Chapter 7. Vision: From Eye to Brain
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By Chris Baraniuk It’s sometimes practically impossible to tell similar colours apart. Even side by side, they look the same. A special pair of spectacles gives us new power to see more distinct colours, and could one day help to spot counterfeit banknotes or counteract camouflage. The glasses, devised by a team at the University of Wisconsin-Madison, basically enhance the user’s colour vision, allowing them to see metamers – colours that look the same but give off different wavelengths of light – as recognisably distinct hues. Human colour vision relies on three types of cone cells that react to short (blue), medium (green) and long (red) wavelengths. While brushing up on his knowledge of the eye before teaching a photonics class, physicist Mikhail Kats had a brainwave. Could the eye be tricked into effectively having another type of cone cell? In theory, this could take our vision from being trichromatic, which uses three colour channels, to tetrachromatic. Some animals see in four (or more) channels. Goldfish, for example, have cells for red, blue, green and ultraviolet light. Some researchers suggest that a very small number of humans may be tetrachromats too. Read more: Human eye proteins detect red beyond red To make their glasses, Kats and his colleagues designed two colour filters, one for each eye that strip out specific parts of the blue light spectrum. With each eye receiving slightly different spectral information about blue things, the team hypothesised that any subtle differences in colour would be more pronounced. And they were right. © Copyright Reed Business Information Ltd
Link ID: 23381 - Posted: 03.21.2017
By DENISE GRADY Three women suffered severe, permanent eye damage after stem cells were injected into their eyes, in an unproven treatment at a loosely regulated clinic in Florida, doctors reported in an article published Wednesday in The New England Journal of Medicine. One, 72, went completely blind from the injections, and the others, 78 and 88, lost much of their eyesight. Before the procedure, all had some visual impairment but could see well enough to drive. The cases expose gaps in the ability of government health agencies to protect consumers from unproven treatments offered by entrepreneurs who promote the supposed healing power of stem cells. The women had macular degeneration, an eye disease that causes vision loss, and they paid $5,000 each to receive stem-cell injections in 2015 at a private clinic in Sunrise, Fla. The clinic was part of a company then called Bioheart, now called U.S. Stem Cell. Staff members there used liposuction to suck fat out of the women’s bellies, and then extracted stem cells from the fat to inject into the women’s eyes. The disastrous results were described in detail in the journal article, by doctors who were not connected to U.S. Stem Cell and treated the patients within days of the injections. An accompanying article by scientists from the Food and Drug Administration warned that stem cells from fat “are being used in practice on the basis of minimal clinical evidence of safety or efficacy, sometimes with the claims that they constitute revolutionary treatments for various conditions.” © 2017 The New York Times Company
By Anna Azvolinsky Delivering a CRISPR/Cas9–based therapy directly to the eye via a viral vector can prevent retinal degeneration in a mouse model of retinitis pigmentosa, a team led by researchers at the National Eye Institute reported in Nature Communications today (March 14). Retinitis pigmentosa, which affects around one in 4,000 people, causes retinal degeneration that eventually leads to blindness. The inherited disorder has been mapped to more than 60 genes (and more than 3,000 mutations), presenting a challenge for researchers working toward a gene therapy. The results of this latest study suggest that a broader, gene-editing–based therapeutic approach could be used to target many of the genetic defects underlying retinitis pigmentosa. “Given the lack of effective therapies for retinal degeneration, particularly the lack of therapies applicable to a broad range of different genetic varieties of this disease, this study represents a very exciting and important advance in our field,” Joseph Corbo, a neuropathologist at the Washington University School of Medicine in St. Louis who was not involved in the work, wrote in an email to The Scientist. This combination of “CRISPR technology with an adeno-associated virus vector, a system tried and true for delivering genetic information to the retina, may represent the first step in a global treatment approach for rod-mediated degenerative disease,” Shannon Boye, whose University of Florida lab develops gene replacement strategies for eye disorders, wrote in an email to The Scientist. © 1986-2017 The Scientist
Link ID: 23364 - Posted: 03.16.2017
By Andy Coghlan A woman in her 80s has become the first person to be successfully treated with induced pluripotent stem (iPS) cells. A slither of laboratory-made retinal cells has protected her eyesight, fighting her age-related macular degeneration – a common form of progressive blindness. Such stem cells can be coaxed to form many other types of cell. Unlike other types of stem cell, such as those found in an embryo, induced pluripotent ones can be made from adult non-stem cells – a discovery that earned a Nobel prize in 2012. Now, more than a decade after they were created, these stem cells have helped someone. Masayo Takahashi at the RIKEN Laboratory for Retinal Regeneration in Kobe, Japan, and her team took skin cells from the woman and turned them into iPS cells. They then encouraged these to form retinal pigment epithelial cells, which are important for supporting and nourishing the retina cells that capture light for vision. The researchers made a slither of cells measuring just 1 by 3 millimetres. Before transplanting this into the woman’s eye in 2014, they first removed diseased tissue on her retina that was gradually destroying her sight. They then inserted the small patch of cells they had created, hoping they would become a part of her eye and stop her eyesight from degenerating. © Copyright Reed Business Information Ltd.
By STEPH YIN Despite being just the size of a rice grain, robber flies, which live all over the world, are champion predators. In field experiments, they can detect targets the size of sand grains from nearly two feet away — 100 times the fly’s body length — and intercept them in under half a second. What’s more, they never miss their mark. A team led by scientists at the University of Cambridge has started to unveil the secrets to the robber fly’s prowess. In a study published Thursday in Current Biology, the team outlined the mechanics of the fly’s pursuit, from its impressive eye anatomy to how it makes a successful catch every time. Notably, the researchers observed a behavior never before described in a flying animal: About 30 centimeters from its prey, the insect slows, turns slightly and brings itself in for a close catch. “This ‘lock-on’ phase and change in behavior during a flight is quite remarkable,” said Sam Fabian, a graduate student at Cambridge and an author of the study. “We would actually expect them to do something very simple — just accelerate and hit the target.” The scientists surveyed robber flies in the field using a “fly teaser,” which consisted of beads on a rapidly moving fishing line controlled by a motor. As the flies charged at the bait, the researchers captured their movements using high-speed cameras. At the start of the robber fly’s conquest, it sits on a perch and scans the sky for passing prey. When it glimpses a potential meal, it takes flight, maintaining a steady angle between itself and its target. This proactive strategy, using a “constant bearing angle,” is also employed by fish, bats and sailors, Mr. Fabian said. © 2017 The New York Times Company
Link ID: 23346 - Posted: 03.11.2017
By JESS BIDGOOD SALEM, Mass. — A few years ago, Bevil Conway, then a neuroscientist at Wellesley College, got an interesting request: Could he give a lecture to the curators and other staff at the Peabody Essex Museum, the art and culture museum here? So Mr. Conway gathered his slides and started from the beginning, teaching the basics of neuroscience — “How neurons work, how neurons talk to each other, issues of evolutionary biology,” Mr. Conway said — to people who run an institution best known for its venerable collections of maritime and Asian art. It was an early step in what has become a galvanizing mission for the museum’s director, Dan L. Monroe: harnessing the lessons of brain science to make the museum more engaging as attendance is falling around the country. “If one’s committed to creating more meaningful and impactful art experiences, it seems a good idea to have a better idea about how our brains work,” he said. “That was the original line of thinking that started us down this path.” The museum, known as P.E.M., has been looking at neuroscience to incorporate its lessons into exhibitions ever since. In an effort to build shows that engage the brain, it has tried breaking up exhibition spaces into smaller pieces; posting questions and quotes on the wall, instead of relying only on explanatory wall text; and experimenting with elements like smell and sound in visual exhibitions. And those efforts are about to increase. The museum recently received a $130,000 grant from the Barr Foundation, a Boston-based philanthropic organization, to bring a neuroscience researcher on staff, add three neuroscientists to the museum as advisers and publish a guide that will help other museums incorporate neuroscience into their exhibition planning. “A lot of what we’re seeing in museums right now is the interpretation of pieces, or artwork,” said E. San San Wong, a senior program officer with the foundation. “What this is looking at is: How do we more actively engage people with art, in multiple senses?” © 2017 The New York Times Company
Researchers at Vanderbilt University in Nashville, Tennessee, have discovered that in zebrafish, decreased levels of the neurotransmitter gamma-aminobutyric acid (GABA) cue the retina, the light-sensing tissue in the back of the eye, to produce stem cells. The finding sheds light on how the zebrafish regenerates its retina after injury and informs efforts to restore vision in people who are blind. The research was funded by the National Eye Institute (NEI) and appears online today in Stem Cell Reports. NEI is part of the National Institutes of Health. “This work opens up new ideas for therapies for blinding diseases and has implications for the broader field of regenerative medicine,” said Tom Greenwell, Ph.D., NEI program officer for retinal neuroscience. For years, vision scientists have studied zebrafish to understand their retinal regenerative capacity. Zebrafish easily recover from retinal injuries that would permanently blind a person. Early studies in zebrafish led to the idea that dying retinal cells release signals that trigger support cells in the retinal called Muller glia to dedifferentiate — return to a stem-like state — and proliferate. However, recent studies in the mouse brain and pancreas suggest GABA, a well-characterized neurotransmitter, might also play an important role in regeneration distinct from its role in communicating local signals from one neuron to the next. Scientists studying a part of the brain called the hippocampus found that GABA levels regulate the activity of neural stem cells. When GABA levels are high, the stem cells stay quiet, and if GABA levels decrease, then the stem cells start to divide, explained James Patton, Ph.D., Stevenson Professor of Biological Sciences at Vanderbilt and senior author of the new study in zebrafish retina. A similar phenomenon was reported in mouse pancreas.
By JANE E. BRODY In letters to The Times, blind readers reacted with heartfelt reassurance and practical guidance to Edward Hoagland’s essay, “Feeling My Way Into Blindness,” published in November. Stanley F. Wainapel, clinical director of physical medicine and rehabilitation at Montefiore Medical Center in the Bronx, admitted that “adapting to vision loss is a major challenge.” But he disputed Mr. Hoagland’s allusion to “enforced passivity,” pointing out that many advances in technology — from screen-reading software for computers to portable devices that read menus or printed letters “with a delay of only seconds” — can keep productivity, creativity and pleasure very much alive for people who can no longer see. Rabbi Michael Levy, president of Yad HaChazakah, the Jewish Disability Empowerment Center, also acknowledged that “transition to a world without sight is far from easy.” But he insisted, “Blindness does not cut me off from the world.” He cited skillful use of a cane, travel devices that tell him where he is and what is around him and periodicals available in real time by telephone among myriad other gadgets that “see” for him. Annika Ariel, a blind student double-majoring in English and political science at Amherst College, wrote that her problems are not with her blindness but rather from people’s attitudes that depict the blind as helpless and dependent. She said she travels independently, uses assistive technologies to complete her work as efficiently as others who can see, and excels academically and socially. Equally inspiring was the response of Mark Riccobono, president of the National Federation of the Blind, who became legally blind at age 5 and lost all useful vision to glaucoma at 14. © 2017 The New York Times Company
Link ID: 23284 - Posted: 02.27.2017
By JANE E. BRODY “Feeling My Way Into Blindness,” an essay published in The New York Times in November by Edward Hoagland, an 84-year-old nature and travel writer and novelist, expressed common fears about the effects of vision loss on quality of life. Mr. Hoagland, who became blind about four years ago, projected deep-seated sadness in describing the challenges he faces of pouring coffee, not missing the toilet, locating a phone number, finding the food on his plate, and knowing to whom he is speaking, not to mention shopping and traveling, when he often must depend on the kindness of strangers. And, of course, he sorely misses nature’s inspiring vistas and inhabitants that fueled his writing, though he can still hear birds chatter in the trees, leaves rustle in the wind and waves crash on the shore. Mr. Hoagland is hardly alone in his distress. According to Action for Blind People, a British support organization, those who have lost some or all sight “struggle with a range of emotions — from shock, anger, sadness and frustration to depression and grief.” When eyesight fails, some people become socially disengaged, leading to isolation and loneliness. Anxiety about a host of issues — falls, medication errors, loss of employment, social blunders — is common. A recent study from researchers at the Wilmer Eye Institute at Johns Hopkins University School of Medicine found that most Americans regard loss of eyesight as the worst ailment that could happen to them, surpassing such conditions as loss of limb, memory, hearing or speech, or having H.I.V./AIDS. Indeed, low vision ranks behind arthritis and heart disease as the third most common chronic cause of impaired functioning in people over 70, Dr. Eric A. Rosenberg of Weill Cornell Medical College and Laura C. Sperazza, a New York optometrist, wrote in American Family Physician. © 2017 The New York Times Company
By Michael Price BOSTON--Among mammals, primates are unique in that certain species have three different types of light-sensitive cone cells in their eyes rather than two. This allows humans and their close relatives to see what we think of as the standard spectrum of color. (Humans with red-green color blindness, of course, see a different spectrum.) The standard explanation for why primates developed trichromacy, as this kind of vision is called, is that it allowed our early ancestors to see colorful ripe fruit more easily against a background of mostly green forest. A particular Old World monkey, the rhesus macaque (pictured), has a genetic distinction that offers a convenient natural test of this hypothesis: a common genetic variation makes some females have three types of cone cells and others have two. Studies with captive macaques has shown that trichromatic females are faster than their dichromatic peers at finding fruit, but attempts to see whether that’s true for wild monkeys has been complicated by the fact that macaques are hard to find, and age and rank also play big roles in determining who eats when. A vision researcher reported today at the annual meeting of AAAS, which publishes Science, that after making more than 20,000 individual observations of 80 different macaques feeding from 30 species of trees on Cayo Santiago, Puerto Rico, she can say with confidence that wild trichromatic female monkeys do indeed appear to locate and eat fruit more quickly than dichromatic ones, lending strong support to the idea that this advantage helped drive the evolution of trichromacy in humans and our relatives. © 2017 American Association for the Advancement of Science.
By LISA SANDERS, M.D. The 3-year-old girl was having a very bad day — a bad week, really. She’d been angry and irritable, screaming and kicking at her mother over nothing. Her mother was embarrassed by this unusual behavior, because her husband’s sister, Amber Bard, was visiting. Bard, a third-year medical student at Michigan State, was staying in the guest room while working with a local medical practice in Grand Rapids so that she could spend a little time with her niece. The behavior was strange, but the mother was more concerned about her child’s left eye. A few days earlier it was red and bloodshot. It no longer was, but now the girl had little bumps near the eye. The mother asked Bard whether she could look at the eye. “I’m a third-year medical student,” Bard told her. “I know approximately nothing.” But Bard was happy to try. She turned to the girl, who immediately averted her face. “Can you show me your eye?” she asked. The girl shouted: “No! No, no, no!” Eventually Bard was able to coax her into allowing her a quick look at the eye. She saw a couple of tiny pimples along the lower lid, near the lashes, and a couple more just next to the eye. The eye itself wasn’t red; the lid wasn’t swollen. She couldn’t see any discharge. Once the child was in bed, Bard opened her laptop and turned to a database she’d been using for the past week when she started to see patients. Called VisualDx, it’s one of a dozen or so programs known as decision-support software, designed to help doctors make a diagnosis. This one focuses mostly on skin findings.
Link ID: 23242 - Posted: 02.17.2017
By Amitha Kalaichandran, When pain researcher Diane Gromala recounts how she started in the field of virtual reality, she seems reflective. She had been researching virtual reality for pain since the early 1990s, but her shift to focusing on how virtual reality could be used for chronic pain management began in 1999, when her own chronic pain became worse. Prior to that, her focus was on VR as entertainment. Gromala, 56, was diagnosed with chronic pain in 1984, but the left-sided pain that extended from her lower stomach to her left leg worsened over the next 15 years. "Taking care of my chronic pain became a full-time job. So at some point I had to make a choice — either stop working or charge full force ahead by making it a motivation for my research. You can guess what I chose," she said. Diane Gromala Pain researcher Diane Gromala found that taking care of her own chronic pain became 'a full-time job.' (Pain studies lab at Simon Fraser University) Now she's finding that immersive VR technology may offer another option for chronic pain, which affects at least one in five Canadians, according to a 2011 University of Alberta study. "We know that there is some evidence supporting immersive VR for acute pain, so it's reasonable to look into how it could help patients that suffer from chronic pain." Gromala has a PhD in human computer interaction and holds the Canada Research Chair in Computational Technologies for Transforming Pain. She also directs the pain studies lab and the Chronic Pain Research Institute at Simon Fraser University in Burnaby, B.C. ©2017 CBC/Radio-Canada.
By Sam Wong Here’s looking at you, squid. Cock-eyed squid have one huge, bulging eye and another normal-sized eye, but the reason has remained a mystery. Now we have an answer. Kate Thomas of Duke University in North Carolina studied 161 videos of the creatures collected over 26 years by remotely operated submarines in Monterey Bay, California. The findings provide the first behavioural evidence that the two eyes are adapted to look in different directions. The large one points upwards to spot prey silhouetted against the sky. The smaller one points downwards to spot bioluminescent organisms against the darkness below. The squid, from the histioteuthid family, live at depths of 200 to 1000 metres, where little light penetrates. The videos show that the squid normally swims with its tail end pointing upwards, but tilted so the large eye is consistently oriented towards the sky. Based on measurements of the eyes and the light levels they would be exposed to, Thomas and her colleagues calculated that having a big upward-pointing eye greatly improves visual perception, while a downward-pointing eye would gain little from being large. “That gives you the context for how this trait might have evolved,” says Thomas. Some of the squid’s prey, such as lanternfish and shrimp, have luminescent undersides so they are camouflaged against the sunlight when seen from below. Yellow pigmentation in the lens of the squid’s large eye may help it distinguish between sunlight and bioluminescence. © Copyright Reed Business Information Ltd.
Noah Charney The Chinese government just arrested a group of people associated with a sham tourist attraction that had lured hundreds of sight-seers to a fake Terracotta Warriors exhibit, comprised entirely of modern replicas. Sotheby’s recently hired Jamie Martin of Orion Analytical, a forensic specialist at testing art, who then discovered that a Parmigianino painting recently sold is actually a modern forgery (Sotheby’s returned the buyer’s money and then sued the person for whom they sold it). And the Ringling Museum in Sarasota, Florida, is hoping that a painting of Philip IV of Spain in their collection will be definitively determined to be by Velazquez, and not a copy in the style of Velazquez. And that’s just in the last week or so. Art forgery and authenticity seems to be in the news just about every week (to my publicist’s delight). But I’m on a bit of a brainstorm. After my interview with Nobel Prize winner Dr. Eric Kandel on the neuroscience behind how we humans understand art, I’ve developed a keen interest in art and the mind. I tackled selfies, self-portraits and facial recognition recently, as well as what happens when the brain fails to function properly and neglects to recognize the value of art. Since my last book was a history of forgery, it was perhaps inevitable that I would wonder about the neurology of the recognition of originals versus copies. But while I looked into forgery from a wide variety of angles for the book, neuroscience was not one of them. © 2017 Salon Media Group, Inc.
by Laura Sanders Most nights I read a book in bed to wind down. But when I run out of my library supply, I read articles on my phone instead. I suspect that this digital substitution messes with my sleep. That’s not good for me — but it’s probably worse for the many children who have screens in their rooms at night. A team of researchers recently combed through the literature looking for associations between mobile devices in the bedroom and poor sleep. Biostatistician Ben Carter of King’s College London and colleagues found that kids between ages 6 and 19 who used screen-based media around bedtime slept worse and were more tired in the day. That’s not surprising: Phones, tablets and laptops make noise and emit blue light that can interfere with the sleep-inducing melatonin. But things got interesting when the researchers compared kids who didn’t have screens in their bedrooms with kids who did have phones or tablets in their rooms but didn’t use them. You might think there wouldn’t be a sleep difference between those groups. None of these kids were up all night texting, gaming or swiping, so neither sounds nor blue light were messing with any of the kids’ sleep. Yet Carter and colleagues found a difference: Kids who had screen-based media in their bedroom, but didn’t use it, didn’t sleep as much as kids without the technology. What’s more, the sleep they did get was worse and they were more tired during the day, the researchers reported in the December JAMA Pediatrics. |© Society for Science & the Public 2000 - 2017
By GRETCHEN REYNOLDS Being nearsighted is far more common than it once was. The prevalence of myopia, the condition’s medical name, in Americans has soared by 66 percent since the early 1970s, according to a 2009 study by the National Eye Institute; in China and other East Asian countries, as many as 90 percent of recent high school graduates are thought to be nearsighted. Myopia results when eyeballs are longer than normal, changing the angle at which light enters the eye and therefore the ability to focus on distant objects. The disorder involves a complex interplay of genetics and environment and usually begins before adolescence, when the eye is growing, but it can worsen in early adulthood. Some experts connect the elevated rates of myopia to the many hours young people stare at computers and other screens. But a recent study published in JAMA Ophthalmology suggests that a greater factor may be a side effect of all that screen-watching — it’s keeping children inside. This new study joins a growing body of research indicating that a lack of direct sunlight may reshape the human eye and impair vision. Researchers at King’s College London, the London School of Hygiene and Tropical Medicine and other institutions gave vision exams to more than 3,100 older European men and women and interviewed them at length about their education, careers and how often they remembered being outside during various stages of their lives. This biographical information was then cross-referenced with historical data about sunlight, originally compiled for research on skin cancer and other conditions. © 2017 The New York Times Company
By Rachael Lallensack A video game is helping researchers learn more about how tiny European starlings keep predators at bay. Their massive flocks, consisting of hundreds to thousands of birds, fly together in a mesmerizing, pulsating pattern called a murmuration. For a long time, researchers have suspected that the bigger the flock, the harder it is for predators like falcons and hawks to take down any one member, something known as “confusion effect.” Now, researchers have analyzed that effect—in human hunters. Using the first 3D computer program to simulate a murmuration, scientists tested how well 25 players, acting as flying predators, could target and pursue virtual starlings, whose movements were simulated based on data from real starling flocks (see video above). The team’s findings reaffirmed the confusion effect: The larger the simulated flocks, the harder it was for the “predators” to single out and catch individual prey, the researchers report this week in Royal Society Open Science. So maybe sometimes, it’s not so bad to get lost in a crowd. © 2017 American Association for the Advancement of Science.
By Anna Azvolinsky Hummingbirds are efficient hoverers, suspending their bodies midair using rapid forward and backward strokes. Aside from their unique ability to hover, the tiny avians are also the only known birds that can fly in any direction, including sideways. Hummingbird brains appear to be adapted for this flying ability, researchers have now shown. According to a study published today (January 5) in Current Biology, a highly conserved area of the brain—the lentiformis mesencephali (LM), which receives panoramic visual motion information directly from the retina—processes the movement of objects from all directions. In contrast, the LMs of other bird species and all other four-limbed vertebrates studied to date predominantly sense back-to-front motion. While the authors had predicted the neurons of this hummingbird brain region would be tuned to slow motion, they in fact found the opposite: LM neurons were sensitive to quick visual motion, most likely because hummingbirds must process and respond to their environments quickly to avoid collisions, both during hovering and in other modes of flight. “This ancient part of the brain the authors studied has one job: to detect the motion of the image in front of the eyes,” explained Michael Ibbotson, a neuroscientist at the University of Melbourne who penned an accompanying editorial but was not involved in the research. The results of this study suggest that “hummingbirds evolved this area of the brain to have fine motor control to be able to hover and push in every direction possible,” Ibbotson said. © 1986-2017 The Scientist
Link ID: 23064 - Posted: 01.07.2017
By Susana Martinez-Conde Our perceptual and cognitive systems like to keep things simple. We describe the line drawings below as a circle and a square, even though their imagined contours consist—in reality—of discontinuous line segments. The Gestalt psychologists of the 19th and early 20th century branded this perceptual legerdemain as the Principle of Closure, by which we tend to recognize shapes and concepts as complete, even in the face of fragmentary information. Now at the end of the year, it is tempting to seek a cognitive kind of closure: we want to close the lid on 2016, wrap it with a bow and start a fresh new year from a blank slate. Of course, it’s just an illusion, the Principle of Closure in one of its many incarnations. The end of the year is just as arbitrary as the end of the month, or the end of the week, or any other date we choose to highlight in the earth’s recurrent journey around the sun. But it feels quite different. That’s why we have lists of New Year’s resolutions, or why we start new diets or exercise regimes on Mondays rather than Thursdays. Researchers have also found that, even though we measure time in a continuous scale, we assign special meaning to idiosyncratic milestones such as entering a new decade. What should we do about our brain’s oversimplification tendencies concerning the New Year—if anything? One strategy would be to fight our feelings of closure and rebirth as we (in truth) seamlessly move from the last day of 2016 to the first day of 2017. But that approach is likely to fail. Try as we might, the Principle of Closure is just too ingrained in our perceptual and cognitive systems. In fact, if you already have the feeling that the beginning of the year is somewhat special (hey, it only happens once a year!), you might as well decide that resistance is futile, and not just embrace the illusion, but do your best to channel it. © 2017 Scientific American
By Stephen L. Macknik Masashi Atarashi, a physics high school teacher from Japan, submitted this wonderful winter illusion to the 2015 Best Illusion of the Year Contest, where it competed as a finalist. Atarashi discovered this effect serendipitously, while watching the snow fall through the venetian window blinds of his school’s faculty lounge—just like his students must sometimes do in the classroom during a lecture! Notice that as the blinds occupy more area on the screen, the speed of the snowfall seems to accelerate. A great illusion to ponder during our white holiday season. Nobody knows how Atarashi’s effect works, but our working hypothesis is that each time the snow disappears behind a blind, or reappears below it, it triggers transient increases in the activity of your visual system’s motion-sensitive neurons. Such transient surges in neural activity are perhaps misinterpreted by your brain as faster motion speed. © 2016 Scientific American,
Link ID: 23022 - Posted: 12.27.2016