Our vision, like all other senses, is malleable and variable depending on experience. Take, for example, those cases when people who are deprived of one sense experience a compensatory increase in others - for example, in the blind, sense of touch and hearing are sharpened. With the help of modern methods, neuroscientists have convincingly proved that the neural circuits of the brain do physically change: sensory centers are rearranged in search of an effective balance between the possibilities of the available neural resources and the demands placed on them by incoming sensory impressions. Research into this phenomenon shows that some sensory zones have a natural tendency towards certain functions, but they also clearly demonstrate the plasticity of the developing brain.
Take a rat that is blind from birth, say due to damage to both retinas. As she grows up, you teach her to go through the maze. Then you lightly damage her visual cortex. You again launch the rat into the maze and compare the time it took before the operation and after. In principle, damage to the visual cortex should not affect the ability of a blind rat to navigate a maze. But the classic experimental finding made by Carl Lashley and his colleagues decades ago is that the rat does worse on the task: apparently, its visual cortex is being invested in the process, although we do not know how.
Around the same time, doctors reported two types of developmental blindness. In the first variant, a patient whose one eye was blind from birth due to cataracts or a rare eyelid disease, after the elimination of this anatomical problem, still remained blind or almost blind to this eye - something prevented its neural pathways from connecting properly. The second option involved children with congenital squint: when they grew up, one of the eyes very often stopped working - the so-called "lazy eye", scientifically - amblyopia. The eye does not really go blind - its retina is functioning - but the person does not see it.
Vision pioneers David Hubel and Thorsten Wiesel, who discovered the principles of image processing in the visual cortex (and received a Nobel Prize for this), in experiments with animals, clarified the neurological basis of amblyopia. The synapses linking retinal cells to the central nervous system are quite malleable during a critical period early in life. If the cortical neurons receive a lot of information from one eye and do not receive from the other, then the axons representing the first eye capture all the synaptic spaces on the cortical neurons. At the same time, the second eye remains functional, but without connections with the neurons of the cortex.
Under normal circumstances, images from both eyes are recorded almost perfectly, and the same spot in the visual scene stimulates one group of cortical neurons. But when Hubel and Wiesel artificially "crooked" the eyes of young animals with a prism that shifted the visible image, the images from the two eyes did not converge properly at the same brain destination. With strabismus, a person sees two separate and contradictory images. The brain is forced to choose one eye. In this case, the connections of the second are suppressed - first temporarily, then permanently, and the eye becomes functionally blind.
Another artful experiment demonstrates a different kind of reorganization of cortical reactions. The retinal “map” is laid out on the visual cortex - of course, it is distorted by the waviness of the cortex surface; nevertheless, it is easy to make sure that neighboring points on the retina are projected onto neighboring points on the visual cortex, organizing a kind of visual scene map on it. Charles Gilbert of Rockefeller University painlessly burned a tiny hole in a monkey's retina with a laser painlessly, then recorded it from the visual cortex to see how the cortical map reacted. At first, there was a hole in it, corresponding to the hole in the retina. But after a while, adjacent areas of the cortex moved over and occupied the vacated space: neighboring areas of the retina now communicated with cortical neurons, which would normally react to the damaged area.
This does not mean that the vision of the damaged area of the retina was restored. If your retina is affected, you will never see anything destroyed - there you now have a blind spot. But even if the brain is unable to compensate for the hole in the retina, the area around it will "own" more cortical neurons than before. We can say that nature thus prevents cortical idleness: the eternal inactivity of a section of the cortex that has ceased to receive signals from a natural source is an impermissible luxury, so that over time it begins to functionally provide intact connections.
Promotional video:
Strong evidence of brain plasticity came from scans of the brain activity of people who were born blind. When the blind volunteers in the scanner used their fingers to read Braille, the brain's primary visual cortex, which normally processes visual signals, was active. Somehow, the processing of tactile information has occupied an unused visual center.
Another striking example is violinists. While playing the violin, you make sweeping movements with one hand, bowing along the strings, and a series of very subtle movements with the other hand, pressing the strings at well-defined points on the neck - very fast if you are a good violinist, and surprisingly fast if you are a star. An extraordinary challenge for speed and accuracy! Professional violinists practice these movements for many hours every day. And this is reflected in the physical location of the connections in their brain. The movements of the fingers are controlled by a specific area of the brain, and in violinists it expands - due to the neighboring brain tissue with its own functions. But this is only true for the bar hand. The same area on the other side of the brain that controls the bowed hand does not expand, because the movements of this hand are relatively coarse.
The opposite situation - deprivation instead of overuse - has also been studied in the laboratory. Cats raised in the dark have lost the ability to correctly combine images from both eyes. Other cats were raised in such conditions that they saw only vertical or horizontal stripes: in the primary visual cortex, they had an abnormally large number of neurons tuned to the vertical and horizontal, respectively. Another group of cats grew up in a dark room illuminated by very short light flashes: such animals could see, but did not perceive movement, since their retinas did not have time to register the movements of objects during flashes and there were no neurons in their cortex that selectively react to movement in different directions.
All this indicates the malleability of the emerging sensory systems. But what if a person grows up without sight at all? Neuropsychologist Donald Hebb predicted that vision can be largely learned. Complex perceptions are formed through experience, by association, and, in his opinion, this should happen at an early age, before the brain has lost the ability to form new necessary assemblies. Basically, his idea was correct: a lot really depends on the visual experience. However, the conclusion that this occurs at a young age seems to be only partly correct.
The evidence comes from experiments with people who were born blind and later gifted with sight. Pavan Sinha of the Massachusetts Institute of Technology, during a visit to his homeland, learned that about 300 thousand children with dense congenital cataracts live in the villages of India. In these children, the lens of the eye is replaced by a cloudy fibrous tissue. Cataracts allow light to pass through and distinguish it from darkness, but there is no need to talk about looking at details. Brilliantly combining science with humanism, Sinha organized a program to find and transport these children to New Delhi, where surgeons in a modern hospital replaced their lenses with artificial analogs (the same cataract operation is done for many elderly people).
Sinha's team tested the vision of young patients before surgery, immediately after surgery, and months or years later. After the removal of the cataract, the vision of the children did not recover quickly. At first, the world seemed hazy and vague to them. But over time, they began to see clearly, and after a few months they could already distinguish details, and not just distinguish light from darkness. Many were now able to walk without a white cane, ride a bicycle on a crowded street, get to know friends and family, attend school, and do other sighted activities.
Yet they never seem to have achieved perfect vision. Its severity remained below normal even after months of training. One patient said that he could read newspaper headlines, but not the fine print. Others had difficulty with specific visual tasks, such as recognizing two overlapping shapes separately. Thus, vision can be restored, but the plasticity of the visual system is not unlimited.
Another evidence of this is the work of special areas of the lower temporal lobe that respond exclusively to faces as a visual stimulus - the so-called "facial spots" (spindle-shaped facial zones). The fact that they are stably found in the same places in different people (or monkeys) suggests that they are naturally embedded in the brain. As Indian children learned to see, their brain activity underwent changes: immediately after the removal of the cataract, the reaction to visual stimuli, including images of faces, was disordered, scattered throughout the cerebral cortex, but soon it was replaced by a series of spots that were located in their normal positions … This shows that the brain knew in advance where the facial spots should be, and indicates a certain predetermination of the visual structures.
Finally, in 2017, Margaret Livingston and others at Harvard Medical School published the results of a solid and elegant experiment on sensory neural plasticity. They raised macaques from birth in such a way that they never saw faces. Neither human, nor ape, nor any other person. The monkeys were cared for with love, but the experimenters wore a welding mask every time to communicate with them.
Otherwise, macaques grew up in a completely normal visual world: they could see everything in their cage and in the rest of the room; could see the experimenter's torso, arms and legs; could see the baby bottle from which they were fed. They could hear the usual sounds of a monkey pack. The only thing they could not see was faces. Macaques developed normally, for the most part, and when they were introduced into the flock, they successfully began to communicate with their relatives and successfully integrated into the monkey society.
The experimenters tested the brain activity of macaques by presenting them with various visual stimuli, including faces. As you might have guessed, they grew up with no facial spots in the brain. It is noteworthy that those areas of the temporal lobe, which would normally serve for face recognition, instead reacted to images of the hands. In a normal social environment, the most important visual objects for a primate are faces. Faces signal anger, fear, hostility, love, and all other emotional information that is important for survival and prosperity. Apparently, the second most important environmental detail for a primate is the hands: the monkeys' own hands and the hands of the experimenters who fed and raised them.
Although their “facial” spots turned into “tame” ones, this replacement turned out to be plastic to a certain extent. About six months after the macaques were finally allowed to see the faces of the experimenters and other monkeys, neurons in these areas of the brain gradually regained receptivity to faces. Obviously, faces convey so much important information that they are able to recapture areas of the brain that were previously captured by hands.
Excerpt from the book "We Know It When We See It" by the American neuroscientist and ophthalmologist Richard Masland (1942–2019)
