Colour vision and colour blindness
- Mechanism
- Exam priority: medium
Three kinds of cones each prefer a different part of the spectrum; the brain reads colour from how strongly each kind responds.
Also called: Trichromacy, Opponent colours, Colour vision deficiency
What it is
Colour vision starts with three cone types whose pigments absorb short, middle and long wavelengths. No single cone knows colour; colour is decoded from the ratio of the three cone responses, then recoded by the retina into opponent channels (red versus green, blue versus yellow, light versus dark). Missing or shifted cone pigments cause inherited colour vision deficiency, most often the X-linked red–green type.
How it works, step by step
- Each cone holds one opsin bound to 11-cis-retinal (from vitamin A); the opsin sets which wavelengths the pigment absorbs best.
- A photon absorbed by any cone produces the same signal; a single cone cannot tell wavelength from intensity (univariance).
- Because the three absorption curves overlap, each wavelength gives a unique ratio of S:M:L activity.
- Retinal circuits subtract cone signals: L versus M gives the red–green channel, S versus (L + M) gives blue–yellow, L + M gives brightness.
- Opponent signals travel through midget (red–green) and small bistratified (blue–yellow) ganglion cells to the LGN and V1.
- Cortical areas, especially V4, compare colours across the scene, so a banana looks yellow in both sunlight and lamplight (colour constancy).
Types of colour vision deficiency
| Type | Cone affected | Inheritance | Note |
|---|---|---|---|
| Protanomaly / protanopia | L (red) shifted / absent | X-linked | Reds look dark; long-wavelength end shortened |
| Deuteranomaly / deuteranopia | M (green) shifted / absent | X-linked | Most common type |
| Tritanomaly / tritanopia | S (blue) | Autosomal dominant | Rare; confuses blue with green, yellow with violet |
| Blue cone monochromacy | Only S cones work | X-linked | Poor acuity, nystagmus, light sensitivity |
| Achromatopsia (rod monochromacy) | No working cones | Autosomal recessive | Sees no colour, very poor acuity, photophobia |
Clinical notes
- Acquired loss is usually asymmetric and may involve blue–yellow: optic neuritis (red looks faded), ethambutol toxicity, and macular or optic nerve disease.
- A carrier mother passes red–green deficiency to half her sons; an affected father passes the gene to all his daughters (carriers) and to none of his sons.
- Screening plates detect the defect; how they are used belongs to clinical eye examination.
Test yourself
Think of the answer, then tap the question to see it.
Why can a single cone type not tell a dim yellow light from a bright red one?
A cone only reports how many photons it catches; any wavelength-intensity mix giving the same catch looks identical. Colour needs a comparison between cone types.
A man with normal colour vision and a carrier woman have children. What is the risk of red–green deficiency for a son?
50%: each son receives one of his mother's X chromosomes, and half of them carry the altered L/M opsin gene.
Why is red–green colour blindness much more common in men than in women?
The L and M opsin genes are on the X chromosome; men have one X, so one altered copy is enough, while women usually have a normal second copy.
Which retinal channel is lost in a tritan defect?
The blue–yellow channel, because S cones are absent or abnormal; the S-versus-(L+M) comparison cannot be made.
Connections
In Biochemistry1
Educational physiology content; not a diagnostic or treatment guide and no substitute for a health professional's advice. Values are approximate references. No doses are given.
Sources: Color vision deficiency: MedlinePlus Genetics (MedlinePlus, US National Library of Medicine, 2024); Color Blindness (National Eye Institute (NIH), 2024); Anatomy, Head and Neck: Retina (StatPearls (NCBI Bookshelf), 2024).
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Representative model, for educational purposes only.