by William Hartridge
Eyes are fundamental to human existence, they allow us to experience the world in high detail and in such a wide variety of colours. How exactly does this work? Like every other process in the body, it is due to a series of chemical reactions. In fact, human vision can be mostly attributed to one molecule and without it, we wouldn’t be able to see at all. This molecule is retinal- a type of molecule called a polyene that features alternating single and double bonds. This allows for an effect called conjugation, whereby the p electron orbitals of atoms overlap to create a network of delocalised electrons. In retinal, this property is responsible for its unique optical characteristics. Retinal can exist as one of two possible stable isomers: 11-cis-retinal and all-trans-retinal and it is the isomerisation of this molecule between its “bent” and “straight” forms that allows for fundamental principle of vision- sensing of light. When energy is provided by a photon of light, it is absorbed by 11-cis-retinal causing a single bond to be formed momentarily between the 11th and 12th carbons that allows for rotation of part of the molecule. After rotation, the double bond is reformed, resulting in retinal now existing in the all-trans-retinal structure. This molecular movement makes vision possible as it acts like a light sensitive switch. Therefore, the next question to be answered is how this molecular motion is converted to a signal that can be interpreted by the brain as an image.
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In the retina of an eye, there exists two types of cell- rods and cones, with rods being responsible for black and white vision at low light levels and cones responsible for full colour vision in the day. Furthermore, there are 3 different types of cone cells, each responsible for sensing a different colour. Inside these cells are proteins, called opsins, that are bound to the previously mentioned retinal molecules and with each type of cell comes a different type of opsin protein: rhodopsins in rods and red, blue or green sensitive photopsins in each type of cone cell.
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Each of these proteins contain a molecule of retinal in the centre and have different conformations to interact with retinal differently, this slightly changes its properties such that each type of opsin is most sensitive to a different wavelength of light. For example, the greatest difference between green and red sensitive photopsins is in three amino acids at positions 180, 277 and 285. In the red sensitive photopsin, these amino acids differ due to added hydroxyl (OH) groups. This causes different interactions with the activated form of retinal, lowering its energy. Consequently, a lower energy of visible light, red, is needed to activate the protein.
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As with any area of the nervous system in the body, the eye generates signals via electrical impulses and it is the activation of these proteins that causes signals to be created. In the dark, positively charged ions, such as sodium and potassium, are always flowing into rod and cone cells through an ion channel gated by a molecule called cGMP. This means that without stimulus, rods and cones are continuously depolarised, so release glutamate neurotransmitters across a synapse to the next cell along, put simply they are always “on”. When the opsins absorb light at their respective most sensitive wavelengths, they activate another protein called transducin which subsequently activates an enzyme called cGMP phosphodiesterase. This enzyme then breaks down cGMP, as cGMP is responsible for the opening of sodium ion channels, these channels now shut due to the lower levels of cGMP, meaning less positive ions can enter the cell. Finally, this reduced level of positively charged ions inside the cell results in hyperpolarisation and a decrease of neurotransmitter (glutamate) release. This is why rods and cones are slightly unique as, conversely to the rest of the body, they generate a signal upon light detection by “turning off” as opposed to “turning on”. Therefore, these signals have to be reversed to allow impulses to be in the format that the brain is used to receiving. This function is carried out by the next cells in line (called bipolar cells) that reverse this signal, converting “off” to “on” and vice versa and then send these impulses to the optic nerve, where they travel to the brain.
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| Stages of activation |
As each photopsin provides light absorption at a different wavelength, it can now be seen that any colour can be sensed by processing the various levels each type of cone cell is activated and combining these signals to determine the final colour.
However vision is not this simple as an issue arises after light has been sensed, due to the irreversible isomerisation of the retinal. In order for the opsin to absorb light again, the system has to be reset. This is carried out by a complex series of reactions that terminate the signal by deactivating all of the involved proteins (that I will not describe) and also the conversion retinal back to its original isomer. Retinal (in the form of all-trans-retinal) first dissociates from opsin as it is no longer the correct shape to bind, then it moves to the epithelium where it is converted back to 11-cis-retinal and finally it is returned to an opsin protein in a rod or cone to be once again ready for light sensing.
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Now the basic mechanism of vision has been outlined, some abnormalities of vision can be further understood, such as colour blindness. As previously mentioned, green and red photopsin proteins are very similar, therefore also have similar genes. This, combined with the close proximity of their genes on the X chromosome, means it is likely that these genes can undergo recombination, where the DNA sequences are combined and rearranged. This can result in either the complete loss of a photopsin gene or the formation of a hybrid protein that absorbs a different wavelength of light. These abnormalities lead to a reduced ability to distinguish between colours, most commonly red and green.
Finally, a deficiency of vitamin A can lead to night blindness (where you cannot see in low light levels) as it is the metabolic precursor for synthesising retinal, the fundamental molecule of vision. This fact partly agrees with the myth that eating carrots can help you see in the dark, as they contain beta-carotene- a precursor to vitamin A. However this can only aid vision if someone is suffering from vitamin A deficiency and cannot actually enhance ordinary vision, especially not to the point where you have full night vision.
Sources:
http://www.chm.bris.ac.uk/motm/retinal/retinalh.htm
https://www.ncbi.nlm.nih.gov/books/NBK22541/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4727664/
https://www.youtube.com/watch?v=GKaFjw8N8zQ&ab_channel=NinjaNerdLectures
https://www.youtube.com/watch?v=dvovtbLGaUw&t=662s&ab_channel=SteveMould
https://www.lenstore.co.uk/eyecare/myth-or-truth
https://www.who.int/data/nutrition/nlis/info/vitamin-a-deficiency
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