I’ll warn you at the beginning. This article will be a bit longer. It’s because I wanted to talk you through the visual signal from the single photon entering your eye to the beautifully sophisticated system of little brain nuclei. By the end of that post, you may be a bit tired, but one I can promise.
You will never see the same way again.
Ready? Let’s start.
The eye and its rods and cones
There are basically two types of photoreceptors in the retina: rods and cones. You must have come across them before, but do you really know the difference? Let’s quickly recap.
Artwork courtesy of ITG staff Janet Sinn-Hanlon in the VMIL, Univeristy of Illinois
Rods are a bit like obese, lazy people: they’re slow in reacting to anything and pretty rubbish at putting things together. That’s why you have to give them information in SLOW, SIMPLE and DISTINCT manner, ideally in the form of a scattered light.
However, it would be quite harsh to write them off completely. Their laziness pays off: rods have a very high light sensitivity and amplification, and they can detect as little as a single photon (i.e. a single light particle)!
Cones are more like an ADD teenager on three red bulls and LSD. Overexcited about everything, recording very high resolution of pictures. They like to see colours and vivid structures like in a drug-intoxicated state, perfectly absorbing axial light rays.
Cones come in three main types, each picking up a different range of the light spectrum (different colour). We used to have four of these back in the days, but apparently evolution had different plans for us. Interestingly, there are some confirmed genetic mutations with women possessing the ability to see 100 of millions of colours with four pigments, condition called tetrachromacy.
This comes at a price: cones have lower sensitivity and lower amplification. They’re mainly found in the fovea (place where our vision is at its best), whereas rods are more distributed and rarely occupy this space.
The Exciting Dark Current
Here’s something a bit counterintuitive: these photoreceptors aren’t facing towards the light in the retina. Their receptors are directly opposite. Why? So that you don’t burn your retina when you look at the sun eclipse, when you were explicitly told not to. Another idiot-proof parental control app in our body. Evolution 2 : Humans 0.
Oh, and also, the receptors aren’t actually excited by light: they are excited all the time, waiting with baited breath and eager anticipation for the moment when photon will appear. This is called the dark current (ca. -40mV).
How it works?
Here is some nerdy explanation. Skip it if not interested.
The photon will change the structure of OPSIN and convert it into TRANSDUCIN; this, in turn, will activate cGMP phosphodiesterase, which will destroy cGMPs. With closure of Na+ gates, the signal is ready to go.
However, it will pass on without action potential. Here’s a diagram showing which type of cells the signal will go through.
OK, you got through that, congratulations! Unless you skipped the entire part, then you don’t deserve a word of recognition, you cheater.
Now – let’s make a little break from the vision. It turns out that ganglion cells (see diagram above) possess some alluring capabilities. Here’s also an interesting thing about how science works. There is a man called prof. Russel Foster (Brasenose, Oxford, JRH Nuffield Department of Neurosciences; previously Bristol University scholar). He discovered that the eye can give us more information than vision. It can also detect brightness. And that brightness has a fundamental influence on our sleep-wake cycle and, consequently, on many other brain processes like learning or memory.
The interesting bit is, no one believed him when he discovered that these photoreceptors may actually lie in the ganglion cells.
“We have studied the eye for a 150 years now, and do you, Sir, suggest there are completely distinct structures outside of the retina that we have missed? You, Sir, must be grossly mistaken!”
You surely must be an idiot, Sir.
Similar remarks were not unusual. Nevertheless, prof. Foster did not give up and pursued his hypothesis, with more and more evidence emerging to back it up. With courage and resilience, he succeeded in shaping modern understanding of circadian rhythm and once again showed us all that we may not be geniuses about our anatomy after all.
Prof. Foster’s work was finally recognised with him joining the Royal Society and his appointment as a Commander of British Empire (CBE) for outstanding services to neurosciences.
Back to the light! We’ve left off our photon somewhere at the back of the eye. Now, the information about that will be sent via optic nerve (CN II). It will then travel to optic chiasm, lateral geniculate nucleus (LGN) in the thalamus, then superior calliculus (just to check up if the visual signal contains something dangerous that requires immediate attention, like a tiger and we need to go NOW. Modern, more civilized example could be you turning your head when you hear a balloon bang).
We’ll skip the bit about on-centre and off-centre ganglion cells and different layers at the LGN. You can read up on that if you want (but it’s not that interesting)
Now, after that, we’ll finally arrive though optic radiation at the terminal station of this journey: Visual Cortex. This Brodmann area 17 structure is located at the very back of your brain (occipital lobe) and gets smashed a bit when you hit the ground (that’s why you see sparkles and stars).
Welcome to the V1 – home of mindblowing fun.
There are a few structures in primary visual cortex (V1) that are particularly interesting.
- Simple and complex cells
These ones deal with linear stimuli. This is one of the areas in neuroscience when things get really cool. How do these cells know when to fire? Why simple cells are more pedantic and must have the exact simple line to trigger firing, and complex are more liberal, with larger receptive fields?
Whatever the answer, what we know is that these guys are mainly responsible for detecting the edges of things. Here’s what’s more exciting: they are grouped in a nice OCD-like way in the V1, with orientation columns and Left/Right ocular dominance columns.
- Colour blobs
These are one of the most intriguing structures, obstructing finely arranged orientation columns. They appear in layers 2 and 3, sometimes 5, but never in layer 4. They have no clue about orientation, but boy can they detect colours!
Just look at how these neurones are grouped by colour and fire when they see the colour of their own.
And now, putting it all together, look what happens:
Diagram courtesy of biopsychology.com 7 edition
Time for signal segmentation
OK, we’ve detected the picture’s edges and colours. We now need to segregate them for further processing. This is done in the secondary visual cortex (V2). This Brodmann area 18 structure lies in front of V1 and acts like a border force agent at the airport. It will scan the visual signal and direct it to where it belongs.
If the signal is vivid and colourful, arising from a bright light, with high-def cone detection, it will go through the parvocellular (P) pathway, temporal pathway, arriving at V4 in temporal lobe for colour analysis.
If the signal is connected with movement, dim light, and is more shadowy, grainy and pixelated, it will be sent right to the parietal lobe to MT centre, via magnocellular (M) cells pathway.
There are a couple of other, more specialised centres, e.g. for disparity, specific distances, disparity movement and complex features like fingers and faces recognition.
Although I won’t go into that much detail, what I would like you to appreciate is how complex, beautiful and simply mind-blowing this system is.
Finally, there are centres responsible for simulating 3D objects, detecting edges and brightness.
And the truth is, most of its functions is yet to be discovered.
Thanks for reading. I hope you can see how many things must occur for you to see. Cool stuff, right?
Finally, for those brave enough to come to the end, here’s a bonus.
Did you know that some blind people can actually see?
This comes back to a famous Oxford experiment, where scientists forced blind people to “guess” what kind of shape is shown to them in the visual field. Contrary to what scientists expected, they performed better than chance, which triggered another series of experiments, when blind people (or monkeys) were shown to avoid obstacles.
One interesting study showed that when presented with a picture and an ambiguous word, e.g. “bank” and a picture of river, they were able to tell whether it is a bank of the river or bank with the money. This is called implicit processing.
In a nutshell, people with some kinds of blindness can still preserve:
- Melatonin reactions
- Sleep wake cycle light stimulation (that’s why they shouldn’t wear sunglasses)
- Pupillary reflex (depending on the site of CN II lesion)
- Implicit processing
This is (most probably) because of a “secret visual pathway”. Some stimuli can travel from the retina to superior calliculus, then to pulvinar nucleus and finally to posterior parietal cortex. This pathway is independent of the previously discussed “traditional” optic nerve pathways, which makes it intact if the main pathway is blocked.
OK – that is finally it. Thank you so much for you reading the article. I would really appreciate if you could write in the comments how much you managed to actually read. I know it wasn’t simple!!!