By Susana Martinez-Conde The many evils of social media notwithstanding, millions of users agree that some of its most delightful aspects include viral illusions and cute cat videos. The potential for synergy was vast in retrospect—but only realized in 2013, when Rasmus Bååth, a cognitive scientist from Lund University in Sweden, blended both elements in a YouTube video of his kitten attacking a printed version of Akiyoshi Kitaoka’s famous “Rotating Snakes” illusion. The clip, which has been viewed more than 6 million times as of this writing, led to subsequent empirical research and an internet survey of cat owners, where 29% of respondents answered that their pets reacted to the Rotating Snakes. The results, published in the journal Psychology in 2014, indicated—though not conclusively—that cats experience illusory motion when they look at the Rotating Snakes pattern, much as most humans do. Now, a team of researchers from University of Padova, Italy, Queen Mary University of London in the UK, and the Parco Natura Viva—Garda Zoological Park in Bussolengo, Italy, has collected additional evidence that cats—in this case, big cats—find the Rotating Snakes Illusion fascinating. Advertisement Intrigued by the earlier study on house cats, Christian Agrillo of the University of Padova and his collaborators set out to determine whether lions at Parco Natura Viva were similarly susceptible to motion illusions, as well as explore the possibility that such patterns might serve as a source of visual enrichment for zoo animals. Their findings were published last month in Frontiers in Psychology. © 2019 Scientific American,

Related chapters from BN8e: Chapter 10: Vision: From Eye to Brain; Chapter 6: Evolution of the Brain and Behavior
Related chapters from MM:Chapter 7: Vision: From Eye to Brain
Link ID: 26826 - Posted: 11.18.2019

By Erica Tennenhouse Live in the urban jungle long enough, and you might start to see things—in particular humanmade objects like cars and furniture. That’s what researchers found when they melded photos of artificial items with images of animals and asked 20 volunteers what they saw. The people, all of whom lived in cities, overwhelmingly noticed the manufactured objects whereas the animals faded into the background. To find out whether built environments can alter peoples’ perception, the researchers gathered hundreds of photos of animals and artificial objects such as bicycles, laptops, or benches. Then, they superimposed them to create hybrid images—like a horse combined with a table (above, top left) or a rhinoceros combined with a car (above, bottom right). As volunteers watched the hybrids flash by on a screen, they categorized each as a small animal, a big animal, a small humanmade object, or a big humanmade object. Overall, volunteers showed a clear bias toward the humanmade objects, especially when they were big, the researchers report today in the Proceedings of the Royal Society B. The bias itself was a measure of how much the researchers had to visually “amp up” an image before participants saw it instead of its partner image. That bias suggests people’s perceptions are fundamentally altered by their environments, the researchers say. Humans often rely on past experiences to process new information—the classic example is mistaking a snake for a garden hose. But in this case, living in industrialized nations—where you are exposed to fewer “natural” objects—could change the way you view the world. © 2019 American Association for the Advancement of Science

Related chapters from BN8e: Chapter 10: Vision: From Eye to Brain; Chapter 18: Attention and Higher Cognition
Related chapters from MM:Chapter 7: Vision: From Eye to Brain; Chapter 14: Attention and Consciousness
Link ID: 26793 - Posted: 11.06.2019

By Kelly Servick CHICAGO, ILLINOIS—In 2014, U.S. regulators approved a futuristic treatment for blindness. The device, called Argus II, sends signals from a glasses-mounted camera to a roughly 3-by-5-millimeter grid of electrodes at the back of eye. Its job: Replace signals from light-sensing cells lost in the genetic condition retinitis pigmentosa. The implant’s maker, Second Sight, estimates that about 350 people in the world now use it. Argus II offers a relatively crude form of artificial vision; users see diffuse spots of light called phosphenes. “None of the patients gave up their white cane or guide dog,” says Daniel Palanker, a physicist who works on visual prostheses at Stanford University in Palo Alto, California. “It’s a very low bar.” But it was a start. He and others are now aiming to raise the bar with more precise ways of stimulating cells in the eye or brain. At the annual meeting of the Society for Neuroscience here last week, scientists shared progress from several such efforts. Some have already advanced to human trials—“a real, final test,” Palanker says. “It’s exciting times.” Several common disorders steal vision by destroying photoreceptors, the first cells in a relay of information from the eye to the brain. The other players in the relay often remain intact: the so-called bipolar cells, which receive photoreceptors’ signals; the retinal ganglion cells, which form the optic nerve and carry those signals to the brain; and the multilayered visual cortex at the back of the brain, which organizes the information into meaningful sight. Because adjacent points in space project onto adjacent points on the retina, and eventually activate neighboring points in an early processing area of the visual cortex, a visual scene can be mapped onto a spatial pattern of signals. But this spatial mapping gets more complex along the relay, so some researchers aim to activate cells as close to the start as possible. © 2019 American Association for the Advancement of Science

Related chapters from BN8e: Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 7: Vision: From Eye to Brain
Link ID: 26779 - Posted: 11.01.2019

By Stephen L. Macknik Most of us look at a bird and see its avian shape in perfect alignment with the colors of its beautiful plumage. How could it be any other way? The shape and color are derived from the same object and so the brain must process shape and color together as a unified percept. Right? Wrong. The brain processes forms and color in separate neural circuits, but because these brain regions communicate with each other, our perception appears unified. To understand how this all works, let’s do an experiment on ourselves to separate (and then recombine in our brains) the colors and shapes from an image. We will use an illusion called the Color Assimilation Grid, developed by Øyvind Kolås, a digital media artist and software developer. First, let’s apply a screen to the birds (above) so that we can sample their colors but get rid of most of their shape information. We simply take the original image and blur it (to break down the shape information, not shown) and then multiply the resultant pixels in a step-by-step, pixel-by-pixel fashion with a grid screen of the same size as the original image. In the screen, white pixels equal 1 and the gray regions equal zero, so the result is a blurry colored plaid sample of the birds’ colors. Now that we have diminished the shape information and sampled the colors, we need to do the opposite: sample the shapes after diminishing the color information, so that we can later mix the two to see how shape and color assimilate in the brain. To create the shape-only image we first turn the original image to grayscale (above) and then we apply the inverse of the screen we used in the color sampling. The result is a grayscale image of the birds with the shape information preserved, superimposed with a tiny grid of empty spaces where we can later add color information without altering the rest of the image. © 2019 Scientific American

Related chapters from BN8e: Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 7: Vision: From Eye to Brain
Link ID: 26760 - Posted: 10.28.2019

By Tanya Lewis The lenses in human eyes lose some ability to focus as they age. Monovision—a popular fix for this issue—involves prescription contacts (or glasses) that focus one eye for near-vision tasks such as reading and the other for far-vision tasks such as driving. About 10 million people in the U.S. currently use this form of correction, but a new study finds it may cause a potentially dangerous optical illusion. Nearly a century ago German physicist Carl Pulfrich described a visual phenomenon now known as the Pulfrich effect: When one eye sees either a darker or a lower-contrast image than the other, an object moving side to side (such as a pendulum) appears to travel in a three-dimensional arc. This is because the brain processes the darker or lower-contrast image more slowly than the lighter or higher-contrast one, creating a lag the brain perceives as 3-D motion. Johannes Burge, a psychologist at the University of Pennsylvania, and his colleagues recently found that monovision can cause a reverse Pulfrich effect. They had participants look through a device showing a different image to each eye—one blurry and one in focus—of an object moving side to side. The researchers found that viewers processed the blurrier image a couple of milliseconds faster than the sharper one, making the object seem to arc in front of the display screen. It appeared closer to the viewer as it moved to the right (if the left eye saw the blurry image) or to the left (if the right eye did). “That does not sound like a very big deal,” Burge says, but it is enough for a driver at an intersection to misjudge the location of a moving cyclist by about the width of a narrow street lane (graphic). © 2019 Scientific American

Related chapters from BN8e: Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 7: Vision: From Eye to Brain
Link ID: 26758 - Posted: 10.28.2019

By Evan Cooper Early one summer morning, I was awakened by a hammering on the inside of my skull. It felt as if a prisoner were trying to Shawshank it out through my left eye socket. When I sat up in bed to reach for the Advil on my nightstand, I became panic-stricken. Both eyes were open, but I could see through only one. I’d been known to leap to worst-case scenarios at the first sign of any physical discomfort. (Pain in my abdomen? Appendicitis! Headache? Definitely a brain tumor.) But this was different: I wasn’t paranoid, I was blind in my left eye. At the ophthalmologist’s office later that morning, I tried not to panic. I was nearly 20 years old, midway through my studies at U.C.L.A. Everything is fine, I told myself. You’re FINE. Like a mantra, I repeated this over and over, determined that, for once, I was not going to catastrophize. I briefly thought I might be imagining it all, conjuring up some drama for attention. Once when I was 11, I called my dad, who lived 3,000 miles away in Los Angeles, and begged him to send an ambulance to my house in Cleveland because I was certain that I had a collapsed lung and my mom was refusing to take me to the hospital. But the doctor I saw told me with some urgency that I needed to see a specialist, immediately. I overheard his assistant quietly consider potential diagnoses: “multiple sclerosis, lupus, another autoimmune disease?” I closed my eyes and imagined myself on the sort of carnival ride where you stick to the wall as you spin round and round until the floor falls away. Beyond disbelief and dread, however, I also felt a familiar swell of self-loathing. Of course I have an incurable, degenerative disease, I reprimanded myself. This is my fault. After all, up until this point, I had lived as if an internal army of drill sergeants were commanding me to eat less, exercise harder, study more, stand out, be The Best. No achievement was ever good enough. And what is an autoimmune disease if not the Self waging a war upon the Self? © 2019 The New York Times Company

Related chapters from BN8e: Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 7: Vision: From Eye to Brain
Link ID: 26680 - Posted: 10.08.2019

Joe Palca It's hard for doctors to do a thorough eye exam on infants. They tend to wiggle around — the babies, that is, not the doctors. But a new smart phone app takes advantage of parents' fondness for snapping pictures of their children to look for signs that a child might be developing a serious eye disease. The app is the culmination of one father's the five-year quest to find a way to catch the earliest signs of eye disease, and prevent devastating loss of vision. Five years ago, NPR reported the story of Bryan Shaw's son Noah, and how he lost an eye to cancer. Doctors diagnosed Noah Shaw's retinoblastoma when he was 4 months old. To make the diagnosis, the doctors shined a light into Noah's eye, and got a pale reflection from the back of the eyeball, an indication that there were tumors there. Noah's father Bryan is a scientist. He wondered if he could see that same pale reflection in flash pictures his wife was always taking of his baby son. Sure enough, he saw the reflection or glow, which doctors call "white eye," in a picture taken right after Noah was born. "We had white eye showing up in pictures at 12 days old," Shaw said at the time, months before his ultimate diagnosis Shaw is a chemist, not an eye doctor nor a computer scientist, but he decided to create software that could scan photos for signs of this reflection. © 2019 npr

Related chapters from BN8e: Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 7: Vision: From Eye to Brain
Link ID: 26679 - Posted: 10.08.2019

By James Gorman When the moon hits your eye like a big pizza pie, it may not be amore at all, but a ghostly white barn owl about to kill and eat you. If you’re a vole, that is. Voles are a favorite meal for barn owls, which come in two shades, reddish brown and white. When the moon is new, both have equal success hunting for their young, snagging about five voles in a night. But when the moon is full and bright, the reddish owls do poorly, dropping to three a night. Barn owls with white faces and breasts do as well as ever, however, even though they should be more easily spotted than their reddish relatives when the lunar light reflects off their feathers. They may well be more easily seen, but it doesn’t matter because of the behavior of their prey. Voles have two responses to owl sightings. They freeze, and hope the owl doesn’t see them. Or they run. But when they see a white owl in bright moonlight, the terrified rodents act like deer caught in headlights and freeze up to five seconds longer than they do for a reddish brown barn owl. This is not what Luis M. San-Jose and Alexandre Roulin, both of the University of Lausanne in Switzerland, expected. They and other scientists reported in Nature Ecology and Evolution on Monday that they expected the white owls to do worse. “The study is a fascinating new look at an old question: How does moonlight affect the plumage of nocturnal predators?” said Richard Prum, an evolutionary biologist and ornithologist at Yale University, who has studied how coloration evolved in birds. He added that authors used “a remarkable array of technologies and methods” to investigate the effect of the variation. Dr. San-Jose, who researches animal coloration, said that there has been little study of color in nocturnal animals in the past, but that has begun to change, producing many surprises in recent years. “Many nocturnal species actually see color at night,” he said. Voles probably don’t. For them, the owls probably appear in shades of gray. Still, the lighter the shade, the more visible the owl. © 2019 The New York Times Company

Related chapters from BN8e: Chapter 10: Vision: From Eye to Brain; Chapter 14: Biological Rhythms, Sleep, and Dreaming
Related chapters from MM:Chapter 7: Vision: From Eye to Brain; Chapter 10: Biological Rhythms and Sleep
Link ID: 26567 - Posted: 09.03.2019

David Cyranoski A Japanese woman in her forties has become the first person in the world to have her cornea repaired using reprogrammed stem cells. At a press conference on 29 August, ophthalmologist Kohji Nishida from Osaka University, Japan, said the woman has a disease in which the stem cells that repair the cornea, a transparent layer that covers and protects the eye, are lost. The condition makes vision blurry and can lead to blindness. How iPS cells changed the world To treat the woman, Nishida says his team created sheets of corneal cells from induced pluripotent stem (iPS) cells. These are made by reprogramming adult skin cells from a donor into an embryonic-like state from which they can transform into other cell types, such as corneal cells. Nishida said that the woman’s cornea remained clear and her vision had improved since the transplant a month ago. Currently people with damaged or diseased corneas are generally treated using tissue from donors who have died, but there is a long waiting list for such tissue in Japan. Japan has been ahead of the curve in approving the clinical use of iPS cells, which were discovered by stem-cell biologist Shinya Yamanaka at Kyoto University, who won a Nobel prize for the work. Japanese physicians have also used iPS cells to treat spinal cord injury, Parkinson’s disease and another eye disease. © 2019 Springer Nature Publishing AG

Related chapters from BN8e: Chapter 10: Vision: From Eye to Brain; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 7: Vision: From Eye to Brain; Chapter 13: Memory, Learning, and Development
Link ID: 26564 - Posted: 09.03.2019

By Michelle Roberts Health editor, BBC News online Experts are warning about the risks of extreme fussy eating after a teenager developed permanent sight loss after living on a diet of chips and crisps. Eye doctors in Bristol cared for the 17-year-old after his vision had deteriorated to the point of blindness. Since leaving primary school, the teen had been eating only French fries, Pringles and white bread, as well as an occasional slice of ham or a sausage. Tests revealed he had severe vitamin deficiencies and malnutrition damage. Extreme picky eater The adolescent, who cannot be named, had seen his GP at the age of 14 because he had been feeling tired and unwell. At that time he was diagnosed with vitamin B12 deficiency and put on supplements, but he did not stick with the treatment or improve his poor diet. Three years later, he was taken to the Bristol Eye Hospital because of progressive sight loss, Annals of Internal Medicine journal reports. Dr Denize Atan, who treated him at the hospital, said: "His diet was essentially a portion of chips from the local fish and chip shop every day. He also used to snack on crisps - Pringles - and sometimes slices of white bread and occasional slices of ham, and not really any fruit and vegetables. "He explained this as an aversion to certain textures of food that he really could not tolerate, and so chips and crisps were really the only types of food that he wanted and felt that he could eat." Dr Atan and her colleagues rechecked the young man's vitamin levels and found he was low in B12 as well as some other important vitamins and minerals - copper, selenium and vitamin D. He was not over or underweight, but was severely malnourished from his eating disorder - avoidant-restrictive food intake disorder. "He had lost minerals from his bone, which was really quite shocking for a boy of his age." He was put on vitamin supplements and referred to a dietitian and a specialist mental health team. In terms of his sight loss, he met the criteria for being registered blind. "He had blind spots right in the middle of his vision," said Dr Atan. "That means he can't drive and would find it really difficult to read, watch TV or discern faces. © 2019 BBC.

Related chapters from BN8e: Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 7: Vision: From Eye to Brain
Link ID: 26563 - Posted: 09.03.2019

By Stephen L. Macknik In normal vision, light falls on the retinas inside the eyes, and is immediately transduced into electrochemical signals before being uploaded to the brain through the optic nerves. So you do not see light itself, but the brain's interpretation of electrochemical signals in the visual parts of the brain. It follows that, if your eyes do not work, but your brain is stimulated just so, your visual neurons will activate (and you will be able to see) just the same as if your eyes were in perfect condition. Sounds easy, but can we do that? Building on decades of research in visual neuroscience, my lab, in collaboration with Susana Martinez-Conde’s, has now conducted some of the studies that validate this idea, completing some of the most important preliminary steps towards a new kind of visual prosthetic. Francis Collins, the Director of the National Institutes of Health, has just posted a blog that highlights our approach. He took notice of our work when we first presented it at this year's meeting for the Principal Investigators of the BRAIN Initiative—the NIH led government funding initiative meant to spur research along on topics like brain implants. The BRAIN Initiative funds several agencies including the NIH, including the National Science Foundation, who kindly funded the grant driving our research thus far. Our starting premise is that vision is fundamentally a thumbnail sketch. Even if 99.9% of your retina works fine, but the central 1/1000th of your visual field is broken, you will be legally blind. That central 0.1% of your visual field is about the same size as your thumbnail held up at arm's length. Because that central 0.1% of the retina is the visual sweet spot, it is the place where the visual magic happens. In fact, much of the remaining 99.9% of the retina’s main job is to help you detect where to move your eyes next. This means that we need to restore central vision in the blind, or we are not really restoring functional vision at all. © 2019 Scientific American

Related chapters from BN8e: Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 7: Vision: From Eye to Brain
Link ID: 26553 - Posted: 08.29.2019

By Cara Giaimo Peppered moth caterpillars live across the Northern Hemisphere, from the forests of China to the backyards of North America. But if you’ve never seen one, don’t feel bad: They’re experts at blending in. Each caterpillar mimics the twig it perches on, straightening its knobbly body into a stick-like shape. It also changes its hue to match the twig’s color, whether birch white, willow green or dark oak brown. They’re so good at this, in fact, that they can do it blindfolded — literally. According to a paper published in Communications Biology in early August, the caterpillars sense the color of their surroundings not only with their eyes, but also with their skin. While other animals, including cuttlefish and lizards, have similar abilities, this is “the most complete demonstration so far that color change can be controlled by cells outside the eyes,” said Martin Stevens, a professor of sensory and evolutionary ecology at the University of Exeter. Dr. Stevens, who was not involved in the study, added that the exact mechanism remains a mystery. The adult peppered moth is famous for a completely different color journey; After soot from the Industrial Revolution darkened tree bark in Britain, peppered moths there evolved to be darker, too. Ilik Saccheri, a professor of ecological genetics at the University of Liverpool and an author of the new paper, normally studies the adult moth. This requires keeping a lot of caterpillars around. Years of observation sparked his curiosity about their color-changing abilities, which happen individually and in a matter of minutes rather than over generations. Each caterpillar hatches tiny and black, and in its early days is blown around by the wind. Once it falls on a plant, it must camouflage itself to avoid being spotted by hungry birds. This process, which involves producing new pigments, plays out over a period of days or weeks. “I was a bit disbelieving that they could change that accurately only using their eyes,” which are quite simple at the larval stage, Dr. Saccheri said. © 2019 The New York Times Company

Related chapters from BN8e: Chapter 10: Vision: From Eye to Brain; Chapter 6: Evolution of the Brain and Behavior
Related chapters from MM:Chapter 7: Vision: From Eye to Brain
Link ID: 26547 - Posted: 08.27.2019

By Susana Martinez-Conde If you’re older than forty, chances are that reading texts or playing with your smart phone is now harder than it used to be. Such difficulty with near focusing is usually the result of presbyopia, the hardening of the lens of the eye that starts to take place in middle age. From eyeglasses to refractive surgery, many available solutions allow GenXers and baby boomers to read small print and conduct other near-vision tasks to their hearts’ content. The problem is, one of the most prevalent treatments for presbyopia could make you less safe on the road. Broadly, people suffering from presbyopia can opt for eyeglasses, contact lenses or surgery. Eyeglasses include reading glasses (used for close-up vision only), as well as glasses with bifocal, multifocal or progressive lenses (which are worn all day and allow vision at a range of distances). Contact lens correction can work just like with eyeglasses, but it also offers an alternative solution for presbyopia, called monovision. In monovision, one eye is corrected for close-up viewing, and the other eye for long-distance viewing. Thus, at any distance (near or far), at least one eye offers clear vision even when the image from the other eye is blurred. Eventually, the brain learns to suppress the blurred images and rely on the crisp images only, so people can enjoy clear vision at all distances. Finally, those with presbyopia can opt for refractive eye surgery, including monovision LASIK, which typically corrects the nondominant eye for near vision while leaving the dominant eye able to see long distance. Among baby boomers, monovision is the most popular contact lens correction for presbyopia, and monovision LASIK is also on the rise for eligible people over the age of 40. Yet, according to new research by Johannes Burge, Victor Rodriguez-Lopez, and Carlos Dorronsoro at the University of Pennsylvania, monovision corrections could present previously unidentified safety concerns, especially while driving. The reason is related to a century-old illusion called the Pulfrich effect. © 2019 Scientific American

Related chapters from BN8e: Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 7: Vision: From Eye to Brain
Link ID: 26489 - Posted: 08.12.2019

By Frank Bruni CHIOS, Greece — Over my 54 years, I’ve pinned my hopes on my parents, my teachers, my romantic partners, God. I’m pinning them now on a shrub. It’s called mastic, it grows in particular abundance on the Greek island of Chios and its resin — the goo exuded when its bark is gashed — has been reputed for millenniums to have powerful curative properties. Ancient Greeks chewed it for oral hygiene. Some biblical scholars think the phrase “balm of Gilead” refers to it. It has been used in creams to reduce inflammation and heal wounds, as a powder to treat irritable bowels and ulcers, as a smoke to manage asthma. I’m now part of a clinical trial in the United States to determine if a clear liquid extracted from mastic resin can, through regular injections, repair ravaged nerves. That would have profound implications for millions of Alzheimer’s patients, stroke survivors — and me. The vision in my right eye was ruined by a condition that devastated the optic nerve behind it, and I’m at risk of the same happening on the left side, in which case I wouldn’t be able to see a paragraph like this one. Will a gnarly evergreen related to the pistachio tree save me? That’s unclear. But in the meantime, I thought I should hop on a plane and meet my medicine. Chios has just 50,000 or so year-round residents. It lies much closer to Turkey than to the Greek mainland. And there’s no separating its history from that of mastic. ImageA 17th-century rendering of the island of Chios. A 17th-century rendering of the island of Chios.CreditBridgeman Images In the 1300s and 1400s, when Chios was governed by the Republic of Genoa, the punishment for stealing up to 10 pounds of mastic resin was the loss of an ear; for more than 200 pounds, you were hanged. The stone villages in the southern part of the island, near the mastic groves, were built in the manner of fortresses — with high exterior walls, only a few entrances and labyrinthine layouts — to foil any attempts by invaders to steal the resin stored there. © 2019 The New York Times Company

Related chapters from BN8e: Chapter 10: Vision: From Eye to Brain; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 7: Vision: From Eye to Brain; Chapter 13: Memory, Learning, and Development
Link ID: 26461 - Posted: 07.29.2019

By Carl Zimmer In a laboratory at the Stanford University School of Medicine, the mice are seeing things. And it’s not because they’ve been given drugs. With new laser technology, scientists have triggered specific hallucinations in mice by switching on a few neurons with beams of light. The researchers reported the results on Thursday in the journal Science. The technique promises to provide clues to how the billions of neurons in the brain make sense of the environment. Eventually the research also may lead to new treatments for psychological disorders, including uncontrollable hallucinations. “This is spectacular — this is the dream,” said Lindsey Glickfeld, a neuroscientist at Duke University, who was not involved in the new study. In the early 2000s, Dr. Karl Deisseroth, a psychiatrist and neuroscientist at Stanford, and other scientists engineered neurons in the brains of living mouse mice to switch on when exposed to a flash of light. The technique is known as optogenetics. In the first wave of these experiments, researchers used light to learn how various types of neurons worked. But Dr. Deisseroth wanted to be able to pick out any individual cell in the brain and turn it on and off with light. So he and his colleagues designed a new device: Instead of just bathing a mouse’s brain in light, it allowed the researchers to deliver tiny beams of red light that could strike dozens of individual brain neurons at once. To try out this new system, Dr. Deisseroth and his colleagues focused on the brain’s perception of the visual world. When light enters the eyes — of a mouse or a human — it triggers nerve endings in the retina that send electrical impulses to the rear of the brain. There, in a region called the visual cortex, neurons quickly detect edges and other patterns, which the brain then assembles into a picture of reality. © 2019 The New York Times Company

Related chapters from BN8e: Chapter 10: Vision: From Eye to Brain; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 7: Vision: From Eye to Brain; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 26433 - Posted: 07.19.2019

Laura Sanders A praying mantis depends on precision targeting when hunting insects. Now, scientists have identified nerve cells that help calculate the depth perception required for these predators’ surgical strikes. In addition to providing clues about insect vision, the principles of these cells’ behavior, described June 28 in Nature Communications, may also lead to advances in robot vision or other automated systems. So far, praying mantises are the only insects known to be able to see in 3-D. In the new study, neuroscientist Ronny Rosner of Newcastle University in England and colleagues used a tiny theater that played praying mantises’ favorite films — moving disks that mimic bugs. The disks appeared in three dimensions because the insects’ eyes were covered with different colored filters, creating minuscule 3-D glasses. As a praying mantis watched the films, electrodes monitored the behavior of individual nerve cells in the optic lobe, a brain structure responsible for many aspects of vision. There, researchers found four types of nerve cells that seem to help merge the two different views from each eye into a complete 3-D picture, a skill that human vision cells use to sense depth, too. One cell type called a TAOpro neuron possesses three elaborate, fan-shaped bundles that receive incoming visual information. Along with the three other cell types, TAOpro neurons are active when each eye’s view of an object is different, a mismatch that’s needed for depth perception. |© Society for Science & the Public 2000 - 2019.

Related chapters from BN8e: Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 7: Vision: From Eye to Brain
Link ID: 26422 - Posted: 07.16.2019

By Elizabeth Pennisi PROVIDENCE—Looking a squid in the eye is eerily like looking in a mirror. Squids, octopuses, and other cephalopods are on a very different part of the tree of life from vertebrates. But both have evolved sophisticated peepers that rely on a lens to focus light and provide excellent vision. This independent evolution of such complexity has puzzled biologists for centuries and has prompted searches for clues about how this might have come about. Evolutionary developmental biologists have now discovered that the genes that guide the initial formation of legs in us and other vertebrates also guide the formation of the squid’s lens (seen in cross section of eye above). The find is yet another example of how nature recruits genes used for one purpose to do another job for the body. The squid lens forms as extra-long membranes jutting out for specialized eye cells overlap to form a tight ball. Our lenses are actually degraded cells themselves packed with a clear protein. To learn how the squid lenses form, these researchers carefully tracked where, when, and which genes turn on and off as embryos of Doryteuthis pealeii, a squid commonly served as fried appetizers, develop. © 2019 American Association for the Advancement of Science

Related chapters from BN8e: Chapter 10: Vision: From Eye to Brain; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 7: Vision: From Eye to Brain; Chapter 13: Memory, Learning, and Development
Link ID: 26421 - Posted: 07.16.2019

By Stephen L. Macknik When Susana Martinez-Conde and I talk to audiences about NeuroMagic—our research initiative to study the brain with magic (and vice-versa), people often ask us how we bring both fields together. They want to know in what ways magic tricks can inform neuroscience, and what a day in the life of a neuromagic scientist looks like. How do we run a neuromagic experiment, from collecting the data to using the results to gain knowledge about the mind's inner secrets? Our new study, led by Anthony Barnhart (aka Magic Tony) and just published in the Journal of Eye Movement Research, illustrates some of the ways in which we investigate magic in the lab. You can download the paper for free, but as it is written for academics, I'll give you the gist here. The experiment addresses how various neural circuits interact in your brain while you watch a magic performance. There's the visual system—critical for perception—there's the oculomotor system—critical for targeting and moving the eyes—and there's the attentional system—critical for filtering out irrelevant information and allowing you to literally and figuratively focus both the visual and oculomotor systems at the right place and at the right time. Without all three of these systems working together, you would be unable to conduct most visual tasks. Advertisement Magic is one of the inroads available to dissect the function of many perceptual and cognitive systems, and especially so in situations that are fairly similar to those we encounter in real life. This concept—ecological validity—is important to testing whether neuroscience theories will hold up outside of the lab, and one of the reasons why magic tricks are attractive for studying everyday perception and cognition. © 2019 Scientific American

Related chapters from BN8e: Chapter 18: Attention and Higher Cognition; Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 14: Attention and Consciousness; Chapter 7: Vision: From Eye to Brain
Link ID: 26412 - Posted: 07.13.2019

Partial sight has been restored to six blind people via an implant that transmits video images directly to the brain. Some vision was made possible – with the participants’ eyes bypassed – by a video camera attached to glasses which sent footage to electrodes implanted in the visual cortex of the brain. University College London lecturer and Optegra Eye Hospital surgeon Alex Shortt said it was a significant development by specialists from Baylor Medical College in Texas and the University of California Los Angeles. “Previously all attempts to create a bionic eye focused on implanting into the eye itself. It required you to have a working eye, a working optic nerve,” Shortt told the Daily Mail. “By bypassing the eye completely you open the potential up to many, many more people. “This is a complete paradigm shift for treating people with complete blindness. It is a real message of hope.” How eye-gaze technology brought creativity back into an artist's life The technology has not been proven on those born blind. The US team behind the study asked participants, each of whom has been completely blind for years, to look at a blacked-out computer screen and identify a white square appearing randomly at different locations on the monitor. The majority of the time, they can find the square. © 2019 Guardian News & Media Limited

Related chapters from BN8e: Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 7: Vision: From Eye to Brain
Link ID: 26411 - Posted: 07.13.2019

By Chris Woolston When Sylvia Groth steps through the doors of the Vanderbilt Eye Institute in Nashville, she knows she has a tough day ahead. Before she goes home, she’ll likely have at least one hard talk with a person whose sight has been ravaged by glaucoma. “When I make a diagnosis of advanced glaucoma, I do it with a heavy heart,” the ophthalmologist says. “It’s such an empty feeling to not be able to do anything.” An incurable eye disease that kills vital nerve cells at the back of the retina, glaucoma is a leading cause of irreversible blindness in the world. More than 70 million people have it, and 3 million of them already are blind. Nothing can be done to restore vision once it’s lost, and even the best treatments can’t always slow disease progression. But researchers foresee a time when they can offer therapies to protect nerve cells in the eye and perhaps even restore lost sight. “We’re making advances with every different type of treatment,” ophthalmologist Leonard Levin of McGill University in Montreal says. Researchers have long understood the basics of the most common form of glaucoma, called open-angle glaucoma. The eye is nourished by a clear fluid called the aqueous humor that keeps the eyeball inflated, plump and healthy. But just like a tire, the eye can become overinflated. If the aqueous humor can’t drain properly, pressure inside the eye grows too high and can crush cells within the optic nerve — the sensory cable that carries images from the retina to the optical centers of the brain. Pressure probably hurts nerve cells in other ways too, ophthalmologist Harry Quigley of Johns Hopkins University says. © 1996-2019 The Washington Post

Related chapters from BN8e: Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 7: Vision: From Eye to Brain
Link ID: 26376 - Posted: 07.02.2019