding the physiologic basis of color vision is essential to detecting abnormalities and devising treatments. This topic reviews the cellular and genetic mechanisms that underlie color perception and applies these mechanisms to characterizing defects in color vision and avenues for treatment.

Issues of Concern

Color vision deficiency can result from various abnormalities, both systemic and specifically within the visual system. Defects in the genes responsible for visual transduction often lead to congenital color vision deficits. Any abnormalities of the retina, optic nerve, optic tract, and visual cortex can cause defects in color vision. As such, systemic diseases like diabetes and eye-specific diseases like glaucoma and cataracts can alter color vision.[1]

Cellular Level

Most mammalian retinae only contain 2 types of cones (dichromats), sensitive to short wavelengths (S-cones, maximally sensitive near the blue end of the visual spectrum) and medium wavelengths (M-cones, maximally sensitive to green wavelength light). Humans, as trichromats, have an additional L-cone, which is sensitive to long-wavelength light at the red end of the visual spectrum. Differential stimulation of these cones creates color axes between red-green and blue-yellow, enabling visualization of mixtures of colors that fall in the range of the visual spectrum. The blue-yellow color axis is somewhat of a misnomer, as it more specifically refers to the ability to differentiate blue from green and yellow from red.[2]

The first step of visual transduction is the light-mediated conformational change of 11-cis-retinal, which activates an associated opsin that acts as a G-protein coupled receptor. Each cone type is associated with a different opsin with other genetic bases. S-cone opsins are autosomally encoded on chromosome 7, whereas M- and L-cone opsins are located nearby on the X chromosome and are nearly identical. M- and L-cone opsin genes are believed to undergo frequent homologous recombination, which underlies changes in normal spectral sensitivity that explain the variations in the severity of red-green color blindness. These defects are far more likely to affect karyotypic males than females as they are sex-linked. S-cone opsin defects are far less common than defects of the M- and L-cones.[3]


Studies indicate that infants have functional color vision by 2 months of age. They can further discriminate between multiple hues independent of luminance and rod function, although their vision differs from that of adults.[4] The refinement and continued development of color vision are not well understood, nor is the age of peak functioning, but likely depends on the strengthening of cone photoreceptor pathways through continued visual experience.[5]

Organ Systems Involved

Normal color perception is a function of the nervous system. It is dependent on visual transduction and relaying of information to the visual cortex.


The evolution of trichromatic color vision is believed to have aided early primates in differentiating red, orange, and yellow fruit from leafy green foliage.[2] In modern-day humans, color vision is vital in household tasks, driving, and many other interactions with the surrounding environment. Loss of functional color vision can impair these everyday tasks, including job performance, and may even preclude specific career choices.[6]


The eye forms images based on differences in the reflectance of light on external objects. Small perturbations, in contrast, are processed through a center-surround system, where surrounding background luminance is subtracted from the center signal, highlighting the local features of the central signal. This system allows for high sensitivity to light-dark contrast. Additionally, the presence of different types of cone photoreceptors in the retina, which is sensitive to varying wavelengths of light, enables contrast of refracted light, providing the basis for visualization and separation of a spectrum of colors.[2]

Cones relay visual information through parvocellular layers to the thalamus's lateral geniculate nucleus (LGN). Neurons in the LGN process the magnitude of contributions from opponent cone signals and continue to relay the signal to the primary visual cortex V1. The mechanisms of color perception beyond the LGN are not as well characterized. Still, functional magnetic resonance imaging (fMRI) studies suggest additional separation and processing of color luminance and color contrast in V1 and other extrastriate visual areas.[7] The fMRI studies of the pathways involved in color perception and processing indicate a potential top-down mechanism in the interaction of the temporoparietal cortex with visual areas V2/3. The relationship may reflect how the language processing center of the left hemisphere aids in color discrimination. Additionally, it may explain why the right visual field has superior color discrimination over the left.[8] An fMRI of the brain also suggests that V4, the ventral occipitotemporal cortex, plays a significant role in color processing, and lesions in this area are associated with achromatopsia or dyschromatopsia.[9]

A variety of additional complex mechanisms influence color perception. The hue, saturation, and brightness of both the center and surrounding areas greatly influence the perception of the central color, such that the same stimulus presented on different backgrounds may be perceived as different colors entirely. Individual differences in color processing also mediate how these factors influence color perception.[10]

Chromatic visual perception appears subject to a high degree of neural plasticity; this seems to be mediated by average background luminance and equilibrating intermediate chromatic stimuli (perception of the standard background color is adjusted to yield equal contributions of opposing color axes). The capability of the visual system to adjust this equilibrium point based on different external environments enables more excellent color contrast.[11] All colors are attainable by additive or subtractive mixing processes within the primary 3 colors

Related Testing

Due to ease of access and use, the most common method of diagnosing color vision defects is with "pseudoisochromatic" plate tests, such as Ishihara plates. However, these tests often fail to differentiate different types of dyschromatopsia. Another diagnostic tool, ordering tests, requires patients to sort other disks based on color progression. Compared to plate tests, these tests are typically more sensitive to detecting color vision abnormalities and better at determining specific diagnoses. Additional diagnostic methods of interest include matching tests, which are attractive due to the possibility of administering and scoring them on a computer. Genetic tests, the examination of retinal morphology (including fundoscopy and optical coherence tomography), and electrophysiological tests (such as electroretinogram) can also aid in diagnosing and characterizing color vision defects.[1]


Abnormal color vision typically subdivides into congenital and acquired forms. The genetic disorders of color vision occur due to defects in genes encoding cone opsins. These genes encode the expression of cone opsins and genes for proteins involved in phototransduction (such as phosphodiesterase and cyclic nucleotide-gated channel subunits). Such defects have a wide range of possible outcomes and may feature different progression rates, retinal degeneration, and loss of visual acuity. Guanylate cyclase deficiencies can lead to Leber congenital amaurosis and severe vision loss early in life. In contrast, rod dystrophies leading to retinitis pigmentosa may cause late color vision abnormalities as degenerating rods affect cone structure and function. Additional causes of color vision defects include fundus albipunctatus and Stargardt disease. Acquired color vision deficiency, or dyschromatopsia, can occur due to any injury or disruption to visual pathways.[1]

Clinical Significance

Defects affecting specific cone opsin types have associated prefixes: protan for L-cones, deutan for M-cones, and Tritan for S-cones. For example, if L-cone opsin is present but abnormal, the patient would be classified as a "protanomalous trichromat." In contrast, a complete loss of L-cone opsin would yield a "protanope dichromat." Such dichromats would be unable to distinguish red and green, only seeing functional combinations of 2 hues. At the same time, anomalous trichromacy can range in severity from normal color vision to functional dichromacy.[3]

Diseases that primarily affect the cone-rich macula, such as age-related macular degeneration, may demonstrate early losses in color discrimination before detectable changes in retinal morphology or visual acuity. The loss of color discrimination can affect the red-green and blue-yellow axes, and severity appears to correlate with increased drusen and reticular pseudodrusen in the retina.[12]

Glaucoma and ocular hypertension, diseases that can result in compression of the optic nerve, may also cause color vision defects. Color perception may suffer alteration before other functional or structural changes are detectable and appear to affect the blue-yellow axis primarily.[13]

Numerous other disorders, specific to the visual system and global, have been associated with color vision abnormalities. Retinal tears and detachments may lead to loss of color vision, as can disorders affecting the optic nerve, including hereditary optic neuropathy, optic neuritis, and optic nerve compression. Many patients with diabetic retinopathy exhibit deficiencies in color vision as well. Multiple drugs have implications in dyschromatopsia, including PDE5 inhibitors, chloroquine, ethambutol, and digoxin, as well as environmental effects such as UV exposure, industrial chemicals, and hypoxia.[1]

Gene therapy is a promising avenue of treatment for many congenital retinal dystrophies. Many genetic disorders in non-human animals are analogous to human conditions. Translational therapies for gene replacement, typically mediated by recombinant adeno-associated virus, have successfully treated multiple congenital disabilities affecting color vision. RPE65 genetic defects, which affect the ability of the retinal pigment epithelium to recycle retinyl esters and can cause Leber congenital amaurosis, were successfully treated with gene therapy in dog models. The treatment has since been extended to humans, yielding the first FDA-approved gene therapy for inherited retinal dystrophy.[14] Other promising treatments include gene therapy for CNGB3 congenital achromatopsia, countering the absence of a cyclic nucleotide-gated channel subunit in cones, which has been successful in dogs, and gene therapy for red-green color blindness in squirrel monkeys.[15][16]

Review Questions


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Lotto RB, Purves D. The empirical basis of color perception. Conscious Cogn. 2002 Dec;11(4):609-29. [PubMed: 12470626]
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Vemala R, Sivaprasad S, Barbur JL. Detection of Early Loss of Color Vision in Age-Related Macular Degeneration - With Emphasis on Drusen and Reticular Pseudodrusen. Invest Ophthalmol Vis Sci. 2017 May 01;58(6):BIO247-BIO254. [PubMed: 28846119]
Papaconstantinou D, Georgalas I, Kalantzis G, Karmiris E, Koutsandrea C, Diagourtas A, Ladas I, Georgopoulos G. Acquired color vision and visual field defects in patients with ocular hypertension and early glaucoma. Clin Ophthalmol. 2009;3:251-7. [PMC free article: PMC2709000] [PubMed: 19668575]
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Disclosure: Nathaniel Pasmanter declares no relevant financial relationships with ineligible companies.

Disclosure: Sunil Munakomi declares no relevant financial relationships with ineligible companies.

Copyright © 2024, StatPearls Publishing LLC.

This book is distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) ( http://creativecommons.org/licenses/by-nc-nd/4.0/ ), which permits others to distribute the work, provided that the article is not altered or used commercially. You are not required to obtain permission to distribute this article, provided that you credit the author and journal.

Bookshelf ID: NBK544355PMID: 31335075


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