Colour Transcript
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Colour Transcript Date: Wednesday, 30 March 2011 - 6:00PM Location: Museum of London 30 March 2011 Colour Professor William Ayliffe Some of you in this audience will be aware that it is the 150th anniversary of the first colour photograph, which was projected at a lecture at the Royal Institute by James Clerk Maxwell. This is the photograph, showing a tartan ribbon, which was taken using the first SLR, invented by Maxwell’s friend. He took three pictures, using three different filters, and was then able to project this gorgeous image, showing three different colours for the first time ever. Colour and Colour Vision This lecture is concerned with the questions: “What is colour?” and “What is colour vision?” - not necessarily the same things. We are going to look at train crashes and colour blindness (which is quite gruesome); the antique use of colour in pigments – ancient red Welsh “Ladies”; the meaning of colour in medieval Europe; discovery of new pigments; talking about colour; language and colour; colour systems and the psychology of colour. So there is a fair amount of ground to cover here, which is appropriate because colour is probably one of the most complex issues that we deal with. The main purpose of this lecture is to give an overview of the whole field of colour, without going into depth with any aspects in particular. Obviously, colour is a function of light because, without light, we cannot see colour. Light is that part of the electromagnetic spectrum that we can see, and that forms only a tiny portion. We cannot see x-rays and microwaves, and neither can we see radio waves or infrared. The sun produces this electromagnetic radiation, and from it we are able to discern only a small portion because of the receptors that we have developed. Without these receptors, we would live in a dark universe. If we had not developed receptors that can feel heat from the infrared end of the spectrum, we would be living in a cold, dark universe, which is what it is. The bit that is not cold and the bit that is not dark is the bit we make up in our heads, which I have discussed, at some length, in previous lectures. Photons of light are captured by the receptors to make an electrical signal, which goes to the brain and allows us to see. However, remember what Isaac Newton said: “For the Rays, to speak properly, have no Colour. In them there is nothing else than a certain power and disposition to stir up a sensation of this Colour or that.” Let me explain what I mean. Colour is actually a noun for the spectral composition of light, and it derives from “color”, the Latin, combined with the Anglo-Norman “culur” - which provides conclusive proof, once and for all, that the Americans cannot spell and we can… Colour vision is the capability of discriminating between light sources on the basis of their emitted or reflected wavelengths, and that is called their spectral content. What do I actually mean by that? Well, if we only have one type of receptor and a mixed bag of radiation coming in - with short wavelengths and long wavelengths – then there is no way to discriminate between the two. What we need is at least two different types of receptors - one that is going to respond maximally to the short wave (often blue light), and one that is going to respond maximally to the longer wavelengths. This leaves us with the ability to differentiate the spectral composition of what is coming in – we can tell whether this light is more reddish or whether it is more bluish. That is not actually done in the retina. It turns out that animals do have different receptors, some responding to the long, some responding to the short, and some responding to those in between; and if you are a mantis shrimp, as I shall explain later, you respond to many wavelengths indeed, including ultraviolet. Spectral sensitivity is how these receptors respond maximally. As you can see in this graph, at this wavelength we get a lot of response; at this wavelength, we get not very much response at all; and at this wavelength, there is no response at all. This particular receptor responds maximally at this wavelength. We could call it a shortwave length receptor or, if you like, a blue receptor, and this one could be a green receptor, but as you can see, it is not exactly green – it is sort of somewhere in between. This one is a long wave receptor, which is red. You will notice that the spectral composition of these two is very close, and that is due to a gene reduplication. They are very closely related genes. Bear in mind that, the receptor, when firing, is simply saying – “I am responding.” It is not saying, “Hey, I am responding and I am greenish.” All it is doing is responding maximally to a certain spectral composition. We reach “greenish” by comparing the responses to any particular gamut of light that comes in and adding them up, and that is done at a different layer. This is a map of the brain. We have seen it in previous lectures, but not this colour wiring. We are looking at these things, called blobs, which are in between, and this is where the colour processing occurs. This is V1, the first visual area. The adjacent bit, surrounding it, is V2, which is the second visual area, and this is composed of thin stripes and thick stripes and things that are called interstripes. We are interested in the thin stripes, and there are clusters of cells that are concerned with the colour of the objects that are being seen. There are also luminance channels that tune this up or tune this down, comparing to the luminance of the stimulus that is being sent up from the blob area. From here, they go to another layer, which is V4 and which was discovered by Semir Zeki at University College London. Here, form and colour come together, which means we can start to classify things in the visual scene as “coloured”. Colour Blindness: Train Crashes and John Dalton Colour blindness is something that vexes people when they first encounter it. Significant research was carried out into the condition by John Dalton, a Quaker from the Lake District who moved to teach at the New College in Manchester (in the eighteenth-century, Oxford and Cambridge excluded students outside of mainstream religions). In 1789, in the Philosophical and Literary Society of Manchester, he published “Extraordinary facts relating to the vision of colours”, which outlined his discovery that he was seeing colours different from other people. He worked out that he was missing something that other people had. This “something” was an “unknown unknown”, as Donald Rumsfeld would put it. It was a very difficult thing to work out and Dalton was a genius for doing so. He went on to pioneer research into atomic theory and discovered colour blindness, often named Daltonism after his theories. What precisely is Daltonism? This slide shows a mother (coloured pink because we are not sexist) and a father (coloured blue because we are not sexist) who have four putative children and, being a democracy, they split the genes up properly and equally. The first son (in blue) has normal colour vision – he has the blue, which is on another chromosome, and the red and green, and so he has three responses. He can now make, across the gamut of light, a pretty average and good response and have a full sensation of primate colour vision. The first daughter has inherited both normal genes, so possesses normal colour vision. The second daughter has inherited this defective gene, where the green is not quite as good because of the middle (M) receptor. However, because she can use the other chromosome (you only need one lot of genes, the other is spare) she makes normal colour, but she is a carrier of the defective gene. She will be like her mother, and has the potential for passing on colour deficiency to any male children. The second son has a problem. As we know, boys are X-deficit females, they possess the different gene. His colour perception is shifted close to the red, so he is going to discriminate less colours than his siblings will. This is called deuteroanomaly, meaning an anomalous second pigment. Dalton’s suffered from a different condition. He actually missed the pigment altogether – the gene was deleted or the effective product from the gene was not being made. We know this because he donated his eyes upon his death, knowing that one day someone would discover the cause of his condition. About fifteen years ago, when I was in Manchester, there was a conference on colour vision, and someone took the eyes out of the bottle and did PCR analysis and found the genetics, and proved that Dalton was right all along – he was missing something. He thought it was because he had coloured oil droplets between the eyes and the receptors which were affecting colour in one of the receptors, and interestingly enough, that is actually how some animals do colour vision – they have different coloured oil drops in their receptors to fine-tune vision. Because it is the second pigment that’s missing, it is called deuteroanopia. He can still make colours because he has this pigment which is not X-linked, from a different chromosome, and he has the red pigment, which is fine, so he can see some colours, but his depth and range of colours, as he describes in the article and in his lecture, are not so good.