What follows is one way this might have happened.

In Part 1, we spoke about multicellular animals and how light sensitivity was rapidly refined into vision through changes in structure that allowed new advantageous behaviours. But light sensing did not begin with multicellular animals. It started eons before. Not figuratively, but 2 full geological eons earlier.

Light-sensing likely arose over 3 billion years ago, with cyanobacteria in the Archean eon. Cyanobacteria are preserved in fossils called stromatolites and are among the earliest evidence of life on Earth. They also provide the first evidence we have of life responding to light. Crucially, they never went extinct, so modern cyanobacteria are direct descendants of that ancient lineage.

Different lines of evidence suggest they had light-sensing capabilities that persist, in modified form, to this day:

• Molecular evidence: Genomic analyses of modern cyanobacteria showed that they possess some of the earliest and most diverse photoreceptor protein families (phytochromes, cyanobacteriochromes, microbial rhodopsins). Phylogenetic analyses place these gene families deep in evolutionary trees, indicating that they originated long before animal opsins evolved.

• Evolutionary continuity: When scientists compare genomes across algae, plants, and animals, they find that many genes involved in light sensing closely resemble those found in cyanobacteria.

• Functional evidence: Modern cyanobacteria show light-driven behaviours. Part 1 explains why this is important. Some of these behaviours are:

  • phototaxis,

  • circadian regulation, and

  • chromatic acclimation. This means adjusting which light-absorbing pigment they use to match the colour of light available at any time. It is so tempting to go down that rabbit hole, but I shan’t.

This suggests that animal photoreceptors may have been built on ancient light-sensing technology. What remains now is to explore how this machinery made it into animal DNA.

The light-sensing cell

In the traditional view, animal photoreceptors arose through gradual reuse and modification of existing cells within early animals. As multicellular organisms evolved, some cells became specialised for electrical signalling and, through small molecular changes, began responding to light.

This view does not assume any direct evolutionary link between animal vision and the light-sensing seen in cyanobacteria, which is treated as a separate, much older phenomenon.

This is about to get fun.

According to one hypothesis, photoreception did not arise only by differentiating an ancestral animal cell type. Instead, it may have been acquired through several layers of endosymbiosis, basically: one organism living inside another. This is why Walter Gehring (2005) calls it the Russian Doll model.

Let us talk endosymbiosis. This refers to an organism engulfing another, but instead of digesting it, they coexist and both benefit from the merger. It is a widely accepted evolutionary mechanism. It is how we think mitochondria entered our cells and became the powerhouse that fuels you. The mitochondrion has its own DNA, which is different from the DNA of the cell that contains it. But I digress.

Here is Gehring’s symbiont hypothesis, step by step.

Step 1: A light-sensitive bacterium

It starts with cyanobacteria. They are a single cell without a nucleus. They can harness light because they contain photopigments, molecules that undergo a reversible chemical change when they absorb photons, allowing cells to notice and respond to light.

Step 2: Engulfed by red algae

At some point, a cyanobacterium was engulfed by a red alga. But instead of being digested, it lent its photosynthetic ability to the alga, making it a chloroplast. This tiny solar panel absorbs light and turns it into energy, more specifically, into food. Have you heard of eating with your eyes?

Step 3: Engulfed again by dinoflagellates

Later still, chloroplasts are engulfed by dinoflagellates, which are single cell plankton, common in marine environments. In some dinoflagellate lineages, the inherited chloroplasts were no longer used primarily for photosynthesis. Instead, they were transformed into elaborate light-sensing organelles.

One species of dinoflagellate, called Warnovia, has an ocelloid, a precursor of an eye (Greuet, 1969). This is not part of our lineage, but this ocelloid has structures that resemble a cornea, a lens, a retina complete with a membrane, and a prominent cup. But the Warnovia is still a single-cell organism. No nervous system. No multicellularity.

Let me say that again. This is, actually, a SINGLE CELL THAT CONTAINS AN EYE.

How cool is that?!

I need a minute to compose myself.

Step 4: Sharing the love – I mean, the DNA

From dinoflagellates onwards, things become more uncertain. Some dinoflagellates live inside other organisms, such as corals and sea anemones. Gehring suggests the possibility that photoreceptor-related genes could have been transferred from the DNA of dinoflagellates into the DNA of animals.

This process is known as horizontal gene transfer, meaning genes pass between symbiont and host, rather than being passed on from parent to offspring. While horizontal transfer itself is a well-established evolutionary mechanism, what remains speculative is whether photoreceptor-related genes made this jump into early animals in a way that contributed to the origin of animal eyes.

In short

The early “Russian dolls” (cyanobacterium → red algae → dinoflagellates) are supported by mainstream endosymbiosis and modern evidence of ocelloids. The idea that this process contributed directly to the origin of animal eyes remains an intriguing possibility rather than an established fact. Scientists are still looking.

Conclusion

Long before animals had eyes, light was already shaping life in single cells. By the time animals appeared, light sensing was a well-developed technology involved in metabolism and survival.

The Russian Doll hypothesis offers one possible bridge between the two worlds. It suggests that ancient light-sensing systems may have entered animal lineages through merger, not mutation alone. If this hypothesis is correct, it would mean that the origin of animal vision may not be located in animals at all, but in much older single-celled life.

Parts of this story are well supported; the final step remains speculative. But this is what gives me chills: the technology we use to see the world is billions of years old, and for the majority of this time, it was not involved in image forming at all! If the hypothesis is right, vision did not start as vision: it began as a way of producing food for the cell, was gradually repurposed for metabolic regulation, then for guiding behaviour, and only much later, refined into what we understand as high-definition vision.

Even if the hypothesis is not correct, vision is still at least about 620 million years old, only without the “producing food” step from the list above. Not any less impressive.

But what is certain is that vision is only a late chapter in a much older story. Long before sight guided behaviour, it fed life itself.

It takes a lot of work and time to write these articles. If you find value in what you just read, there are many ways to support my work. You can:

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REFERENCES:

Gehring, W. J. (2005). New perspectives on eye development and the evolution of eyes and photoreceptors. Journal of Heredity, 96(3), 171-184.

Gehring, W. J. (2014). The evolution of vision. Wiley Interdisciplinary Reviews: Developmental Biology, 3(1), 1-40.

Greuet, C., & Ferru, G. (1969). Etude morphologique et ultrastructurale du trophonte d'Erythropsis pavillardi Kofoid et Swezy. Protistologica, 5(4), 481-503.

What troubled Darwin was not simply that the eye was complex, but that all its parts worked together so precisely. It was difficult to imagine intermediate stages that could also be functional. In his words:

“To suppose that the eye, with all its inimitable contrivances for adjusting the focus to different distances, for admitting different amounts of light, and for the correction of spherical and chromatic aberration, could have been formed by natural selection, seems, I freely confess, absurd in the highest possible degree.”
Charles Darwin, The Origin of Species (1859).

Darwin was not alone. Decades later, the same scientist who managed to unravel how the brain communicates and established the neuron doctrine that overturned the belief at the time, also found himself stopped by the eye. Santiago Ramón y Cajal, the father of neuroscience, admitted that no structure challenged him more:

“In the study of [the retina] I for the first time felt my faith in Darwinism (hypothesis of natural selection) weakened, being amazed and confounded by the supreme constructive ingenuity revealed not only in the retina … but even in the meanest insect eye. I felt more profoundly than in any other subject of study the shuddering sensation of the unfathomable mystery of life.”
Santiago Ramón y Cajal. Recollections of My Life (1898), p. 576

Ask anyone. The more you know about the eye, the closer it feels to magic than chance.

We now know vastly more than Darwin and Ramón y Cajal could have imagined, and it remains equally breathtaking. To put this complexity in perspective: while the human heart has a sophisticated network of roughly 60 cell subtypes, the eye relies on nearly 160, with over 120 specialised types packed into the retina alone. This dense biological machinery allows your eyes to see objects kilometres away and read words centimetres from your face, detect rapid movement in the periphery, and operate across a brightness range spanning nearly a billion-fold, from starlight to sunlight. Not for nothing, vision is the only sense with its own dedicated brain lobe.

If you are still not impressed, you can read here about how cones and rods work to give you maximum flexibility and incredible precision..

But Darwin did not stop there, he pointed a way forward:

“Yet reason tells me, that if numerous gradations from a perfect and complex eye to one very imperfect and simple, each grade being useful to its possessor, can be shown to exist; if further, the eye does vary ever so slightly, and the variations be inherited, which is certainly the case; and if any variation or modification in the organ be ever useful to an animal under changing conditions of life, then the difficulty of believing that a perfect and complex eye could be formed by natural selection, though insuperable by our imagination, can hardly be considered real.”
Darwin (1859).

Let us unpack that.

He does not deny that the eye could evolve. He accepts an imperfect eye, but insists that each successive improvement must give the organism an advantage great enough to be passed on.

The task becomes easier if we flip the question and ask what an organism can do with a slightly better eye. Each new small improvement gives the animal an opportunity to do something new in its environment. Dan-Eric Nilsson (2013) argues that if an innovation in eye development leads to a behaviour change, then the evolution of the eye is really the evolution of visually guided behaviour. Let us explore what this means with a story. Come a little closer.

The evolution of visually guided behaviours.

Let’s imagine a very simple organism. Let’s call him Jonas.

(I)

Jonas lives in the sea, long before complex animals appeared. He is a soft, flat-bodied organism, little more than a sheet of cells drifting about. He does not have eyes, but he just gained a single light-sensitive cell that converts light into an electrical signal. This may not sound impressive to you, but for Jonas, this is the difference between night and day. Literally. Jonas can now notice when there is daylight and regulate his circadian rhythm. Not only this, but as a marine animal, this light sensitivity gives Jonas some information about depth, because light is rapidly absorbed and scattered by water. Darker means deeper.

This is not vision as we know it. Jonas can only detect very slow changes in ambient light.

(II)

Millions of years have passed, and, among other innovations, Jonas has gained a pigment cell. This cell acts as a screen, absorbing light and shielding one side of the light-sensitive cell.

Light can now reach Jonas only from the unshielded side, which means that now he can tell where the light is coming from. Yet, direction becomes meaningful to Jonas only if he has the ability to move. And he does. With this new trick, he can move towards or away from light, a behaviour called phototaxis. He can also orient himself, because he now knows where he is in relation to the light.

Around the same time, inside the light-sensitive cell itself, another subtle change is taking place. The light-sensitive membrane begins to fold inward, creating folds that increase the surface area exposed to light. More membrane means greater sensitivity. This simple structural change dramatically boosts sensitivity without changing the cell’s overall size.

(III)

Some more millions of years have passed and Jonas has many more photoreceptors, and his once flat eye has folded inward, forming a shallow cup. This changes everything. Light entering the cup now strikes different receptors depending on its direction, allowing Jonas to form a crude spatial pattern.

Jonas can now, for the first time, form an image.

Life looks extremely blurry, more like shifting patches of light and dark, but even this coarse spatial pattern allows him to steer more accurately, avoid obstacles, and navigate through his environment with intention rather than drift.

As the cup deepens and the opening narrows further, direction becomes more precise. A shadow moving across his eyes could mean a predator, so now Jonas can see the danger and escape.

(IV)

Some millions of years later, Jonas’ eyes have continued to refine. As the cup deepens, it becomes easier to determine the direction of incoming light. Yet, the most important change is the gradual appearance of a lens.

This may have begun as a transparent layer serving a protective role against debris or harmful UV light, but over time it became a powerful optical innovation. By bending incoming light, the lens concentrates rays onto a smaller region of the retina, now densely packed with photoreceptors. This dramatically increases contrast and sharpness.

This refinement transforms vision and comes with a bigger eye to accommodate the optics. Jonas can now resolve finer details, distinguish objects from their background, and judge distance with greater accuracy. This means he can not only avoid predators but actively hunt, tracking prey, planning movement and interacting visually with other animals. Vision becomes a powerful guide for behaviour and interaction.

Other Ways of Seeing

Jonas has come a long way, and you have seen only snapshots in an endless sequence of small advances. But this story follows only one evolutionary route: the one that leads to a single-chamber, camera-type eye, the path taken by humans, frogs, and leopards. Jonas got an eye built for fine detail.

Other lineages branched off at different times and produced eye structures best suited to their own environmental challenges. You can learn more about how here.

Jonas’ cousin Marina did not develop a single chamber. Instead, the surface of her eye formed multiple shallow folds, each with its own lens and its own sampling direction. This gave Marina a dramatically wider field of view than Jonas had, an eye built for vigilance rather than detail, ideal for spotting predators approaching from any direction. Flies have this type of eye. Have you ever tried catching a fly with your hand?

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From zero to eye in 170,000,000 years flat

What Jonas experienced as a story corresponds to a well-supported evolutionary sequence. Dan-Eric Nilsson describes eye evolution as progressing through four main stages of structural and behavioural innovation:

Class I - Non-directional light-sensing → regulation of circadian rhythm
Class II - Directional light-seeing → phototaxis and orientation
Class III - Low-resolution vision → navigation, obstacle avoidance
Class IV - High-resolution vision → active predation, visual communication

Nilsson and Pelger (1994) estimate that the transition from a simple light-sensitive patch to a fully developed camera-type eye could have taken as little as 170 million years, and that this process was likely completed by the early Cambrian (~530 million years ago). Using conservative assumptions, the researchers calculate that fewer than 400,000 generations would have been sufficient.

This means that once light sensitivity existed, eye evolution developed fast, propelled by immediate behavioural gains under constant environmental pressure.

Hard evidence

Fossil records support Nilsson’s rapid timeline. By the early Cambrian, around 515 million years ago, animals already possessed anatomically sophisticated eyes. These are two examples of arthropods, the evolutionary ancestors of insects, spiders, and crustaceans:

• Anomalocaris: a large predatory animal, up to a metre in length, and likely the dominant hunter of its time, with large eyes mounted on flexible stalks that projected from the head. These would be compound eyes (like Marina’s eyes) with thousands of tiny lenses arranged in a hexagonal grid, possibly as many as 16,700 lenses per eye (Paterson et al., 2011).

• Microdictyon sinicum: an animal resembling a worm with legs, representing a transitional step between soft-bodied worms and the jointed, armoured arthropods. Fossils show lens-like structures on each body segment, suggesting that early eyes could have been distributed in the body instead of being in the head.

Could vision have accelerated evolution?

The Cambrian explosion was a brief period of about 20-25 million years (540 - 515 million years ago). During this time, animal life changed rapidly from small soft-bodied organisms to large, interacting animals with specialised tissues and hard parts, like shells and exoskeletons, which could fossilise. We are still talking about marine life only, no terrestrial ecosystems yet.

The timeline for eye development suggests something counterintuitive: complex, high-quality vision appears around the beginning of this evolutionary burst, not as a late refinement.

In this context, researchers argue that vision could have intensified evolutionary pressure. Better eyes raised the stakes on both sides: seeing predators and prey at a distance favoured the evolution of speed, armour, camouflage, and ever faster and more specialised perception.

Where Jonas lives on today: modern animals

Evolution does not move towards complexity for its own sake. If a sensory system fits the brief of what the animal needs and the environment does not demand any more, there is no pressure to change. For this reason, many animals alive today still rely on visual systems similar to the stages we followed with Jonas, not because evolution stalled, but because these designs remain excellent solutions.

Class I – Non-directional light sensing

Some simple marine animals like corals and sea anemones use light sensitivity to track day-night cycles.

Class II – Directional light sensing

Flatworms are soft-bodied and vulnerable to desiccation and UV damage. A simple photoreceptor paired with a pigment cell gives them enough directional information to find shelter under rocks.

Class III – Low-resolution vision

The nautilus and some molluscs have cup-shaped eyes without a lens. These form low-resolution images sufficient for detecting shape and movement, supporting navigation and basic obstacle avoidance.

Class IV – High-resolution vision

It is hard to choose an example because there is a great variety of eye systems that are familiar to us. Three major groups belong here: vertebrates, cephalopods and arthropods. These animals have lenses, sometimes multiple ones, and the ability to form sharp, detailed images. Some use this sharp vision to hunt prey, while others use it to order food online.

If this raised questions rather than answers, that is precisely what this is about. Feel free to share what you are still wondering about below.

Leave a comment

All together now…

Function drives evolution. Eyes did not evolve because complexity is inherently “better”, but because each small improvement enabled a new behavioural advantage, exactly as Darwin said, and those advantages compounded over time.

Vision changed the rules. Once organisms could sense the direction of light and form even crude images, natural selection intensified. Predator and prey were no longer reacting on contact but at a distance, reshaping how animals moved, hid, hunted, and survived.

Darwin was right to hesitate. Even today, with genetics, high-resolution imaging and computational models, the eye remains one of the most astonishing systems evolution has produced. Explaining how it evolved does not drain it of its wonder. If anything, the deeper we look, the more unfathomable the eye becomes.

And so, it feels fitting to end where Darwin himself paused:

Coming next…

So far, we have spoken about multicellular animals and how light sensitivity was rapidly refined into vision. But light sensing did not begin with animals, it began billions of years earlier.

Join me in Part 2 as we go back to where life first sensed light.

It takes a lot of work and time to write these articles. If you find value in what you just read and want to support my work, you can buy me a coffee.

In any case, if you got this far, please like and restack, and feel free to drop any questions in the comments.

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REFERENCES:

Cajal, S. R. Y. (1989). Recollections of my life (Vol. 8). MIT press.

Darwin, C. (1964). On the origin of species: A facsimile of the first edition. Harvard University Press.

Nilsson, D. E. (2013). Eye evolution and its functional basis. Visual neuroscience, 30(1-2), 5-20.

Nilsson, D. E., & Pelger, S. (1994). A pessimistic estimate of the time required for an eye to evolve. Proceedings of the Royal Society of London. Series B: Biological Sciences, 256(1345), 53-58.

Paterson, J. R., García-Bellido, D. C., Lee, M. S., Brock, G. A., Jago, J. B., & Edgecombe, G. D. (2011). Acute vision in the giant Cambrian predator Anomalocaris and the origin of compound eyes. Nature, 480(7376), 237-240.

Even Darwin found the complexity of eyes difficult to explain.

To suppose that the eye, with all its inimitable contrivances … could have been formed by natural selection, seems, I freely confess, absurd in the highest possible degree. Darwin (1859)

There are vast differences between the eyes of insects, mammals, molluscs, birds and others. Not only do they have entirely different eye structures, but are also differences in the numbers and placement of eyes (not always on the head). Some animals have functioning eyes that produce no images at all. It is hard to think that all eyes evolved from an earlier version.

Why would evolution invent eyes again and again? What does that tell us about the fundamental importance of vision for survival?

The neo-Darwinist view, argued by figures like Ernst Mayr (Salvini-Plawen & Mayr, 1977), was that eyes evolved independently, some secondary sources citing between 40 and 60 times. When organisms which are not related evolve similar traits independently, this is called convergent evolution. For example, both octopodes (yes, octopuses) and humans have developed camera-type eyes with a lens that focuses the image onto one spot in the retina. However, even though the design is similar, the tissue that forms the eye in the embryo comes from different cells: in the octopus, it comes from the same tissue that forms skin, while in the human, it comes from tissue that forms the brain.

How different are animal eyes?

To understand why scientists believed eyes must have evolved many times, it helps to look at just how different eyes appear across the animal world.

a) Different architectures.

There are many designs beyond camera eyes. For example:

• insects have compound eyes made of hundreds of tiny lenses,

• scallops see using mirrors made of crystals that reflect light onto the retina, and

• jellyfish have simple light-sensing spots and no image-forming vision.

b) Different photoreceptors, opsins and supporting molecules

Animals use different opsins (light-sensitive proteins), and crystallins (proteins that form the lens), and different supporting molecules.

c) Different developmental origins

Retinas in the eye can form from different tissues. For example, most invertebrate eyes (insects, crustaceans, many molluscs, cnidarians) derive from epidermis (skin-forming tissue), while vertebrates’ retinas are formed from neural tissue, literally as an outgrowth of the brain.

This rich diversity of eyes suggests that evolution independently stumbled upon different ways of solving the problem of detecting light, producing entirely different eye infrastructure across different animal groups. This view of multiple origins is called the polyphyletic origin of eyes.

Now, if all these eyes evolved separately, should we expect to find any patterns between them?

The case of the missing eyes

In 1915, Mildred Hoge noticed that some fruit flies (Drosophila) were born with no eyes. She recognised this was a congenital defect, but genes were not cloned at the time. She called this disorder eyeless.

Decades later, a similar condition was noticed in mice. A single defective gene called Pax6 would cause a mouse to have very small eyes, and if the mouse inherited this gene in both chromosomes, it would die before birth, lacking eyes, nose and parts of the forebrain (Hill et al., 1991). This defect was named small eye. This mouse discovery was relevant because it could help us understand a similar condition in humans, called aniridia: a genetic condition that causes people with a defective gene to be born with very small irises or no irises at all. Inheriting both defective genes is rare, but when it happens, the embryos fail to develop eyes, a nose and have severe brain damage, and consequently die before birth.

A mouse, a fly and a human walk into a lab…

In the 1990s, scientists isolated the genes behind the small eye in the mouse (Walther & Gruss, 1991) and aniridia in humans (Ton et al., 1991). It turned out they were both versions of the same gene, Pax6. So, we know Pax6 is necessary for eye formation in mammals because when it is missing, eyes do not form. But does it exist outside mammals?

Shortly after, in Walter Gehring’s lab in Basel, Quiring and colleagues (1994) sequenced the fly gene they called ey (for eyeless), responsible for the eyeless fruit fly, and found that it was homologous to the mammal Pax6. Homologous means derived from a common ancestral gene, suggesting a common ancient origin for producing eyes across mice, humans and flies.

Can these genes be “turning on” eye formation?

Now, in scientific terms, this is still not enough. Correlation does not… You know how it goes.

All we know this far is that when the Pax6 gene is not working, eyes fail to develop, and that this is true across different phyla (insect and mammal). However, this only suggests that Pax6 is necessary for eyes to develop. This does not necessarily mean that it is the switch that triggers eye formation.

How can we test this? Have a think before you read on.

The gain-of-function experiment

Can the Pax6 fly equivalent gene ey create eyes where they are not supposed to be?

Fly → Fly

Halder, Callaerts & Gehring (1995) performed a groundbreaking experiment. They induced the ey gene (homolog to Pax6) into a different section of their genome that codes for appendages. The result? The flies grew fully formed eyes— on legs, on wings, even on the antennae. These are called ectopic eyes because they appeared outside of their usual location.

What have we learnt? This Pax6-homologue gene -by itself- seems to be enough to trigger the entire cascade of events for eye formation. So Pax6 is not only necessary, but on its own, it is sufficient to initiate eye development, acting as a master switch that says “build eyes here”.

But if this gene is present in different species, we should be able to transfer this gene across species, right?

Mouse → Fly

Fly and mouse eyes are very different: the fly’s compound eyes are mosaics made of hundreds of tiny lenses, while the mouse has a camera-type eye with a single lens focusing light onto a retina, like human eyes.

To get a closer definition of the function of Pax6, the next step was to introduce foreign Pax6, this time from a mouse, into the fly. The result will shock you! (I am sorry, I could not help myself.) But it is crazy: not only did the fly developed ectopic eyes, not only were they also fully formed and functional, but they were compound fly eyes, built under the instructions of the mouse gene.

This confirmed that Pax6 triggers the process, acting as a master switch, but the genetic recipe for making the new eyes comes from the host.

Fly → Frog

In the late 1990s, Callaerts and colleagues (1997) and Chow and colleagues (1999) attempted to produce ectopic eyes on frogs using the eyeless fly gene (homolog to Pax6). The result was patches of retinal tissue and lens structures, but no fully functioning eyes. Many reasons can be at play: the gene can activate the pathway, but to develop a full working eye, it needs the correct signals from local surrounding tissue to tell it how and when to develop the eye (Callaerts). It is also possible that the regulatory genes that act downstream of Pax6 may not be compatible in the frog. so the cascade cannot run to completion (Chow).

Pax6 in earlier animals: how far back can we trace this gene?

Pax6 has been found in an astonishing range of animals, from simple worms to vertebrates. It is so fundamental to early nervous-system patterning that even animals that have lost their eyes over evolution still retain this gene. For example, C. elegans is a nematode (a worm) that has no photoreceptors at all, yet it has conserved its Pax6 homologue. Remarkably, this gene from C. elegans can still induce new eyes when introduced into flies.

This suggests that Pax6 could have existed before eyes evolved, where it likely helped regulate the development of early neural structures, and was later “recruited” into also controlling eye formation when photoreceptive organs began to appear.

One eye to see them all

This evidence points to a single origin and is consistent with Darwin’s proposal of a simple ancestral photoreceptive system: a proto-eye.

The theory of a single origin for all eyes, called monophyletic theory, argues that a core group of regulatory genes, with Pax6 (or its ancestral paralogue PaxB) at the top, was conserved throughout evolution and repeatedly used to build eyes in different animal groups (Gehring & Ikeo, 1999).

The fact that the Pax family of genes are present in such a wide range of species indicates that this regulatory toolkit must have existed in a common ancestor that lived before the cnidarian-bilaterian split, about 620 million years ago. Quite the survival record. That places Pax6 just before the Cambrian explosion, the burst of evolutionary innovation that produced most major animal body plans. See the phylogenetic tree below.

- Bilaterians include all animals with a symmetrical organisation, i.e. with a front-back and left-right axis, such as flies, humans, frogs, spiders and scallops.

- Cnidarians, in contrast, are radially symmetrical: jellyfish, corals, sea anemones and others.

Intercalary evolution: from one eye to many eyes

A proto-eye would have been regulated by an ancestral Pax6-like gene which would initiate eye formation. Further downstream, additional genes would provide more specific instructions for all the stages involved in building the eye. Over evolutionary time, new genes were added, modified or removed. Intercalary evolution suggests that while the regulatory genes at the top remain the same, different steps were inserted in between the older ones, resulting in eyes with increasing developmental complexity without altering the ancient core.

There are two main mechanisms for new genes to enter the pathway:

Gene duplication:

A gene is accidentally duplicated, and the spare copy is free to specialise into a new function. For example, some insects have only a single Pax6 gene, but in flies its Pax-like gene duplicated, resulting in 2 regulatory genes: ey and toy (twin of ey), which now form a two-step regulatory loop but still sits at the top of the pathway.

Enhancer fusion (gene recruitment):

A gene that was not involved in vision is “recruited” into a new function. An example of this is a gene called drosocrystallin, which made the protein used to build the insect’s exoskeleton. This gene was recruited, and part of the protein it made became the lens in the eye, contributing to its transparency and refractive function. The name is confusing, but an “enhancer” is simply a short DNA sequence that initiates a process.

Over millions of such iterations, these additions accumulated in different lineages and formed all the designs that exist today. This also explains how eyes can be so wildly different in structure, optics and development, while still conserving the same regulatory gene.

Choose-your-own-adventure — but for genes

It is easy to imagine this as a linear process with Pax6 at the top of a neat top-down chain, but in reality, it is more of a network where each gene’s activity depends on the combined input of several others. This distinction matters because it explains how the same genetic toolkit can “order” such radically different eyes.

At the core of this network is the set of genes known as the Retinal Determination Gene Network (Kumar, 2009a,2009b). For simplicity, I will talk about the fruit fly but homologues of these genes exist in most bilaterians. See the network diagram,

In the fly, the regulatory network is made up of the eye determination genes: ey and toy (the Pax6 homologues), So, Eya, Dach, and Atonal. All of these genes regulate one another, for example, via feedback loops, dampening or activating each other, allowing fine control over the process. There is no single switch but rather a flexible regulating system that provides both stability and flexibility to the eye design.

A second regulatory layer comes from external signalling pathways (Hth, Dpp, and EGF), which feed into the network at multiple points. These genes provide timing and positioning cues to ensure that at the local level, the different processes that build the eye happen in the right order and in the right place; they provide the context.

The same regulatory genes can be reused or rewired to produce new forms. Evolution often works with old parts in new ways.

Once we see that eye development relies on an interconnected network where all genes are “listening to many voices”, it becomes clear that evolution does not need to reinvent a new system to create a novel eye. Simply tweaking a single interaction, weakening a connection, or introducing a new gene (by duplication or enhancer fusion), or even bypassing a gene entirely, will produce new eye type.

This flexibility explains why eyes can differ so dramatically across animals while still sharing a conserved set of regulatory genes, and why having the same genes does not guarantee identical organs. For example, even within cnidarians, the range of complexity of eyes is astonishing: the box jellyfish has 4 clusters of eyes, each cluster containing 3 different types of eyes, allowing it to extract different kinds of information from their environment. In contrast, sea anemones (also cnidarians) have no image-forming vision at all but have light-sensing organs to orient themselves.

Bringing it together

For a long time, it was thought that eyes had been invented multiple times independently. But the molecular evidence now points to a single point of origin.

Now comes the kicker…

Conclusion: Why does any of this matter?

Because it forces us to confront how improbable vision really is.

We trust our eyes more than any other sense, and we are right to do so: vision gives us the richest, most reliable grasp of the world, with roughly half of our brain involved in processing vision. Our eyes make it possible to understand others (humans and animals), to recognise emotions, and even to read these very words. It even allows us to understand things that we cannot actually see: science would not exist without the ability to lock in and pass on knowledge in written form.

Let this be your takeaway, if nothing else: this entire system that allows us to see beautiful landscapes, be moved by art, and look into someone’s eyes… All of this… almost did not happen. We owe this to a random mutation in a tiny cluster of cells over 600 million years ago, a genetic accident, that snowballed into everything we now experience as our visual world.

Are we not lucky?

It takes a lot of work and time to write these articles. If you find value in what you just read and want to support my work, you can buy me a coffee.

In any case, if you got this far, please like and restack, and feel free to drop any questions in the comments.

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Coming next…

Now, if you want to know how eyes came about, stay tuned for the next edition, where we talk about how and why the first ever eye appeared. Spoiler alert: for millions of years, eyes were blind.

REFERENCES:

Callaerts, P., Halder, G., & Gehring, W. J. (1997). PAX-6 in development and evolution. Annual review of neuroscience, 20(1), 483-532.

Chow, R. L., Altmann, C. R., Lang, R. A., & Hemmati-Brivanlou, A. (1999). Pax6 induces ectopic eyes in a vertebrate. Development, 126(19), 4213-4222.

Gehring, W. J. (2005). New perspectives on eye development and the evolution of eyes and photoreceptors. Journal of Heredity, 96(3), 171-184.

Gehring, W. J., & Ikeo, K. (1999). Pax 6: mastering eye morphogenesis and eye evolution. Trends in genetics, 15(9), 371-377.

Halder, G., Callaerts, P., & Gehring, W. J. (1995). Induction of ectopic eyes by targeted expression of the eyeless gene in Drosophila. Science, 267(5205), 1788-1792.

Hill, R. E., Favor, J., Hogan, B. L., Ton, C. C., Saunders, G. F., Hanson, I. M., ... & Heyningen, V. V. (1991). Mouse small eye results from mutations in a paired-like homeobox-containing gene. Nature, 354(6354), 522-525.

Hoge, M. A. (1915). Another gene in the fourth chromosome of Drosophila. The American Naturalist, 49(577), 47-49.

Kumar, J. P. (2009). The molecular circuitry governing retinal determination. Biochimica et Biophysica Acta (BBA)-Gene Regulatory Mechanisms, 1789(4), 306-314.

Kumar, J. P. (2009). The sine oculis homeobox (SIX) family of transcription factors as regulators of development and disease. Cellular and Molecular Life Sciences, 66(4), 565.

Kumar, J. P. (2010). Retinal determination: the beginning of eye development. Current topics in developmental biology, 93, 1-28.

Quiring, R., Walldorf, U., Kloter, U., & Gehring, W. J. (1994). Homology of the eyeless gene of Drosophila to the Small eye gene in mice and Aniridia in humans. Science, 265(5173), 785-789.

Samadi, L., Schmid, A., & Eriksson, B. J. (2015). Differential expression of retinal determination genes in the principal and secondary eyes of Cupiennius salei Keyserling (1877). EvoDevo, 6(1), 16.

Salvini-Plawen, L. v., & Mayr, E. (1977). On the evolution of photoreceptors and eyes. In M. K. Hecht, W. C. Steere, & B. Wallace (Eds.), Evolutionary biology (Vol. 10, pp. 207–263). Plenum Press.

Ton, C. C., Hirvonen, H., Miwa, H., Weil, M. M., Monaghan, P., Jordan, T., ... & Saunders, G. F. (1991). Positional cloning and characterization of a paired box-and homeobox-containing gene from the aniridia region. Cell, 67(6), 1059-1074.

Walther, C., & Gruss, P. (1991). Pax-6, a murine paired box gene, is expressed in the developing CNS. Development, 113(4), 1435-1449.

Have you ever disagreed so vehemently about the colour of something?

Who is right? Neither.

The backpack has no colour at all. This is true for literally everything around us. The world has no colour; colour is in the brain of the beholder, if you will.

That said, if that backpack were to have a colour, it would so definitely be green.

We all see colours a little differently. For example, what I call white is not the same shade you call white. But there are some people who see colours more differently than others.

Colour blindness is very common. People who are colourblind do not see only in black and white, as the name suggests, but they see different colours than most people. That said, achromatopsia (a deficiency that makes people see only in shades of grey) does exist, but it is extremely rare.

Here are some facts:

• Colour deficiency is estimated to affect 300 million people worldwide.

• Roughly 8% of all men and 0.5% of all women are colourblind, with some distribution patterns across geographies and ethnic backgrounds.

• There are different types of colour blindness, with 95% of all colour deficiency being related to red-green deficiency.

A little history

John Dalton was the first person to scientifically document colour blindness in 1798, based on observations of his own experience, as he was red-green colourblind himself. When he looked at the light split by a prism, he could not see the 7 colours that Newton had described.

“To me it is quite otherwise: —I see only two or at most three distinctions. These I should call yellow and blue; or yellow, blue and purple. My yellow comprehends the red, orange, yellow and green of others; and my blue and purple coincide with theirs” (Dalton, 1798, p. 31)

Dalton thought his vitreous humour (the gel inside his eyes) was tinted blue and filtering out the reds. He asked a physician and friend, Dr. Joseph Ransome to do a postmortem examination of his eyes. In 1844, the day after Dalton died, his friend complied and refuted his theory (Musselman, 2000).

It was Thomas Young in 1802, who first suggested the real cause lay in the retina. Before we knew about photoreceptors, he theorised that 3 light-sensitive particles would be sufficient for us to see all the colours, and that colour deficiencies came from missing or altered ones.

Most of us are trichromats

Our eyes have two types of photoreceptors: rods, used for night vision, and cones for colour and detail. Read this excellent deep dive on cones and rods. Cones contain light-sensitive proteins called opsins, each tuned to a specific range of wavelengths. Humans are rare amongst mammals in that they have three types of cones, with peak sensitivities at roughly long (~560 nm), medium (~530 nm) and short (~420 nm) wavelengths. Most mammals, like cats and dogs, are dichromats (two cones). (If you are curious about how your pet sees colour, that is coming in the future.)

These cones are often called red, green and blue, but this is misleading because cones cannot see colours, nor convey colour information. For example, if you miss the “blue” cone, you can still see turquoise but not yellow. Confused? Good.

This is the part explainers leave out

This is why you come to me. Why does losing the function of a single cone (any of them) shift your entire colour perception instead of just knocking down that colour?

Cones convert light into electrical impulses. Cones can only indicate when light is hitting them. You could say they are colourblind in the literal sense. The colours we see are the result of a computation, a comparison of the inputs from the different cones.

The brain creates colour by comparing cone signals. The electrical information generated by the cones is rearranged into three new separate pathways. As you can see in the image above, there is a broad overlap in the sensitivity of the three cones. Any wavelength will stimulate most cones at the same time, but each to a different degree. To determine a colour, neurons need to compare how each of the cones responds to that light.

Neurons literally add and subtract cone inputs to build “opponent channels.” Information from each channel is grouped into 3 new pathways. The cool thing is that the same cone inputs are compared in different ways to obtain different kinds of information.

• The red-green channel subtracts the M-cone input to the L-cone input → L – M.

• The blue-yellow channel compares S-cone input against the combined input of the other two → S – (L + M).

• Luminance is obtained by adding the input from L and M → L + M

Graphically:

These three pathways remain largely separate, all the way from the retina, through the lateral geniculate nucleus (the brain’s sensory relay station), and only begin to converge once they reach the visual cortex (V1) at the back of the brain.

This is also why we cannot see a reddish-green or a blueish-yellow. Those colours cancel each other out along the opponent axes.

From this wiring, it follows that there can be different types of colour vision depending on how many cones are affected, and specifically, which ones.

How can genes go wrong [or coding errors]

We rely on cones and their opsins for colour vision. The instructions for both the cones and their light-sensitive opsin sit in our genes. Mutations, deletions, or rearrangements in these genes during cell division can disrupt colour perception in different ways:

• A cone altered → The cone is present and functioning, but the sensitivity of the opsin is shifted to a slightly different peak wavelength. Vision still relies on three cones, but some colours appear less distinct and duller. This results in anomalous trichromacy, and depending on the cone affected, it is called protanomaly (L), deuteranomaly (M), or tritanomaly (S)*.

• A cone missing or silenced → Alterations in the gene for a cone or an opsin can silence or delete an entire cone type. This reduces vision to two cones, which is known as dichromacy. The deficiencies are: protanopia, deuteranopia and tritanopia.

• All cones knocked out →In very rare cases, mutations in genes that code for the proteins involved in the phototransduction cascade can silence cone function entirely. This is the process that turns light into electrical signals and will affect all the cones, leaving vision to rely only on rods. This is called achromatopsia. This comes accompanied by blurry vision, light sensitivity (if you have read my cones and rods article, you surely know why), and sometimes nystagmus (involuntary eye movement).

* Names in vision science are not very creative - they often refer to the order of discovery (think V1, V2, V3…). In this case, inspiration came from Greek: protos = first; deuter = second; tritos = third. (Meanwhile, scientists who get to name proteins get all the fun: Sonic hedgehog, Ken and Barbie, and my favourite: fuzzy; are all actual protein names. But I digress…)

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These genetic coding errors give rise to the congenital (inherited) types of colour vision in humans, from the common red–green deficiencies to the very rare complete loss of cone function.

Not the Same Rainbow

Here are some examples of how colour blind people see.

These images are only for reference. Colour blindness is different for each person. It ranges from a mild difficulty in distinguishing colours to an inability to see certain colours. Some people are not even aware of their colour blindness.

Notice above how the protanopia and deuteranopia images look rather similar. This is because the input from red and green cones combines into the same axis. In fact, John Dalton was thought to be a protanope, based on his description of his own colour perception, but in 1995, an analysis of tissue from his eyes confirmed him to be a deuteranope (Hunt et al.). Yes, they still have his eyes. You can visit them at the Science and Industry Museum in Manchester (item Y1997.6.38).

Do you see colours differently from people around you? Which colours do you struggle with most?

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Why is red-green colour deficiency more common than blue-yellow?

Red-green problems

The L and M (red and green) cones are very similar; their sensitivity curves almost overlap, as shown in the first image. The genes that code for them, OPN1LW and OPN1MW respectively, sit side by side in the chromosome and share nearly 98% of their nucleotide material. This closeness and similarity makes them especially prone to mistakes during cell division: the genetic material can be confused, leading to errors such as unequal recombination, mutations and deletions.

Blue-yellow problems

In contrast, the gene that codes for the S cone (blue) sits on an entirely different chromosome, completely separate from the L and M genes on the X. It also shares only about 40% of its sequence with them. This distance and distinctiveness make it much more stable and less prone to the recombination errors that plague the red–green pair.

Why is colour deficiency most common in men?

We humans have 23 pairs of chromosomes, 22 shared by everyone and 1 that determines the sex: males carry an XY pair, while females carry XX. The genes that code for the L and M cones sit on the X chromosome. This means women have a spare one, so as long as one copy works normally, they will experience normal trichromatic vision. They will still carry the defective gene and pass it on.

Can we say then that, if a man and a woman disagree about the colour of, say, a backpack, the woman is statistically more likely to be right?

I withdraw the question, Your Honour.

Can we have more than 3 cones?

Yes. But only if you are a woman.

Tetrachromacy means that a visual system relies on 4 cone types. In humans, this possibility exists only in women, because the L and M opsin genes sit on the X chromosome, and women have two of them.

Women who are carriers of anomalous trichromacy inherit one normal opsin gene and one shifted version. As a result, they may express both, giving them S, M, a “normal” L, and a shifted L or M cone — four in total.

So does having four cones actually mean you see a richer rainbow? When 24 women with this genetic setup were tested behaviourally (using colour tests to identify what they saw), only one showed clear evidence of using all four cones in colour perception (Jordan et al., 2010).

How can we explain that? Most likely because our visual system evolved to support three cones, and adding a fourth one does not mean the brain will necessarily exploit it. What we perceive is limited by our brain infrastructure. Have I said that before? Probably. But it is a hill I will happily die on: perception is built in the brain.

The genetics at a glance

Different colour vision deficiencies follow different inheritance rules:

• Red–green → X-linked recessive. A single mutated X causes a deficiency in men, but women need both Xs mutated.

• Blue–yellow → Autosomal dominant. Caused by mutations on chromosome 7, not a sex chromosome, and therefore affects both men and women equally.

• Achromatopsia → Autosomal recessive. Both parents must pass on a defective copy. It involves multiple gene variants (e.g., CNGB3 or CNGA3) and affects men and women equally, although it is very rare.

Can colour blindness be acquired?

So far, we have talked about colour vision deficiencies that are inherited, which are by far the most common, but colour blindness can also be acquired later in life.

Why it happens

Acquired colour vision deficiency becomes more common with age, because many diseases that affect vision are age-related. Here are some examples (the list is much, much longer):

• Retinal disease: macular degeneration, diabetic retinopathy, retinal detachment, retinitis pigmentosa.

• Optic nerve problems: glaucoma, optic neuritis.

• Neurological disease: Parkinson’s disease, Alzheimer’s disease , multiple sclerosis.

• Cortical damage: very rare; injury to area V4 can erase colour from our vision.

• Medications, toxins: hydroxychloroquine, ethambutol, carbon monoxide, lead.

• Lifestyle factors: heavy alcohol use in adolescence/early adulthood may subtly impair colour vision (Brasil et al., 2015).

Inherited vs acquired – the key differences

• They affect mostly different axes.

  About 95% of inherited cases affect the red–green axis, while acquired deficiencies more often disrupt the blue–yellow axis. In a study of 865 people aged 58–102, Schenk and colleagues (2014) found that perceptual losses along the blue–yellow axis were about three times as common as red–green losses.

• Congenital is more stable

  Congenital colour deficiency tends to affect all cones of the same type in both eyes, it is present across the entire visual field, and remains stable from birth throughout life. On the contrary, acquired colour vision deficiency is a little messier. It can affect only a portion of the visual field or a single eye, or it can affect both eyes differently. It can also progress or reverse over time.

Awareness matters

Knowing how prevalent colour vision deficiency is matters not only for increasing awareness and implementing accessible design, but also for shaping policies such as early testing, which can be reliably done from the age of 4.

Without early testing, symptoms in children can go unnoticed or be misinterpreted as inattention or poor performance. Think science, biology, art or any topic that involves colour-coded graphics and maps. In some cases, children have erroneously been placed in lower academic tracks. This can cause frustration and self-esteem issues.

Accessible design goes beyond individual accommodations; it makes information more inclusive in all industries. In science, for example, a lot of information is locked inside colour-coded figures.

Daily life, work and workarounds

Colour deficiency is not disabling, but it can be inconvenient. Colourblind people may struggle to identify when fruit is ripe or if meat is cooked through. They learn to rely on other cues or remember the order of the colours.

Most challenges come from living in a world built for trichromats, when a lot of the communication is encoded in colour, from traffic lights to charts and signage.

Colour blindness can also limit career options. Regulations vary by country and profession, but generally, jobs in aviation, transport, engineering, and the military have strict standards, as colour is regularly used for signalling. Some roles in technical or medical fields may also be restrictive.

That said, many people go through life without realising they are colourblind. And those who do know, are often well adapted and may not feel the need to see more colours.

Recommendations

If you work with visuals or teaching materials and want to do your part, here are a few easy changes that make a big difference for people with colour vision deficiency:

• Check your visuals. Run your images through a colour blindness simulator if you can. If not, just switch to greyscale and look for contrast. You would be surprised how much information lives in luminance alone.

• Do not pack all your information into colour alone. Use textures, labels or symbols to make figures and charts more accessible.

• Check your circle. Find out if anyone you regularly work with has any colour needs. You can use desktop simulators to help you design.

• Encourage your team to keep accessibility in mind when creating content.

  Or make it easier on yourself → 👇 just share this article with them.

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Conclusion

All that is happening is that we are seeing the same world differently.

People with colour blindness are not seeing the wrong colours, they are just picking up a different wavelength. The colours we all see are equally real, even if they are different.

There are many (many!) different reasons for colour vision deficiency. The fact that so many different genes, proteins, and pathways can affect colour perception speaks of the many moving parts and the unique balance that is our visual system.

From a biological perspective, there is no survival threat for colour blindness. The inconvenience comes from living in a society designed around a trichromatic standard.

Colour vision is just another reminder that reality is different for everyone.

If you had a colour deficiency, would you want to know? Would you feel robbed to find out X% of people see colours you cannot see? Are you colourblind? If so, how does it affect you? Let me know in the comments.

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An entirely unrelated question

Before you go, can you help me with a survey? Only one question:

Look at the object below and tell me, what colour do you see?

If you enjoyed this, share it with someone who sees the world a little differently.

It takes a lot of work and time to write these articles. If you find value in what you just read and want to support my work, you can buy me a coffee.

In any case, if you got this far, please like and restack, and feel free to drop any questions in the comments.

Buy me a coffee ☕️

Share

References:

Brasil, A., Castro, A. J. O., Martins, I. C. V., Lacerda, E. M. C., Souza, G. S., Herculano, A. M., ... & Silveira, L. C. L. (2015). Colour vision impairment in young alcohol consumers. PLoS One, 10(10), e0140169.

Dalton, J. (1798). Extraordinary facts relating to the vision of colours: With observations. Memoirs of the Literary and Philosophical Society of Manchester, 5(1), 28–45. https://digital.sciencehistory.org/works/fb4949523

Hunt, D. M., Dulai, K. S., Bowmaker, J. K., & Mollon, J. D. (1995). The chemistry of John Dalton’s color blindness. Science, 267(5200), 984-988.

Jordan, G., Deeb, S. S., Bosten, J. M., & Mollon, J. D. (2010). The dimensionality of color vision in carriers of anomalous trichromacy. Journal of vision, 10(8), 12-12.

Neitz, J., & Neitz, M. (2011). The genetics of normal and defective color vision. Vision research, 51(7), 633-651.

Musselman, E. G. (2000). Local colour: John Dalton and the politics of colour blindness. History of science, 38(4), 401-424.

Schneck, M. E., Haegerstrom-Portnoy, G., Lott, L. A., & Brabyn, J. A. (2014). Comparison of panel D-15 tests in a large older population. Optometry and Vision Science, 91(3), 284-290.

A quick note before we start. This article is a bit more abstract. Here, we start with patients’ experiences of conscious and unconscious vision, then we look at their brain activity to narrow down on where consciousness sits. And finally, we extrapolate some abstract claims about what and where consciousness is. If you get lost, just keep reading and the pieces should fall into place by the end.

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Ready? Here we go.

Catching up from Part 1: Last time, we looked at Riddoch syndrome, a disorder where patients who are blind from damage to the main visual cortex (V1) can still be consciously aware of something moving in their blind field, although it looks ghostly and shapeless. Back in 1917, V1 was considered the sole seat of conscious vision, but neuroimaging studies confirmed that alternate pathways bypass V1 and send coarse information directly to V5, the brain’s motion processing area. That is how Riddoch patients see moving shadows without a primary visual cortex.

You should know by now that I chose my words very carefully, yet I just said “Consciously aware”. This may sound redundant, but you will soon see it is not.

Roll cameras.

What if I told you that there are blind patients who can act as if they can see? They can navigate around obstacles, even squeeze through narrow spaces, and even ride a bike safely!

The Blindsight story

Patient DB was one of the first blindsight patients (Weiskrantz et al., 1974). Surgeons removed an abnormal tangle of blood vessels in his right occipital lobe, which left him blind in his left visual field.

He insisted that he could not see, but when he was pressed to “guess” the direction of a line, point at an object in his blind field, or guess the direction of something moving, he could do that with surprising accuracy.

What looked like lucky guesses was actual proof that the brain can process visual information, and even guide behaviour, while the patient remains unaware.

The test

Blindsight is studied using a forced-choice paradigm. This simply means that the patient is required to give an answer, even when they insist that they cannot see. If they perform at chance (around 50% correct), they are just guessing. But if their performance is consistently above that, then it cannot be explained by chance, and therefore, they “know” … Even if they do not know that they know. In other words, they are aware of the visual stimulus, just not consciously aware. – See what I did there? Brought it right back.

Blindsight in action: Watch a blindsight patient navigate a busy hallway.

Patient TN was a doctor who suffered two consecutive strokes one month apart, each damaging one side of his visual cortex, leaving him blind over his entire visual field.

“He walked like a blind man, using his stick to track obstacles and requiring guidance by another person when walking around the various laboratory buildings during testing” (de Gelder et al., 2008).

To test his blindsight navigation skills, de Gelder and colleagues asked him to walk to the other side of a cluttered hallway, without assistance and without his cane. Remarkably, TN walked smoothly around obstacles of different sizes and heights. At some point, he even turned sideways to squeeze between a box and a wall. “He walked much faster than we had expected, without hesitation or any kind of exploration,” said de Gelder (Robson, 2008). When asked, TN said he had not seen anything and was not aware of avoiding any objects.

This video (de Gelder, et al., 2008) is one of the most compelling demonstrations of the brain guiding movement in the absence of visual awareness. (The person following TN closely was Dr Lawrence Weiskrantz, who also studied DB).

Something to think about:

If patients can respond to unconscious input without realising it, could we too be reacting to cues we do not notice? Can you think of the last time you had a hunch that proved right, or sensed something was “off” before you knew why? I would love to hear about it.

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Blindsight vs. Riddoch

But what do these syndromes have in common, and how do they differ? They both involve visual information getting through in their blind field. In Riddoch syndrome, patients are consciously aware of motion, even though they cannot see the moving object itself and are entirely blind to anything stationary. In blindsight, patients report no awareness at all but behave as if they can unconsciously discriminate objects around them. In other words:

The most famous blindsight patient

We met patient GY in Part 1, as his case was key in showing V5’s role in conscious motion perception (Barbur et al., 1993).

He was only 8 years old when a car accident damaged his occipital lobe, and he lost vision in his right visual field. For decades, he insisted he could see nothing at all. But he became the most studied blindsight patient, undergoing PET, fMRI, MEG and psychophysics tests.

GY’s case was unusual: he responded differently depending on the stimulus. Sometimes, he reported seeing ghostly shadows (conscious awareness, classic Riddoch syndrome), and sometimes he performed well above chance while insisting he saw nothing (classic blindsight).

This offered Semir Zeki and Dominic Ffytche (1998) a rare opportunity to ask: Does the brain look different when vision is conscious compared to when it is unconscious? They used different stimuli to trigger each response and imaged GY’s brain during both responses. Since one response involved conscious awareness and the other one unconscious awareness, looking at brain activity could tell us something about the neural bases for consciousness.

Brain activity during conscious and unconscious vision

Zeki and Ffytche found that different brain regions were active depending on whether GY was conscious of movement or not. They could classify GY’s state of awareness just by looking at the brain activation.

• Conscious awareness (the classic Riddoch syndrome): There was activity in V5, showing yet again that V5 can support conscious motion awareness even when V1 is damaged.

• Discrimination without awareness (blindsight): There was no activation in V5, even though there was activity in V3 and other neighbouring areas, showing that the brain was receiving the information.

How the researchers explained it

Zeki & Ffytche showed that conscious and unconscious vision can be anatomically dissociated.

Long story short, they concluded that blindsight is only one manifestation within the broader Riddoch syndrome.

Long story long, they proposed that damage to V1 uncouples two processes that normally run together: the brain’s ability to discriminate a stimulus and our awareness of perceiving it. In everyday vision, these two are fused, so we experience it as the same thing. But the researchers propose that with V1 gone, the two can drift apart.

The difference may seem subtle, but it is one thing for the brain to notice something (discrimination) and even act on it, and another to consciously know that we are perceiving it (conscious awareness). Zeki and Ffytche offer us a visual aid (the red writing is mine):

Hallucination and consciousness

More recently, in 2023, Beyh and colleagues (including both Zeki and Ffytche) revisited the question of V5’s role in conscious vision with a more fine-grained analysis. Their patient, ST, was a man in his early 50s with partial blindness from a V1 lesion. He could see motion in his blind field and fit the classic description of Riddoch syndrome.

By carefully changing the stimulus, the researchers could elicit different perceptual responses, and then link each to distinct brain activity patterns:

• When ST consciously saw motion, decodable patterns of activity appeared in V5

• When ST reported seeing nothing (while being presented with motion): early visual areas were active but V5 showed no activity.

In other words, they could tell from the brain scans alone whether ST was aware or not. They could see that visual information was getting through to the brain because they found activation in early visual areas. But there was no conscious vision if V5 was not active. As the authors put it:

“Moving stimuli may give rise to neural activity in medial visual areas, but unless this is associated with V5 activity, they remain unseen” (Beyh & Zeki).

But the study did not stop there

By changing the contrast and speed of the stimulus, the researchers could study two more perceptual responses:

• False confidence: In some trials, ST reported seeing motion with high confidence, yet his answers were no better than chance. Sometimes he misjudged the direction of movement, other times the movement itself. Brain activity during these trials pointed to the inferior frontal gyrus, an area linked to conflict monitoring and decision-making under uncertainty.

• Hallucinatory motion: In blank trials with no movement at all, ST sometimes reported seeing motion. This correlated with activity in the hippocampus, a region important for memory and spatial navigation. The authors suggested these were internally generated perceptions, possibly triggered by the brain’s predictive machinery.

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But was V5 active?

There was activity in V5 in three of the four conditions:

• When ST could see motion

• False confidence

• Hallucinatory movement

The only time when there was no activity in V5 was when ST reported not seeing the stimulus, even though moving stimuli were present and other early visual areas in his brain were active.

This suggests that V5 is not just a motion detector. Its activity seems tied to whether motion reaches conscious awareness at all.

And motion is not unique in this respect: V4 plays a similar role for colour. When V4 is damaged, patients lose conscious colour perception, even though their eyes still register wavelengths. They can describe shapes and motion, but the world appears in greyscale, a condition known as cerebral achromatopsia.

Asking the right questions

There is clear value in these approaches of teasing out different degrees of awareness, as shown by Zeki & Ffytche and by Beyh and colleagues. There is not always a clear divide between seeing and not seeing. In the classic blindsight studies by Weiskrantz and colleagues, patients could only answer yes or no when asked, “Did you see anything?” A patient with a vague perception might well say “no,” and still perform above chance. In 2008, Overgaard and colleagues introduced the Perceptual Awareness Scale, where patients could respond with clear image, almost clear image, weak glimpse, or not seen. Their behavioural results tracked with what they reported. What looks like blindsight could in fact be degraded but genuine conscious vision.

What / where is Consciousness?

The implication of this is that conscious vision is not a single, all-or-nothing event but that it might be modular, relying on several micro-consciousness areas distributed across the brain (Zeki, 2003).

“Consciousness is not a unity, and there are instead many consciousnesses that are distributed in time and space” (Zeki, 2003).

Zeki’s “theory of multiple consciousnesses” is based on the idea that consciousness builds on distinct specialised areas, each geographically and functionally separate. Each mini-consciousness area contributes its own slice to our awareness, and the brain binds them together into the illusion of a unified flow of experience, what Zeki calls global consciousness.

Damage to any of those slices results in an alternative visual reality. Word choice again: it is an alternative visual reality but not a false one, since all perception is itself a constructed representation.

And a bonus one for the road

If Zeki’s theory shows us how consciousness is about integrating different pieces, here comes one more case that shows us how the brain can reassemble the puzzle in surprising new ways.

MB was a 21-year-old male patient whose occipital lobes were damaged around the time he was born. Since childhood, he “behaved as profoundly visually impaired,” yet he could guess the direction of fast-moving objects with 100% accuracy. Remarkably, he could ride a bike safely.

“He participated in various ball games and running events. He rode a bicycle and safely avoided people and parked and moving cars. He also played video games that were based on movement” (Giaschi et al., 2003).

An fMRI of MB’s brain showed no activation in V1 (as expected) but also no activity in V5 either. And yet, he could still see motion, consciously. What part of his brain was processing this motion? The activity appeared in the right premotor cortex, the precuneus (linked to memory and self-awareness) and the posterior superior temporal sulcus.

Because MB’s damage occurred so early in life, his brain was still in a critical period of development. The young brain is extraordinarily plastic, and so other regions could take over the task of processing motion.

Consciousness may be more like a sense-making computer, developing networks wherever it can to interpret the world by whichever method is available. The brain finds a way to get the job done, to help you navigate the world and keep you safe. It is not about elegance; it is about existing.

Consciousness is whatever the brain does to make sense of the world.

Final reflections

If conscious visual experience, which feels so direct and unified to us, can be supported by all these varied visual pathways, what does this say about the fundamental nature of consciousness itself? Is it tied rigidly to specific structures, or is it something that emerges from complex integrated activity, wherever it happens in the brain?

Conclusion: what perception disorders tell us about consciousness

The cases of Riddoch syndrome and blindsight challenge our everyday assumption that seeing is knowing. Vision is not a singular faculty neatly housed in one brain area. And neither is consciousness. They emerge from a network of regions, each contributing fragments of awareness. Even when the usual pathways are gone, the brain uses what remains to keep us connected to the world.

Perception disorders reveal something profound: consciousness is not a fixed essence but a state of sense-making, a biological necessity for survival. The brain assembles whatever pieces it can into a workable version of reality, enabling conscious perception when necessary and guiding behaviour even behind our awareness.

This all tells us that awareness goes far beyond just seeing. Your brain knows more than it tells you. Consciousness does not mean having access to everything but knowing enough. The line between conscious and unconscious, seen and unseen, is a bit blurred as the brain tirelessly attempts to interpret, predict, and give you enough to navigate the world in real time.

Acknowledgement:

A warm thank you to Dr. Ahmad Beyh for taking the time to read this article (Parts 1 and 2) and share thoughtful feedback.

It takes a lot of work and time to write these articles. If you find value in what you just read and want to support my work, you can buy me a coffee.

In any case, if you got this far, please like and restack, and feel free to drop any questions in the comments.

Buy me a coffee ☕️

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REFERENCES

Barbur, J. L., Watson, J. D., Frackowiak, R. S., & Zeki, S. (1993). Conscious visual perception without V1. Brain, 116(6), 1293-1302.

Beyh, A., Rasche, S. E., Leff, A., Ffytche, D., & Zeki, S. (2023). Neural patterns of conscious visual awareness in the Riddoch syndrome. Journal of Neurology, 270(11), 5360-5371.

De Gelder, B., Tamietto, M., van Boxtel, G., Goebel, R., Sahraie, A., Van den Stock, J., ... & Pegna, A. (2008). Intact navigation skills after bilateral loss of striate cortex. Current biology, 18(24), R1128-R1129.

Giaschi, D., Jan, J. E., Bjornson, B., Au, S., Lyons, C. J., & KH, P. (2003). Conscious visual abilities in a patient with early bilateral occipital damage. Developmental Medicine & Child Neurology, 45(11), 772-781.

Overgaard, M., Fehl, K., Mouridsen, K., Bergholt, B., & Cleeremans, A. (2008). Seeing without seeing? Degraded conscious vision in a blindsight patient. PloS one, 3(8), e3028.

Robson, D. (2008, December 22). Blind man ‘sees’ his way past obstacles. New Scientist. https://www.newscientist.com/article/dn16324-blind-man-sees-his-way-past-obstacles/

Weiskrantz, L., Warrington, E. K., Sanders, M. D., & Marshall, J. (1974). Visual capacity in the hemianopic field following a restricted occipital ablation. Brain, 97(1), 709-728.

Zeki, S. (2003). The disunity of consciousness. Trends in cognitive sciences, 7(5), 214-218.

Zeki, S., & Ffytche, D. H. (1998). The Riddoch syndrome: insights into the neurobiology of conscious vision. Brain: a journal of neurology, 121(1), 25-45.

We have spoken about LM, a woman who, despite having perfect sight, had lost the ability to see motion and could see the world only as a series of still images. If you have not read that, you can catch up here. But what if the opposite is also possible? Can someone see an object move while not being able to see the object itself? If so, what do they see?

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Vision is associated with the primary visual cortex, also called V1, at the back of the brain. In 1905, anatomist Paul Flechsig wrote that V1 was “the only entering place of the visual radiation into the organ of psyche”, and by that he meant that V1 is the only place where visual information enters consciousness.

WW1 and ghostly motion

British neurologist Captain George Riddoch served as an officer in the Royal Army Medical Corps during the First World War. He treated soldiers who were blind due to gunshot wounds to the primary visual cortex (V1). This was a common wound as the helmets left the back of the head exposed.

Riddoch mapped the visual fields of each patient to define the size and shape of their blind field. To his surprise, some patients reported that sometimes they could see “something moving” inside their blind fields. For example, one soldier could see the motion of the feet of the people walking by, but nothing above the ankles. Another said he could see the motion of the spoon when he was being fed. Even though they were convinced they could see something, what they saw was “so vague and shadowy” (Riddoch, 1917).” The soldiers found it difficult to describe what they saw:

“The ‘moving things’ had no form, and the nearest approach to colour that he could attribute to them was a shadowy grey” (Riddoch, 1917).

Could it be that motion was not merely a component of vision but a separate feature of visual perception altogether?

What is Riddoch syndrome?

Riddoch syndrome is a rare neurological disorder in which people blind from damage to the primary visual cortex can still consciously perceive movement in their blind field, while remaining unable to see shape or colour. Depending on how much of the cortex is damaged, the blind field may cover the whole visual field or a portion of it.

What Riddoch saw

Riddoch’s 1917 paper challenged the accepted view of vision. At the time, V1 was considered the only gateway to conscious sight, and vision itself was thought of as a single sense, divided into light, colour, and form. Motion was not even in the picture. Riddoch’s observations suggested otherwise. By suggesting that patients could see motion without having a functioning V1, he was proposing that motion has its own neural basis outside the brain’s “visual centre.” Riddoch went further and suggested that vision was not unitary but made up of distinct perceptions and that they could fail independently.

Not surprisingly, his idea did not catch on. Not only because it was a heretic notion at the time, but also because there was another plausible explanation.

Same front, same side, different interpretation

At the same time Riddoch was studying this phenomenon, same war, same side, same city, Irish neurologist Gordon Holmes was also finding patients who could see movement inside their blind fields.

Holmes was stationed at No.13 Stationary Hospital in Boulogne, barely 2 km from the Empire Hospital, where Riddoch worked. But, while Riddoch was treating a handful of wounded officers in a repurposed private clinic, Holmes was treating soldiers on a ratio of 90 patients to 1 doctor (secondary account, but many, in any case).

Under those conditions, Holmes mapped the visual fields of around 400 soldiers who had damage to their visual area due to gunshot wounds. But if he found the same phenomenon, why did he disagree with Riddoch? Well… asking the right question is everything. Both men were mapping visual charts by asking patients to report when they saw a disk on a screen, and then plotting that on their chart (see image above). But Riddoch did not ask his patients to report only when they saw the object, but also when they saw it move. By comparing the answers, he could show that soldiers were detecting movement in the same area where they were blind.

Holmes dismissed Riddoch’s findings, suggesting that this “shadowy” visions could be explained by small patches of V1 that had survived. Holmes’ opinion carried more weight, as he was already a recognised neurologist and Riddoch’s former teacher. Riddoch’s theory was dismissed.

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What evidence was missing?

To challenge Holmes’ rebuttal, Riddoch needed to show a double dissociation. It is not enough to see motion without shape and colour; he would also need the reverse: shape and colour without motion. If only such a case had been reported… (and if you have read this article, you are probably smiling…). However, that took a long time to come.

Riddoch is back, baby!

In 1983, Zihl and colleagues published the case of patient LM, a woman with clear vision of colour and form but no motion. She had intact V1 but damage to area V5 (more on V5 soon). This was the missing puzzle piece that finally cemented V5 as an area dedicated to visual motion, confirming what Riddoch had proposed 66 years earlier.

[Riddoch died in 1947, aged 58]

By the time LM appeared, the old idea that V1 was the only visual processing area was already beginning to crack. Research on animals in the 1960s–70s had already uncovered new visual areas beyond the primary visual cortex: V2 and V3 for integrating form, V4 for colour, and V5 for motion. Animal brains are useful models for mapping pathways, but they are not identical to ours, so findings always need to be confirmed in humans. That is where LM fits in: her case proved that perceiving shape and colour can be separated from perceiving motion, and confirmed what Riddoch had anticipated: that different visual features could fail independently.

If you are curious about the chronology, see here:

• 1960s – Hubel & Wiesel: Single-unit recordings in cat and monkey visual cortex; discovered orientation-selective cells and hierarchical processing. This set the stage for mapping extrastriate areas (outside of V1).

• Early 1970s – V2 and V3: First outlined by Semir Zeki; mapped in detail by David Van Essen and John Allman.

• 1973 – V4 (colour): Identified by Zeki as a colour-selective region; later expanded by Margaret Livingstone & David Hubel in the 1980s.

• 1970s – V5 / MT (motion): Described by Zeki; its functional role confirmed in the 1980s by William Newsome, William Movshon, David Albright, and Ralph Siegel, who showed MT activity was tightly linked to motion perception.

I have left the references out to keep this timeline light. All of these findings come from classic visual neuroscience papers.

The science: understanding the visual brain

Vision is not processed in a single location in the brain. Instead, it is distributed across a network of specialised regions, and information about each feature (colour, shape, motion) is processed as separate streams and then integrated into what we experience as a seamless image.

The Role of Area V5 in Motion Vision

Riddoch patients could see motion because the area V5 in their brain (also called V5/MT) was intact. V5 is the brain’s motion centre. When it is damaged, as in LM, the fluidity of the world itself disappears. Cars appear to jump from one spot to another, people seem to teleport across rooms, and lips move out of sync with voices. Motion is simply gone. This condition, known as akinetopsia or motion blindness, is the mirror opposite of Riddoch syndrome.

Where Riddoch syndrome preserves motion vision without conscious form, akinetopsia (motion blindness) removes motion from a world otherwise fully visible. The two conditions represent opposite disruptions in the visual pathway and underscore the modular nature of perception.

Area V5

In normal vision, V5 receives its main input from V1 (Cragg, 1969; Zeki, 1969, 1971). But if Riddoch patients do not have a working V1, how does V5 still get the information?

See? You are already a step ahead of me. There are indeed alternate pathways to V5.

Alternative routes

Over the last few decades, studies in monkeys showed that several subcortical pathways bypass V1 and project directly to V5:

• The superior colliculus —> It detects sudden movement and drives the eyes and head towards it. It also processes unconscious visual information. It connects to V5 via the pulvinar.

• The pulvinar (in the thalamus) —> It integrates information from several visual areas and acts as a“gatekeeper,” prioritising signals and linking them to attention and emotion. It also connects to the amygdala.

• Lateral geniculate nucleus (LGN, also in the thalamus) —> It is the retina's main relay to the cortex. Most of its visual output goes to V1, but a small shortcut goes straight to V5.

These circuits do not carry fine detail. The signal is fast and coarse, but it offers a survival advantage: it provides a fast lane that warns you if something is hurling towards you.

Modern times – neuroimaging evidence

Until now, all evidence was based on behavioural tests. Barbur and colleagues (1993) were the first to show the brain activity that matched what Riddoch had proposed. They used PET to study patient GY, a 36-year-old patient who was blind in half of his visual field (called hemianopia) due to a car accident at the age of 8. This provides neuroimaging evidence for the first time that V5 could be activated even when there is no activity in V1, and that this activation corresponded with conscious perception of visual movement.

This tells us three important things:

• V5 receives information even when V1 is not functioning

• Activity in V5 is enough to produce a conscious experience of movement

• V1 is not the sole seat of vision, and is not the only place where visual information enters consciousness

Since 1993, fMRI and MEG have taken this much further. Over three decades of work have refined our understanding of how V5, subcortical inputs, and consciousness fit together.

Why this matters

Conscious awareness had long been linked to the primary visual cortex. But Riddoch shows that motion, at least, can breach consciousness without V1. This forces us to confront the fluid boundaries between seeing and not seeing, knowing and not knowing. This calls for a more nuanced model of how awareness emerges from the brain.

Consciousness in fragments

We know now that vision is not unitary but rather different features such as colour, shape, motion, integrated back together. It is not an “all or nothing” phenomenon, and patients with different lesions can see different aspects of the world. But what about consciousness? Is consciousness all or nothing? Or is it a patchwork of separate fragments of awareness?

Coming next…

Riddoch’s patients could see ghostly shadows move in their blind fields. LM could see the world frozen in still frames. But what if I told you that some blind patients can avoid obstacles without knowing they are doing it? Basically, they can see, but they are not aware that they can see. These cases gave rise to the concept of blindsight (vision without awareness) and forced science to rethink not just how we see, but what it means to be conscious.

Continue to Part 2 here.

Acknowledgement:

A warm thank you to Dr. Ahmad Beyh for taking the time to read this article (Parts 1 and 2) and share thoughtful feedback.

It takes a lot of work and time to write these articles. If you find value in what you just read and want to support my work, you can buy me a coffee.

In any case, if you got this far, please like and restack, and feel free to drop any questions in the comments.

Buy me a coffee ☕️

Share

References:

Barbur, J. L., Watson, J. D., Frackowiak, R. S., & Zeki, S. (1993). Conscious visual perception without VI. Brain, 116(6), 1293-1302.

Cragg, B. G. (1969). The topography of the afferent projections in the circumstriate visual cortex of the monkey studied by the Nauta method. Vision research, 9(7), 733-747.

Campbell, A. W. (1905). Histological studies on the localisation of cerebral function. University Press.

McFadyen, J. (2019). Investigating the subcortical route to the amygdala across species and in disordered fear responses. Journal of Experimental Neuroscience, 13, 1179069519846445.

Riddoch, G. (1917). Dissociation of visual perceptions due to occipital injuries, with especial reference to appreciation of movement. Brain, 40(1), 15-57.

Zeki, S. M. (1969). Representation of central visual fields in prestriate cortex of monkey. Brain research, 14(2), 271-291.

Zeki, S. M. (1971). Cortical projections from two prestriate areas in the monkey. Brain research, 34(1), 19-35.

Zihl, J., Von Cramon, D., & Mai, N. (1983). Selective disturbance of movement vision after bilateral brain damage. Brain, 106(2), 313-340.

How is the sharpest part of our vision so bad at seeing… well, sharply?

As a child, I often stayed at my grandmother's house. At night, as I lay in bed in the dark, I could make out a small statue on a shelf, always on the edge of my vision. But every time I looked directly at it, it would vanish. Every single time. I was not the magical thinking type, even then, but not understanding why bothered me.

Now I know the mechanism behind this, and it is one of my favourite evolutionary adaptations in neuroscience.

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The illusion of effortless vision

We trust that we open our eyes and reality simply filters in. The whole scene presents itself instantly and fully formed, sharp and in rich detail. We can see both in bright daylight and in near darkness. And we can also see very fast, enabling us to avoid collisions and see movement.

Yet vision is not so effortless. There are simultaneous, complementary systems at play that, combined, give us a seamless experience of sight and the illusion of a complete scene in focus. In truth, our eyes can only see sharp detail in a tiny fraction of the visual field at any given moment. The rest is computational magic.

The brain is very expensive, and light-sensitive cells are particularly energy hungry. We need to detect different features in all light conditions, very fast, but also as economically as possible... Enter the cones and rods.

Introducing the cones and rods

We manage fast, sharp vision by relying on the two main photoreceptor types: cones and rods, each with different specialisations. Both respond to light by converting photons (the smallest unit of light) into electrical impulses. In evolutionary terms, the cones evolved from rods, so the underlying mechanisms are the same, even though their functions are almost opposite (more on functions later).

Remarkably, it is how they are wired into the visual pathway and their distribution across the retina that determines how much detail and light we can detect. This setup provides a flexible system, capable of high detail, fast response and impressive sensitivity in near-total darkness – and that is what gives us this wonderfully rich visual experience.

Same but different

I said earlier that cones evolved from rods, yet they have almost the opposite function. There is a bonus table at the end of the article comparing them side by side, so you can just enjoy the reading for now.

What they have in common: they convert light to electrical signals.

Light enters the eye and is absorbed by opsin proteins inside hundreds of stacked disks in the outer segments of the photoreceptors. When activated, these proteins change shape and shut ion channels in the membrane, altering the cell’s electrical charge. This triggers a cascade of events that generate an electrical impulse, which is the currency of neurons.

This process is called phototransduction because it transforms (“transduces”) light into electrical impulses.

What sets them apart: their opsins

Cones and rods have different opsins: rhodopsin in rods and cone opsins in cones; they have different sensitivities.

The opsins in cones: masters of speed.

Cone opsins respond to light very fast and can shut off the photoreceptor membrane in 3-5 milliseconds. The entire process, from photon to electrical impulse, can happen in 9 to 18ms. Not only that, but cones can recover fast and be ready to fire again in just 3ms (compared to hundreds of milliseconds in rods) (Lamb, 2022). This allows us to see fast changes in light, and therefore, we can see smooth movement. Our cones can detect flickering light at a frequency of 100 times per second or 100 Hz (Tyler & Hamer, 1990), which is why motion appears fluid rather than jumpy or stuttered.

As a side note, cone opsins are responsible for our ability to see colour. Each cone contains one of three opsins, each tuned to a particular wavelength of light. These three types together form the basis for colour vision. This is very eloquently explained here (scroll to “How we see colour”).

The opsins in rods: masters of amplification.

Unlike cones, which require a bright light (many photons) to respond, rods only need a single photon to fire a spike. This is because a single rhodopsin molecule initiates a cascade of internal reactions that amplifies the signal dramatically at every stage (Baylor et al., 1979; Lamb, 2016). This amplification allows us to make the most of very little light.

Here is the downside: rods have a very slow recovery time until they can fire again. We notice this when walking from a bright area into a dark room, it takes time before we can see clearly again. Research has timed this at a maximum of 40 minutes for optimal vision after an intense light exposure (Lamb & Pugh, 2004).

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The deceptively simple solution: Conversion

This is my favourite concept in neuroscience because it illustrates how delightfully simple mechanisms can serve very complex features.

In the image (below), light comes from the left and is picked up by the cones and rods at the back of the retina. That might feel counterintuitive, but retinal cells are transparent, allowing light to pass through.

Photoreceptors respond to light by generating small electrical signals (graded potentials). These signals are passed on to bipolar cells, which then relay them to ganglion cells. The axons of the ganglion cells bundle together to form the optic nerve, which carries visual signals to the visual cortex via the thalamus. This setup means that the signals are integrated and modulated at every stage, even before they leave the retina.

Crucially, the way the cones and rods connect to ganglion cells is different, and this is the core engineering principle that gives us both high sensitivity and high resolution with a simple design.

Many rods converge onto a single ganglion cell.

Conversion gives the ganglion cell a very high light sensitivity. It gives it a broad receptive field – a wide map of photoreceptors that increases the chances of catching any light. If any of the photoreceptors is hit by a photon, the ganglion cell knows about it. The trade-off is that it cannot know where (which rod) the light is coming from. So, we say that the spatial specificity is very low, resulting in a blurry image.

But this is not all, there is also a summation effect. Think of the sound of a single person gasping versus that of a crowd gasping. Pulling together signals from many photoreceptors results in a stronger signal. This is why rod vision gives us high sensitivity to light, allowing us to see in very dim conditions but at the cost of a rather low resolution.

By contrast, each cone relays information to its own ganglion cell.

This means that this ganglion cell knows exactly where the light is coming from, resulting in excellent spatial resolution and a sharp image. The downside of only receiving input from a single photoreceptor is that this ganglion cell will require more light (that is, more photons hitting that single cone) to “summate” enough input together to trigger an electrical impulse. This is why cones only activate in bright environments while rods take over in low lighting.

Location, location, location

Vision is not equally sharp across the retina. This is because we do not need detailed information from every part of our visual field at once. The brain is highly energy hungry, and photoreceptors are some of the most metabolically expensive cells in the body. It is therefore most useful to detect fine detail only when and where we need it and conserve energy.

The light that enters the eye is bent primarily by the cornea and further adjusted by the lens to converge on a central area called the fovea. This region contains only cones (Curcio et al., 1990) and is therefore specialised to detect fine detail. It is what allows us to read interesting articles like this one, or to see the excitement on someone’s expression as you tell them about cones and rods.

However, cone density drops sharply just outside the fovea and, even though there are still cones in the periphery, this area is dominated by rods (see chart below).

This is because we do not need high detail in the periphery of our vision; a few cones are enough. What is crucial for survival is to detect fast changes in light in the corner of our eye: we just need to sense that something is coming at us. If it turns out to be a car or a tiger (I do not know where you take your walks), it is less urgent. A built-in bias to flinch when something comes at us gives us enough time to look at it (thus making the image land on the fovea) and figure out what it is.

Rods are a different kind of hero. Rods are far more abundant than cones, in a ratio of about 20:1 (or 95% of all photoreceptors), and they are found exclusively outside the fovea. They are not specialised for sharp vision but for detecting faint light in very dim conditions. It needs to be quite dark for rods to take over, which typically happens at night. Fittingly, the time it takes for rods to recover after exposure to bright light (up to 40 minutes) can easily accommodate the time it takes for dusk to fall.

This elegant configuration combines the ability to perceive the smallest details without sacrificing the ability to react instantly to potential threats. And we have the added superpower of night vision.

           It is an optimised system that balances precision with sensitivity:
           Foveal vision: only cones, high detail, low sensitivity.   
           Peripheral vision: mostly rods and fewer cones, high light sensitivity, low detail
           (Remember that cones in the periphery still support daytime vision.)

Night vision

Our visual system operates in different modes depending on light levels:

• cone-driven photopic vision in bright light,

• rod-driven scotopic vision in darkness, and

• combined input in mesopic vision in conditions such as dawn, dusk or streetlight.

Mesopic vision is far too complex to include here, but for now, it suffices to know that it is not either/or, but that there is an overlap when both cones and rods contribute to vision. If you are observant, you can tell when you are using mesopic vision because colours look a bit strange. Ask me about this at your own peril.

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Cones require bright light to trigger an electrical impulse, so they do not get activated in the dark. Rods, in contrast, are optimised to amplify scarce light and, for this reason, in bright environments they become overwhelmed or “bleached”. So, while cones are active in bright daylight, rods take over in darkness.

Once our eyes have adjusted to near darkness (almost pitch-black), the high light sensitivity of rod vision allows us to detect shapes and movement even in starlight. However, since rod-driven vision has very poor spatial specificity, we cannot see sharp detail in the dark. Objects also appear colourless because colour is mediated by cones, which are now inactive.

This transition between rod-driven and cone-driven vision is another way our visual system optimises perception. Between the two photoreceptor types, it covers a vast range of light conditions, from 0.000001 to 100,000,000 nits. That is an impressive 14 orders of magnitude.

Now, if you are thinking our night vision is not really all that good, consider when was the last time you used your scotopic (rod-driven) vision? Think about it: to enter full superpower rod-driven mode, you must be in near pitch-black (below 0.001 nits) for up to 40 continuous minutes. That is the light level of a moonless night in the countryside.

To help you work this out, I found you some numbers: if you read in bed, you will need about 10-20 nits of light on the page. A typical phone screen emits around 300-400 nits, going up to 2,000 nits. A 55-inch television screen has a luminance of 400 nits. All of those are within the photopic (cone only) range.

You are equipped to see in the dark. Are you not tempted to test your night vision superpowers?

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All of this for the illusion of effortless sight

Despite having the same core mechanism, photoreceptors have evolved complementary strengths: rods amplify light, cones deliver sharp, smooth movement and colour vision. Together, they give us the illusion of a rich and detailed vision in all lighting conditions.

All of this happens so fast; to see the world, clearly, sharply, in motion, across bright and dark environments. We rarely consider the enormous computational power and feats of biological engineering required to just open our eyes and let the world simply filter in.

Vision is the most exciting magic trick!

I bet you were having so much fun, you forgot the question that started this. Go on, have a go:

        Why do stars in the night sky seem to vanish when you look straight at them?  

           A. Because the star’s light is scattered by the lens. 
           B. Because cones are more sensitive to dim light. 
           C. Because the centre of your vision does not contain the very light-                                                                                                                                                     
                sensitive rods. 
           D. Because stars are shy.

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In this article, we have only looked into the retina. I have not touched on how the brain uses this information to see edges, colour, contrast, movement or biological motion and how all of this links to emotion or recognising familiarity. Or even how we manage not to get dizzy every time we move our eyes! All of this is coming in due time. Although about visual motion, you can already check out this link.

If you enjoyed this, do subscribe for more. I am always open to questions and challenges, so feel free to suggest new topics.

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• Bonus Content: Quick comparison of cones and rods (table below)

What you have learnt:

• Duplex theory of cones and rods and their different specialisations

• Conversion: light sensitivity vs spatial resolution

• Spatial distribution: cones in the fovea, rods (and fewer cones) in the periphery

• Visual modes: scotopic, photopic and mesopic vision

• Seamless integration for a rich visual experience, capable of simultaneously having sharp perception and a fast response to danger

It takes a lot of work and time to write these articles. If you find value in what you just read and want to support my work, you can buy me a coffee.

In any case, if you got this far, please like and restack, and feel free to drop any questions in the comments.

Buy me a coffee ☕️

Share

References:

Baylor, D. A., Lamb, T. D., & Yau, K. W. (1979). Responses of retinal rods to single photons. The Journal of physiology, 288(1), 613-634. https://doi.org/10.1113/jphysiol.1979.sp012716

Curcio, C. A., Sloan, K. R., Kalina, R. E., & Hendrickson, A. E. (1990). Human photoreceptor topography. Journal of comparative neurology, 292(4), 497-523. https://doi.org/10.1002/cne.902920402

Lamb, T. D., & Pugh, E. N. (2004). Dark adaptation and the retinoid cycle of vision. Progress in retinal and eye research, 23(3), 307-380. https://doi.org/10.1016/j.preteyeres.2004.03.001

Lamb, T. D. (2016). Why rods and cones? Eye, 30(2), 179-185. https://doi.org/10.1038/eye.2015.236

Lamb, T. D. (2022). Photoreceptor physiology and evolution: Cellular and molecular basis of rod and cone phototransduction. The Journal of Physiology, 600(21), 4585-4601. https://doi.org/10.1113/JP282058

Osterberg, G. A. (1935). Topography of the layer of rods and cones in the human retina. Acta Ophthalmologica. Supplementum, 6, 1–103.

Tyler, C. W., & Hamer, R. D. (1990). Analysis of visual modulation sensitivity. IV. Validity of the Ferry–Porter law. Journal of the Optical Society of America A, 7(4), 743-758. https://doi.org/10.1364/JOSAA.7.000743

A world without motion

In 1983, Zihl, von Cramon and Mai published a remarkable case study that shaped our understanding of motion vision. The patient, referred to as LM, was 43 years old and had suffered a brain haemorrhage that affected both sides of her brain, in a region near the back, known as the lateral temporo-occipital lobe. The injury was outside the primary visual cortex considered the only visual area at the time. Despite having sharp, clear vision, she was unable to perceive motion. She was initially misdiagnosed with a “bizarre visual disorder mimicking agoraphobia,” but her condition was far more complex.

“People, dogs and cars appear restless, are suddenly here and then there, but disappear in between. Very often I don’t even know where they have left because they move too fast”(Zihl et al., 1983).

LM could not see fluid movement. To her, the moving world appeared as a collection of frozen images, and simple daily tasks, such as pouring tea or crossing the street, were extremely difficult. Her reluctance to social spaces was not rooted in a phobia, but a disconnect. To her, people would suddenly appear in a room and then disappear before her eyes. Talking to people was particularly unnerving as they would appear to speak without moving their lips.

"When I'm looking at the car first, it seems far away. But then, when I want to cross the road, suddenly the car is very near.”

The case of LM advanced our understanding of the brain

LM was not the first reported case of motion blindness, but hers was the first case in which the symptoms and brain damage were so precisely linked. Reports dating back to 1911 described patients with motion blindness. However, those patients had additional impairments, such as anomic aphasia (an inability to name objects despite recognising them) and sometimes, also concentric vision loss. See Potzl and Redlich (1911) and Goldstein and Gelb (1918) for details.

What made LM’s case particularly significant was the combination of the selectivity and specificity of her condition (Zihl & Heywood, 2015). Selectivity refers to the clearly defined impairment that exclusively affected her motion vision and spared all other visual functions, such as form, colour, depth, object and face recognition. Specificity means that her motion blindness could not be explained by any deficits, making it a clear consequence of her bilateral injury to the visual brain. This suggested that motion is a distinct visual function, relying on mechanisms beyond the primary visual cortex.

“The selectivity of the visual disturbance supports the idea that movement vision is a separate visual function depending on neuronal mechanisms beyond the primary visual cortex” (Zihl & Heywood, 2015).

Defining the MT/V5 area

CT scans revealed damage in LM’s lateral temporo-occipital cortex, corresponding to the middle temporal area (MT). Given both the location and the nature of her visual loss, Zihl and colleagues (1983) proposed that this region was the human equivalent of area V5 in rhesus monkeys, where Semir Zeki (1974) had found a dense concentration of direction-sensitive neurons which responded selectively to motion in a specific direction.

Just a quick note on the terminology: you will often see the names MT, V5 and MT/V5 used interchangeably. V5 comes from functional mapping studies and is commonly used when discussing visual function. MT (Middle Temporal area) refers to its anatomical location. While we are on this topic, V1, the primary visual cortex, also has several names: striate cortex, area 17 or Brodmann area 17.

In 1969, Hubel and Wiesel identified direction-selective cells in V1. At the time of LM, the dominant view was that motion processing happened primarily in this area. Zeki’s later discovery of direction-sensitive neurons in V5 suggested that motion signals from V1 could be further processed there, but the idea that V5 played a central role in motion perception was still speculative.

Then came the case of LM. Her motion blindness, caused by damage to the human equivalent of V5, provided compelling evidence that V5 was essential for the experience of visual motion.

How V5 Builds motion

The retina in the eye is a mosaic of tiny receptive fields. Think of a receptive field as the area that a neuron can "see." As visual information travels through the brain, neurons combine inputs from earlier stages, creating progressively larger receptive fields capable of detecting more complex features.

Neurons in V1 have smaller receptive fields than V5 and can only detect local motion. This is known as the aperture problem, illustrated below. As seen from V1, the movement is ambiguous and does not reveal the actual global direction of movement.

Area V5 is particularly tuned for motion. Neurons here are sensitive to speed and direction of movement across all axes. Neurons in V5, with a larger receptive field, solve the aperture problem by integrating input across multiple V1 neurons, allowing the brain to reconstruct the global motion of the entire object, rather than the local motion of its parts.

If you would like to know precisely how the neurons at any stage reconstruct visual information, ask away.

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V5 does not just add motion signals, it integrates them

V5 does not simply summate movement input but rather integrates it into a unified coherent perception. This has been demonstrated in macaque monkeys, where researchers recorded neuronal responses to different motion stimuli (see image below). In this experiment, two moving gratings, drifting in different orthogonal directions, were combined to form a plaid pattern. This created the illusion of movement in a new, diagonal direction (see orange arrow). The monkeys were shown all three types of motion stimuli.

As mentioned earlier, the direction-selective neurons in V1 respond maximally to motion in a specific direction, with different neurons responding to different preferred directions.

When the stimuli were shown to the monkeys, V1 neurons responded strongly to the individual gratings, according to their preferred direction (horizontal or vertical). They also responded during the plaid stimulus, since it is made of two overlapping gratings. However, a section of neurons in V5 responded only to the overall motion of the plaid and not to the individual gratings. This suggests that V5 is not just summing inputs but actively computing a new, global direction of motion. In doing so, V5 creates a higher-level representation of movement.

V5 in daily life

The profound impact of V5 damage on LM's quality of life highlights the importance of this area. It contributes to several aspects of visual processing, including but not limited to:

• Depth perception through motion parallax. Video gamers will recognise this. It involves extracting depth cues from the relative movement of objects as we move through the environment. Objects closer to us appear to move faster than those further away.

• Biological motion. This refers to recognising movement patterns in living beings, such as recognising a friend by their walk. Biological motion is also key for interpreting social cues, such as body language.

• Eye tracking and coordination. This includes tracking a moving object or seeing people walk in and out of rooms and generally interacting in the world. It is also necessary for writing, which was slower for LM as she could not track fast hand movements.

• Interpreting dynamic social cues This includes facial expressions and gestures, which are crucial for understanding the actions and intentions of others.

Without these functions, the world becomes fragmented. Reading intentions and emotions in others becomes difficult, face-to-face conversations feel disorienting and communication overall loses its natural rhythm.

How LM managed

Despite her life-changing condition, LM faced her challenges head-on. She was resilient and showed no symptoms of depression or anxiety. She learnt to manage her condition by avoiding crowded places and situations with multiple moving stimuli. She adopted clever strategies, such as avoiding looking directly at moving objects and focusing her gaze on stationary features in her environment. She relied on other senses, like focusing on hearing to estimate the distance of cars, and overall tried to keep her autonomy as much as possible (Zihl & Heywood, 2015).

LM's contribution

LM's generosity to science was invaluable. She volunteered for countless, exhausting tests for over two decades, knowing that they would only help others. All aspects of her perception and psychological state were tested repeatedly, particularly as methods improved over the years. Her patience, strength and collaboration allowed researchers to understand motion in ways that go beyond what I can cover here. MT/V5 is currently the most studied visual area and is now known to be involved in integrating motion input from other senses (audio, touch) and to have links to attention and emotion.

Conclusion: Why her story matters

The story of LM is my favourite case study in neuroscience because it so clearly illustrates the complexity and fragility of human perception. It reveals how deeply we rely on our senses, not just to navigate the world but to connect with others and find belonging and meaning in everyday life. It also fosters compassion and awe of how wonderful it is to see.

It is easy to assume that as long as our vision is sharp, losing the ability to see motion could be manageable. But LM’s experience reveals how disorienting, isolating, and even frightening it can be when just one part of our perception goes missing.

Her case is a direct example of how every aspect of perception shapes our emotional and social life and is a reminder that science is built on the struggles and generosity of others. Next time you pour yourself a cup of tea, think of LM and how wonderful it is to see motion at all.

What is another aspect of your own perception that you take for granted? How would your life change without it?

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If LM’s story moved you, subscribe for more stories and insights into how the brain constructs our experience of reality and connection with others.

References

Gelb, A., & Goldstein, K. (1918). Psychologische Analysen hirnpathologischer Fälle auf Grund von Untersuchungen Hirnverletzter. I. Zeitschrift für die gesamte Neurologie und Psychiatrie, 41, 1-142.

Hubel, D. H., & Wiesel, T. N. (1969). Visual area of the lateral suprasylvian gyrus (Clare-Bishop area) of the cat. The Journal of Physiology, 202(1), 251-260.

Movshon, J. A., Adelson, E. H., Gizzi, M. S., & Newsome, W. T. (1986). The analysis of moving visual patterns. In C. Chagas, R. Gattass, & C. Gross (Eds.), Pattern recognition mechanisms (pp. 117–151). Vatican City: Pontificia Academia Scientiarum.

Potzl, O., & Redlich, E. (1911). Demonstration eines Falles von bilateraler Affektion beider Occipitallapen. Weiner Klinsche Wochenschrift, 24, 517-18.

Zeki, S. M. (1974). Functional organization of a visual area in the posterior bank of the superior temporal sulcus of the rhesus monkey. The Journal of physiology, 236(3), 549-573.

Zihl, J., & Heywood, C. A. (2015). The contribution of LM to the neuroscience of movement vision. Frontiers in Integrative Neuroscience, 9, 6.

Zihl, J., von Cramon, D., & Mai, N. (1983). Selective disturbance of movement vision after bilateral brain damage. Brain, 106(2), 313-340.

Some say olo blurs the distinction between reality and perception. I believe it sharpens it. Keep reading.

What exactly is olo?

Olo is a colour that can only be seen when induced by laser light under very specific conditions. It has been described as a peacock blue or teal more vibrant than anything found in nature (Manke, 2025). The colour was discovered by a team led by Professors Austin Roorda and Ren Ng at the University of California, Berkeley, in collaboration with researchers from the University of Washington. Their goal was to explore whether the human brain could perceive a completely new colour by stimulating just one type of light-sensitive cell in the eye, specifically, the M cones. Using advanced optics and precise laser targeting, they isolated these cells and found that this produced a perceptual experience that people had never had before: a new colour, now known as olo.

Who has seen it and what did they see?

At the time the paper was published, only five people, all with normal colour vision, had seen olo. One of them, Professor Roorda, described the experience as seeing “a profoundly saturated teal… the most saturated natural color was just pale by comparison” (Fong, 2025). Others described it as “an intensely saturated teal” and “a blue-green of unmatched saturation.”

It is worth noting that participants did not see olo across their entire visual field. Instead, it appeared as a small patch in the periphery. This is because the cones in the centre of the visual field (the fovea) are too tightly packed for precise stimulation. Peripheral cones, however, are more spaced out, allowing the laser to isolate them more reliably. The perception of olo lasted only as long as the cones were being stimulated.

How do we know what colour they saw?

The participants were asked to match the colour they perceived using two methods: by tuning a laser wavelength and by adjusting free-wheeling dials on an RGB projector to modify the hue, saturation and brightness. Both systems also had a further dial to add white light. The participants stated that olo did not match the vividness of any known colour and its intensity and richness were such that they needed to “wash out” the colour with a significant amount of white light to approximate a known colour. The resulting match resembled a blue-green that sits outside the colour range displayable by standard means.

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How was olo created?

The Oz device uses extremely precise imaging technology that allows researchers to identify and track specific cells in the retina. The research team mapped the locations of the different cones (light-sensitive cells) in the retina for each participant and then used microscopic doses of laser light, targeted at specific cone types. This method enables them to study how individual cones contribute to perception. The laser stimulation creates a visual perception that the researchers call an “Oz percept.” To produce the percept of the new colour olo, they targeted the laser exclusively at the M cones.

What are these cones, you ask? Glad you did.

How does the brain create colours?

This part digs deeper into how colour vision works. Feel free to skip ahead if this is not your thing.

Physiologically, colour is the perceptual experience that results from our eyes experiencing different wavelengths of light. Cones are the photoreceptors in the back of the eye involved in picking up this information. The actual experience of colour happens further into the brain and it is the result of neuronal processes across different parts of the brain.

1) Light is detected by the cones in the retina

When light enters the eye, it is absorbed by photoreceptors in the retina that convert energy to electrical impulses. The photoreceptors that are sensitive to different wavelengths of light are the cones. Typically, humans have 3 cone types (S, M and L), each containing photopigments (opsins) that are maximally sensitive to different wavelengths: short (S, blue), medium (M, green) and long (L, red) (see chart below). Assigning colours to the wavelengths is an oversimplification, but it will do for now. As the chart shows, there is a certain overlap in the wavelength sensitivity of each cone. This is crucial for colour perception, as it means that no naturally occurring wavelength stimulates only one cone type. For example, light at 550 nanometres (nm) activates L cones, but it activates M cones more strongly.

2) Further neural processing happens in the visual cortex.

This colour information travels down the optic nerve towards the visual cortex, where it is processed by comparing the relative activation of all three cone types, rather than interpreting the signal from any cone in isolation. All the colours that we perceive result from the computation of input from these three cone types. “Is there no yellow cone?” you ask. We do not need a yellow cone. A wavelength of about 570-590 nm would stimulate both M and L cones. The brain interprets high L + M activation as yellow. By the way, the 550 nm mentioned earlier is perceived as yellow-green, or “chartreuse” if you are familiar with design colour charts… or liqueurs.

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Clarification: “maximally sensitive” means that cones respond to a range of wavelengths but respond more strongly to a particular one. For example, the S cone responds maximally at 420 nm, and half as strongly at 400 nm and at 440 nm. Because different combinations of wavelengths can produce the same pattern of cone activation, we can perceive the same colour from physically different light sources, these are called metamers. But I digress.

What makes olo so special?

Researchers used light with a wavelength of 543 nm to evoke olo. This wavelength was chosen because it strongly stimulates M cones while minimising activation of S cones, and it is a standard, reliable laser wavelength commonly used in vision research. Under natural conditions, 543 nm light typically appears green. Due to the overlapping sensitivity of the three cone types, any light we encounter usually stimulates more than one cone type. In this case, 543 nm light primarily activates M cones (which peak around 530 nm), but also stimulates L cones (peaking around 560 nm) to a lesser degree and may slightly stimulate S cones (peaking around 420 nm), if at all.

What makes olo fundamentally different, and the reason it cannot be seen outside a lab setting, is that researchers targeted the 543 nm laser light exclusively to hit M cones, bypassing both S and L cones. This precise, isolated stimulation led to the unprecedented perceptual experience of olo: a colour literally never seen before.

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Why the name olo?

The name olo was coined to reflect the binary code 010, representing the input for each cone type: 0 (S cone), 1 (M cone) and 0 (L cone).

Same wavelength, many colours.

Here’s a twist: the same 543 nm wavelength that evoked olo also induced other colours. The team experimented targeting different cone types and configurations while keeping the wavelength constant to examine how this isolated stimulation affects the colour perceived. As a result, participants reported seeing orange, yellow, green, and blue-green. As the authors note, “the appearance of light depends strongly on the identity of the cone targeted,” even when the physical stimulus remains the same. This highlights the importance of the spectral sensitivity overlap of L, M, and S cones and demonstrates that colour perception arises from comparative processing across cone types.

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Reception of the news and debates

The discovery of a new colour doesn’t happen often. Naturally, olo has sparked interest, raised questions, and unsettled a few assumptions. But beyond the novelty, what does this research actually show us? And what does it help reveal about how we perceive and make sense of the world?

Is olo really a colour if most people cannot see it?

Even among humans, colour is not a fixed experience, meaning that the same wavelength can evoke different colour perceptions from person to person. A common genetic variation makes some women tetrachromats, giving them a fourth cone and allowing them to see an entire range of colours that are invisible to most. But the colours they see are as real as those we all see. The existence of a colour does not depend on how many people can see it, but on whether it reliably produces a consistent and specific neural response.

Some argue that since olo cannot be seen in nature, it is not a real colour. However, olo meets the definition of colour: it is a phenomenological experience that arises when the brain processes light information received by the photoreceptors (albeit via a laser). I disagree that it cannot be experienced naturally; the stimulation is artificial, but the perception is as real as with any colour and is produced by the same neural mechanisms.

Is olo a novel colour?

The researchers claim that this is a new colour, as it remains outside of the usual gamut. Some experts argue that olo falls within the blue-green spectrum, and therefore it does not truly constitute a novel hue but rather an extreme variation of existing hues. A challenge is that describing a colour to people who have never experienced it inevitably relies on comparisons to the colours they already know, making it difficult to determine if olo is truly distinct.

Is the sample size too small?

Some media commentary and online discussions, particularly on platforms like Reddit, have questioned the small number of participants in the olo study. With only five people taking part, it is reasonable to ask: is that enough?

Yes, it is. This research was not designed to define a new colour but rather to serve as a proof of concept, to test whether a novel perceptual experience could be induced at all through precise, cone-specific stimulation. This type of research requires intensive preparation, including high-resolution retinal mapping for each participant and multiple sessions of cone stimulation and colour matching. The focus is on collecting rich, highly controlled data from each individual, and for this, a small sample size is standard practice and is scientifically appropriate.

Why is this research significant?

One of the central challenges in neuroscience is isolating variables tightly enough to draw clear conclusions. What makes this study remarkable is that researchers were able to do just that: stimulate specific cone types directly and produce a precise, repeatable percept.

This was not the first time the Oz technology was used, but it was the first time it stimulated a large enough number of cones to generate a full perceptual experience. As the authors write, "These results are proof-of-principle for programmable control over individual photoreceptors at population scale” (Fong et al., 2025).

Olo confirms that colour is a neural event. Light is only the source, but our experience of colour is shaped by our neural architecture.

That said, our perceptual experience also physically shapes our brain, but that is a topic for another day.

What could this mean for the future?

The precision of the Oz system opens up new ways to study the visual system at an unprecedented scale and with a degree of control not available before. It allows researchers to explore how the brain integrates new visual inputs. Crucially, it can simulate the effects of adding new cone types in a completely non-invasive way. This includes the potential to restore colour perception in colourblind individuals, and even to induce forms of tetrachromacy, allowing humans to experience a broader and previously inaccessible range of colours. Researchers are also exploring how Oz could be used to simulate cone loss in healthy individuals, allowing them to model and study visual disorders caused by cone deficiencies.

Final thoughts: what olo teaches us about reality

Olo is described as a colour more vivid than any found in nature, yet it cannot be made into a pigment or seen without being induced. Some argue this blurs the boundary between perception and reality. I believe differently, I think olo sharpens this distinction. The fact that olo can be induced through artificial stimulation of our sensory system emphasises that colour exists as a neural event. In this sense, olo does not challenge our understanding of reality; it underscores that what we perceive as “real” is a construct of our unique neural architecture.

Acknowledgement:

A warm thank you to Dr. Austin Roorda for taking the time to read this article and share thoughtful feedback.

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If this post made you think differently about colour or perception, you will probably enjoy what is coming next. I will be writing more about vision, sensory illusions, case studies and all things brain.

If you find value in what you just read and want to support my work, you can buy me a coffee. In any case, if you got this far, please like and restack, and feel free to drop any questions in the comments.

References

Fong, J., Doyle, H. K., Wang, C., Boehm, A. E., Herbeck, S. R., Pandiyan, V. P., Schmidt, B. P., Tiruveedhula, P., Vanston, J. E., Tuten, W. S., Sabesan, R., Roorda, A., & Ng, R. (2025). Novel color via stimulation of individual photoreceptors at population scale. Science Advances, 11(16), eadu1052. https://doi.org/10.1126/sciadv.adu1052

Lanese, N. (2025, April 18). Scientists hijacked the human eye to get it to see a brand-new color. It's called 'olo.' Live Science. https://www.livescience.com/health/neuroscience/scientists-hijacked-the-human-eye-to-get-it-to-see-a-brand-new-color-its-called-olo

Manke, K. (2025, April 22). Scientists trick the eye into seeing new color ‘olo’. Berkeley News. https://news.berkeley.edu/2025/04/22/scientists-trick-the-eye-into-seeing-new-color-olo/

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Hi, I am Vane. I am glad you found your way here.

I am a neuroscientist with a fine arts background. As a researcher, I study how the brain constructs our visual experience, how connectivity between brain areas is crucial for even the simplest actions, and how sensory information shapes our reality. As an artist, I explore how to trick the eye into seeing depth and movement through colour.

What connects both is a deep curiosity about how we see, feel, and interpret the world around us, not as it is, but as our brains make it.

Why Neuroscience Unwrapped

We live in a world shaped by what we see, but we rarely question our perceptions. I created Neuroscience Unwrapped to make the science of perception accessible to everyone, and to share my enduring fascination with this incredible brain of ours… or any brain, really. I just like brains.

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This project shares the wonderfully complex and deceptively simple science of perception, clearly, critically. Because when we uncover the mechanisms behind perception, we become more aware, more empathetic and more capable of questioning the assumptions that quietly run our lives.

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