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1 February 2023

Why is a squid eye “better evolved” than a human eye?

Squid swimming in the sea

This article was originally written for Insight magazine.

No, sadly it’s not the start of a joke. Squid eyes really are, by some measures, more intuitively designed than human eyes.

In the summer edition of Insight, we explained the role of rods and cones in helping us see in colour and detect motion. In a sweep of simplicity, we stated that the rods and cones are in the retina, and that an electrical impulse is sent from there to the brain, resulting in vision. In fact, the structure of the retina, and how the signals are sent to the brain, is rather complicated.

Certain cells within the retina are also of interest in glaucoma research. This article is going to explain the structure of the retina, how the signals initiated by rods and cones actually make it to the brain, and why this is of relevance to glaucoma – as well as why squid eyes are better than human ones!

The structure of the retina

In humans, as in all vertebrates, the retina forms a bowl shape at the back of the eye. Behind it sits the choroid, which provides a rich blood supply to the retina. We can divide the retina into four layers, based on the processing that’s happening at each stage.

These stages or layers are:

  1. Photoreceptors, called rods and cones, detect light and send the signal to the bipolar cells. For more information, see the article Motion in technicolour: how we see movement and colour (published in Insight in Summer 2022).
  2. Bipolar cells (supported by other cells called horizontal cells) carry out basic processing of the signals received by the rods and cones. The processing determines what’s going on around those rods or cones – whether adjacent cells are also receiving light signals or not. This helps with identifying edges and contrast associated with objects we can see.
  3. Retinal ganglion cells (RGCs) continue the processing, collating signals from a number of bipolar
    cells. Depending on the type of ganglion cell, these can help identify direction of movement, rapid changes in light intensity, or patches of a particular colour.
  4. Nerve fibre layer: the axons of the RGCs (see A simple introduction to nerve cells below) come together from across the retina to form the optic nerve, which transmits the signals to the brain. Imagine this as being like the hairs on our scalp being bundled together to form a ponytail. The signals are sent to the visual processing centres within the cortex of our brain, to create an understanding of what we are seeing.

Why a squid retina is (arguably) superior to the human retina

There is an evolutionary peculiarity to the structure of the retina: the layers are arranged back to front! The photoreceptors are at the BACK of the retina. That means light must travel through all the other layers before reaching the photoreceptors. These layers also contain supporting tissue such as blood capillaries. As a result, some of the light which enters the eye never reaches the photoreceptors, because it’s absorbed by other cells in the way. The other problem this generates is the blind spot, where the nerve fibres congregate and form the optic nerve, which passes through the retina. Because the optic nerve cuts through the retina, there is a small area with no photoreceptors.

Intriguingly, squids and related animals have a retina which is arranged the other way around, with the photoreceptors at the front. This means less light is “lost” on the journey through the eye, and also there is no blind spot as the optic nerve sits behind the retina.

So why is the vertebrate retina arranged the way it is? Well, evolution just happens, so there is no “why” in any case. But there are advantages: it’s easier to provide a rich blood supply to the energy-demanding photoreceptors via the choroid. Another potential advantage is to reduce the light intensity of light hitting the photoreceptors, to prevent them from being “dazzled” – possibly a relic from our evolutionary ancestors living deep in the ocean.

Diagram of a human eye alongside a diagram of a squid eye.

A simple introduction to nerve cells

There are several different types of nerve cells, or neurons. In the simplest terms, their role is to send and receive signals between other cells (including muscle or hormone-releasing cells, as well as other nerve cells). The exact structure varies, but all have at the very least:

  • A cell body, with a nucleus (containing genetic material);
  • An axon, to send impulses along;
  • Dendrites, to form connections to other cells.

Signals are sent along axons as an electrical impulse. Nerve cells send signals to other cells across a gap called a synapse. Signals cross the synapse in the form of a chemical, often called a neurotransmitter, or an electrical impulse (like a static shock being passed between cells). Drugs such as alcohol or painkillers often act as neurotransmitters, changing how nerve cells interact with one another.

What’s all this got to do with glaucoma?

You may be aware that examination of the optic disc forms an important part of glaucoma monitoring. That looks at where the bundle of nerves leaves the back of the eye and travels to the brain. If you have glaucoma, the bundle is thinner – imagine a ponytail formed by thin hair compared to thick hair – and you have “cupping” (see “Making sense of the jargon” in our Spring 2021 edition of Insight for more information).

You may also have optical coherence tomography (OCT) tests done as part of the monitoring of your glaucoma. These scans of the back of the eye look at the different layers in the retina. The key metric for glaucoma is looking at the thickness of the retinal nerve fibre layer, or RNFL. The RNFL is generally thinner in people with glaucoma than in the rest of the population.

Both cupping and thinning of the RNFL are caused by nerve fibres dying. If the nerve fibres are dying, the signals can’t be sent to the brain and we have glaucoma. As explained above, those nerve fibres are formed from the axons of retinal ganglion cells (RGCs). Lots of research is underway looking at RGCs. For example, research might be looking at:

  • What causes RGCs to die;
  • Why RGCs in some people are more vulnerable to the effects of increased pressure than in other people;
  • How to prevent or slow down RGC death.

As well as the research described on page 25, we’ve just funded some research, through our UKEGS grant, for Professor James Morgan at Cardiff School of Optometry and Vision Sciences to research RGC damage in glaucoma. This research is investigating the role of yet another type of cell in the retina, called microglial cells, in protecting or damaging RGCs. We hope to provide more information about this research in a future edition of Insight.

It is hoped that a better understanding of RGC death, and how to prevent it, will provide new opportunities for glaucoma treatments.