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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

Laura Sanders Some nerve cells in the brain are multitaskers, responding to both color and shape, a survey of over 4,000 neurons in the visual systems of macaque monkeys finds. The finding, described in the June 28 Science, counters earlier ideas that vision cells nestled in the back of the brain each handle information about only one aspect of sight: an object’s color or its orientation, an element of shape. Some scientists had thought that those aspects were then put together by other brain cells in later stages of visual processing to form a more complete picture of the world. In the new experiment, four macaques looked at a series of sights made of moving lines on a screen. Each time, the lines were one of 12 possible colors and moved at particular angles, creating an effect similar to a spinning candy cane in two dimensions. Using genetic tricks that made nerve cells glow when active, the researchers watched for action among the monkeys’ cells in an area of the brain that handles vision. Called V1, this stretch at the back of the brain is one of the first areas to interpret sight signals. Most of the cells that had a favorite color, indicated by their activity, also had a favorite orientation of lines, the researchers found. “Thus, textbook models of primate V1 must be updated,” the team writes. PUTTING IT TOGETHER This video captures nerve cells in a monkey’s visual system firing off signals. Some of these cells respond both to a favorite color and favorite shape. The discovery counters previous ideas that information about color is processed separately from information about shape in the brain. |© 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: 26374 - Posted: 07.02.2019

By Tim Vernimmen The image above, “A Sunday Afternoon on the Island of La Grande Jatte,” was painted in 1884 by French artist Georges Seurat. The black lines crisscrossing it are not the work of a toddler wreaking havoc with a permanent marker, but that of neuroscientist Robert Wurtz of the National Eye Institute in the US. Ten years ago, he asked a colleague to look at the painting while wearing a contact lens–like contraption that recorded the colleague’s eye movements. These were then translated into the graffiti you see here. Art lovers may cringe, yet it is likely that Seurat would have been intrigued by this augmentation of his work. The movement Seurat kick-started with this painting — Neo-Impressionism — drew inspiration from the scientific study of how our vision works. Particularly influential was the pioneering research of Hermann von Helmholtz, a German physician, physicist and philosopher and author of a seminal 1867 book, Handbook of Physiological Optics, on the way we perceive depth, color and motion. One of the questions that occupied Helmholtz, and quite possibly Seurat, is why we don’t perceive the constant eye movements we make when we are scanning our surroundings (or a painted representation of them). Consider that the lines above were drawn in just three minutes. If we saw all those movements as we made them, our view of the world would be a blur of constant motion. As Wurtz and his Italian colleagues Paola Binda and Maria Concetta Morrone explain in two articles in the Annual Review of Vision Science, there’s a lot we know about why that doesn’t happen — and more yet to learn.

Related chapters from BN8e: Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 7: Vision: From Eye to Brain
Link ID: 26341 - Posted: 06.20.2019

By Madison Dapcevich An optical illusion designed by researchers to test how contrast deceives the brain appears to show a diamond moving across the screen, twitching up and down and left to right, without ever physically changing location. Dubbed the “Perceptual Diamond”, the illusion “produces motion continuously and unambiguously” to trick the viewer into thinking it is moving around the screen, yet it remains steady and slightly illuminated. Rather, its motion is mimicked by changing the contrast between the edges of strips around the diamond’s edges and the background. Shifts in contrasts around the edges, like in this illusion, can create the perception of motion. The Perpetual Diamond illusion provides no clues as to its orientation or direction until it is animated, generating movement through contrast signals alone, wrote the authors in i-Perception. "We often take the perception of motion for granted because we assume that motion corresponds to objects shifting location in the real world," explained study author Arthur Shapiro, from the American University in Washington DC, in an email to IFLScience. "However, the brain has many processes that can lead to the perception of motion, and there are many types of images that can stimulate these processes." Depending on the combination of illuminated edges, the diamond will appear to move in different directions. For example, if the two top edges blink between black and white and the two bottom edges do the opposite, the diamond appears to continuously move upward.

Related chapters from BN8e: Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 7: Vision: From Eye to Brain
Link ID: 26337 - Posted: 06.19.2019

By Elizabeth Pennisi When the ancestors of cave fish and certain crickets moved into pitchblack caverns, their eyes virtually disappeared over generations. But fish that ply the sea at depths greater than sunlight can penetrate have developed super-vision, highly attuned to the faint glow and twinkle given off by other creatures. They owe this power, evolutionary biologists have learned, to an extraordinary increase in the number of genes for rod opsins, retinal proteins that detect dim light. Those extra genes have diversified to produce proteins capable of capturing every possible photon at multiple wavelengths—which could mean that despite the darkness, the fish roaming the deep ocean actually see in color. The finding "really shakes up the dogma of deep-sea vision," says Megan Porter, an evolutionary biologist studying vision at the University of Hawaii in Honolulu who was not involved in the work. Researchers had observed that the deeper a fish lives, the simpler its visual system is, a trend they assumed would continue to the bottom. "That [the deepest dwellers] have all these opsins means there's a lot more complexity in the interplay between light and evolution in the deep sea than we realized," Porter says. At a depth of 1000 meters, the last glimmer of sunlight is gone. But over the past 15 years, researchers have realized that the depths are pervaded by a faint bioluminescence from flashing shrimp, octopus, bacteria, and even fish. Most vertebrate eyes could barely detect this subtle shimmer. To learn how fish can see it, a team led by evolutionary biologist Walter Salzburger from the University of Basel in Switzerland studied deep-sea fishes' opsin proteins. Variation in the opsins' amino acid sequences changes the wavelength of light detected, so multiple opsins make color vision possible. One opsin, RH1, works well in low light. Found in the eye's rod cells, it enables humans to see in the dark—but only in black and white. © 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: 26224 - Posted: 05.10.2019

Maria Temming New artwork created by artificial intelligence does weird things to the primate brain. When shown to macaques, AI-generated images purposefully caused nerve cells in the monkeys’ brains to fire more than pictures of real-world objects. The AI could also design patterns that activated specific neurons while suppressing others, researchers report in the May 3 Science. This unprecedented control over neural activity using images may lead to new kinds of neuroscience experiments or treatments for mental disorders. The AI’s ability to play the primate brain like a fiddle also offers insight into how closely AIs can emulate brain function. The AI responsible for the new mind-bending images is an artificial neural network — a computer model composed of virtual neurons — modeled after the ventral stream. This is a neural pathway in the brain involved in vision (SN Online: 8/12/09). The AI learned to “see” by studying a library of about 1.3 million labeled images. Researchers then instructed the AI to design pictures that would affect specific ventral stream neurons in the brain. Viewing any image triggers some kind of neural activity in a brain. But neuroscientist Kohitij Kar of MIT and colleagues wanted to see whether the AI’s deliberately designed images could induce specific neural responses of the team’s choosing. The researchers showed these images to three macaques fitted with neuron-monitoring microelectrodes. |© 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: 26206 - Posted: 05.03.2019

Ruth Williams Showing monkeys a series of computer-generated images and simultaneously recording the animals’ brain cell activities enables deep machine learning systems to generate new images that ramp up the cells’ excitation, according to two papers published today (May 2) in Cell and Science. “It’s exciting because it’s bridging the fields of deep learning and neuroscience . . . to try and understand what is represented in different parts of the brain,” says neuroscientist Andreas Tolias of Baylor College of Medicine who was not involved with either of the studies, but has carried out similar experiments in mice. “I think these methods and their further development could provide a more systematic way for us to open the black box of the brain,” he says. It’s a goal of sensory neuroscience to understand exactly which stimuli activate which brain cells. In the primate visual system, certain neurons in the visual cortex and inferior temporal cortex (two key vision areas) are known to respond preferentially to certain stimuli—such as colors, specific directions of motion, curves, and even faces. But, says neuroscientist Carlos Ponce of Washington University School of Medicine in St. Louis, who co-authored the Cell paper, “the problem is, we’ve never quite known whether, in our selection of pictures, we have the secret true image that the cell really is encoding.” Maybe, he suggests, a cell isn’t responding to a face, but to an arrangement of features and shapes found in a face that may also be found in other images. And with countless available images, “it’s impossible to test all of them,” he says. In short, it has been impossible to determine the exact visual stimulus that would maximally activate a given neuron. © 1986–2019 The Scientist.

Related chapters from BN8e: Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 7: Vision: From Eye to Brain
Link ID: 26205 - Posted: 05.03.2019

By Susana Martinez-Conde Human night vision is not as precise as day vision. That’s why getting up barefoot in the middle of the night comes with a much higher risk of stepping on painful Lego pieces than walking along the same path during the day. I have three kids of ages twelve and under, so I know. But the specific ways in which our night vision is worse than our day vision are surprisingly counterintuitive to most of us. I remember learning in college that night-vision is achromatic (meaning that we only see in grayscale at night) and not really believing it. It took some careful night-time observation to conclude that my professor was right: objects that were colorful during the day had no hue at night. Most shocking of all was the realization that, though I had always suffered from night-time color blindness (as all of us do), I had never been aware of my deficiency. A recent study by Alejandro Gloriani and Alexander Schütz, from the University of Marburg, Germany, published earlier this month in Current Biology, shows that our night vision self-delusion is even more pervasive than previously thought. Advertisement To appreciate Gloriani and Schütz’s discovery, the first thing to understand is that day and night vision rely on the activity of different types of photoreceptors (these are the retinal cells that convert light energy into electrical signals, which your brain can then process). ‘Cones’ are active during the day (or when you turn the lights on at night). ‘Rods’ are active during the night (or at very dim light levels). © 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: 26181 - Posted: 04.29.2019

National Institutes of Health scientists studying the progression of inherited and infectious eye diseases that can cause blindness have found that microglia, a type of nervous system cell suspected to cause retinal damage, surprisingly had no damaging role during prion disease in mice. In contrast, the study findings indicated that microglia might delay disease progression. The discovery could apply to studies of inherited photoreceptor degeneration diseases in people, known as retinitis pigmentosa. In retinitis pigmentosa cases, scientists find an influx of microglia near the photoreceptors, which led to the belief that microglia contribute to retina damage. These inherited diseases appear to damage the retina similarly to prion diseases. Prion diseases are slow degenerative diseases of the central nervous system that occur in people and various other mammals. No vaccines or treatments are available, and the diseases are almost always fatal. Prion diseases primarily involve the brain but also can affect the retina and other tissues. Expanding on work published in 2018, scientists at NIH’s National Institute of Allergy and Infectious Diseases (NIAID) used an experimental drug to eliminate microglia in prion-infected mice. They studied prion disease progression in the retina to see if they could discover additional details that might be obscured in the more complex structure of the brain. When the scientists examined their prion-infected study mice, they found that photoreceptor damage still occurred – even somewhat faster – despite the absence of microglia. They also observed early signs of new prion disease in the photoreceptor cells, which may provide clues as to how prions damage photoreceptors. Their work appears in Acta Neuropathologica Communications.

Related chapters from BN8e: Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 7: Vision: From Eye to Brain
Link ID: 26088 - Posted: 03.28.2019

David Cyranoski A Japanese committee has provisionally approved the use of reprogrammed stem cells to treat diseased or damaged corneas. Researchers are now waiting for final approval from the health ministry to test the treatment in people with corneal blindness, which affects millions of people around the world. The cornea, a transparent layer that covers and protects the eye, contains stem cells that repair it when damaged. But these can be destroyed by disease or by trauma from chemicals or burns, which can result in patients losing their vision. Currently, cornea transplants from donors who have died are used to treat damaged or diseased corneas, but good-quality tissue is scarce. A team led by ophthalmologist Kohji Nishida at Osaka University plans to treat damaged corneas using sheets of tissue made from induced pluripotent stem cells. These are created by reprogramming cells from a donor into an embryonic-like state that can then transform into other tissue, such as corneal cells. Nishida’s team plans to lay 0.05-millimetre-thick sheets of corneal cells across patients’ eyes. Animal studies have shown1 that this can save or restore vision. The health ministry is expected to decide soon. If Nishida and his team receive approval, they will treat four people, whom they will then monitor for a year to check the safety and efficacy of the treatment. The first treatment is planned to take place before the end of July. Other Japanese researchers have carried out clinical studies using induced pluripotent stem 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: 26045 - Posted: 03.18.2019

Matthew Warren Cue the super-mouse. Scientists have engineered mice that can see infrared light normally invisible to mammals — including humans. To do so, they injected into the rodents’ eyes nanoparticles that convert infrared light into visible wavelengths1. Humans and mice, like other mammals, cannot see infrared light, which has wavelengths slightly longer than red light — between 700 nanometres and 1 millimetre. But Tian Xue, a neuroscientist at the University of Science and Technology of China in Hefei, and his colleagues developed nanoparticles that convert infrared wavelengths into visible light. The nanoparticles absorb photons at wavelengths of around 980 nanometres and emit them at shorter wavelengths, around 535 nanometres, corresponding to green light. Xue’s team attached the nanoparticles to proteins that bind to photoreceptors — the cells in the eye that convert light into electrical impulses — and then injected them into mice. The researchers showed that the nanoparticles successfully attached to the photoreceptors, which in turn responded to infrared light by producing electrical signals and activating the visual-processing areas of the brain. The team conducted experiments to show that the mice did actually detect and respond to infrared light.

Related chapters from BN8e: Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 7: Vision: From Eye to Brain
Link ID: 25999 - Posted: 03.01.2019

Nicola Davis The mystery of how the zebra got its stripes might have been solved: researchers say the pattern appears to confuse flies, discouraging them from touching down for a quick bite. The study, published in the journal Plos One, involved horses, zebras, and horses dressed as zebras. The team said the research not only supported previous work suggesting stripes might act as an insect deterrent, but helped unpick why, revealing the patterns only produced an effect when the flies got close. Dr Martin How, co-author of the research from the University of Bristol, said: “The flies seemed to be behaving relatively naturally around both [zebras and horses], until it comes to landing. “We saw that these horseflies were coming in quite fast and almost turning away or sometimes even colliding with the zebra, rather than doing a nice, controlled flight.” Researchers made their discovery by spending more than 16 hours standing in fields and noting how horseflies interacted with nine horses and three zebras – including one somewhat bemusingly called Spot. While horseflies circled or touched the animals at similar rates, landing was a different matter, with a lower rate seen for zebras than horses. To check the effect was not caused by a different smell of zebras and horses, for example, the researchers put black, white and zebra-striped coats on seven horses in turn. While there was no difference in the rate at which the flies landed on the horses’ exposed heads, they touched and landed on the zebra coat far less often than either the black or white garment. © 2019 Guardian News & Media Limited

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: 25977 - Posted: 02.21.2019

Fergus Walsh Medical correspondent A woman from Oxford has become the first person in the world to have gene therapy to try to halt the most common form of blindness in the Western world. Surgeons injected a synthetic gene into the back of Janet Osborne's eye in a bid to prevent more cells from dying. It is the first treatment to target the underlying genetic cause of age-related macular degeneration (AMD). About 600,000 people in the UK are affected by AMD, most of whom are severely sight impaired. Janet Osborne told BBC News: "I find it difficult to recognise faces with my left eye because my central vision is blurred - and if this treatment could stop that getting worse, it would be amazing." The treatment was carried out under local anaesthetic last month at Oxford Eye Hospital by Robert MacLaren, professor of ophthalmology at the University of Oxford. He told BBC News: "A genetic treatment administered early on to preserve vision in patients who would otherwise lose their sight would be a tremendous breakthrough in ophthalmology and certainly something I hope to see in the near future." Mrs Osborne, 80, is the first of 10 patients with AMD taking part in a trial of the gene therapy treatment, manufactured by Gyroscope Therapeutics, funded by Syncona, the Wellcome Trust founded investment firm. The macula is part of the retina and responsible for central vision and fine detail. In age-related macular degeneration, the retinal cells die and are not renewed. The risk of getting AMD increases with age. © 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: 25974 - Posted: 02.19.2019

By Zoe Dubno When I was 12, I became part of the very select group of people who have had a life-changing experience at a fondue restaurant. After repeatedly grabbing my brother’s green fondue fork and eating his steak from the broth pot, I found myself accused of elder-sibling entitlement. But my father, who is colorblind, said I had done nothing wrong; like me, he was unable to see any difference between my brother’s green fork and my orange one. The Ishihara color-vision test he administered on his computer later that night confirmed that I was among those few women with red-green colorblindness. He was excited that I saw “correctly” — which is to say, like him. Back then, the ability to understand his frame of reference was mostly limited to other people barred from becoming astronauts. Now there’s an app for it. Colorblindness can be sort of a fun affliction. Sometimes I see my own private colors, and objects lose their prescribed meanings. Someone’s fashionable, Instagram-friendly sand-colored apartment might become, just for me, a garish baby-food green. The English scientist John Dalton described something similar in “Extraordinary Facts Relating to the Vision of Colours” (1794), the first known scientific study of anomalous color vision: He would often earnestly ask people whether a flower was blue or pink “but was generally considered to be in jest.” I attended a liberal-arts college, so I know full well that philosophizing about the subjective experience of color is best done barefoot in a field while listening to Alice Coltrane music. Biologically, though, the mechanics are relatively straightforward. Humans are trichromats: We see color because three sets of cones inside the eye absorb light at different wavelengths, from red to blue. Colorblindness is, typically, a congenital weakness in one set or another. The cones in my eyes that are meant to detect long red wavelengths are abnormal; I may see red and orange, but they’re dim and green-tinted, their energy registering partly on the cones that detect medium-length green wavelengths. (For some colorblind people, the entire season of “autumn” must feel like an elaborate prank.) Those with no working cones in one group — dichromats — experience almost total blindness of that color. Red becomes black. Orange, now redless, becomes yellow. © 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: 25957 - Posted: 02.13.2019

Using a novel patient-specific stem cell-based therapy, researchers at the National Eye Institute (NEI) prevented blindness in animal models of geographic atrophy, the advanced "dry" form of age-related macular degeneration (AMD), which is a leading cause of vision loss among people age 65 and older. The protocols established by the animal study, published January 16 in Science Translational Medicine (STM), set the stage for a first-in-human clinical trial testing the therapy in people with geographic atrophy, for which there is currently no treatment. "If the clinical trial moves forward, it would be the first ever to test a stem cell-based therapy derived from induced pluripotent stem cells (iPSC) for treating a disease," said Kapil Bharti, Ph.D., a Stadtman Investigator and head of the NEI Unit on Ocular and Stem Cell Translational Research. Bharti was the lead investigator for the animal-model study published in STM. The NEI is part of the National Institutes of Health. The therapy involves taking a patient’s blood cells and, in a lab, converting them into iPS cells, which can become any type of cell in the body. The iPS cells are programmed to become retinal pigment epithelial cells, the type of cell that dies early in the geographic atrophy stage of macular degeneration. RPE cells nurture photoreceptors, the light-sensing cells in the retina. In geographic atrophy, once RPE cells die, photoreceptors eventually also die, resulting in blindness. The therapy is an attempt to shore up the health of remaining photoreceptors by replacing dying RPE with iPSC-derived RPE.

Related chapters from BN8e: Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 7: Vision: From Eye to Brain
Link ID: 25873 - Posted: 01.17.2019

Kohske Takahashi We report a novel illusion––curvature blindness illusion: a wavy line is perceived as a zigzag line. The following are required for this illusion to occur. First, the luminance contrast polarity of the wavy line against the background is reversed at the turning points. Second, the curvature of the wavy line is somewhat low; the right angle is too steep to be perceived as an illusion. This illusion implies that, in order to perceive a gentle curve, it is necessary to satisfy more conditions––constant contrast polarity––than perceiving an obtuse corner. It is notable that observers exactly “see” an illusory zigzag line against a physically wavy line, rather than have an impaired perception. We propose that the underlying mechanisms for the gentle curve perception and those of obtuse corner perception are competing with each other in an imbalanced way and the percepts of corner might be dominant in the visual system. Perception of contour and shape is one of basic functions of vision. To this end, visual system processes information in a hierarchical way; first it extracts local orientations, then it integrates the local orientations into intermediate representations of contour, and finally it forms global shape percepts (Loffler, 2008). The intermediate representation of contour would include concavity, convexity, corner angle, curvature, and so forth. Although it is obvious that the physical shape is determined by combination of the local orientations, perceptual shape is susceptible to several factors. Accordingly, as visual illusions demonstrate, percepts are not necessarily veridical. For example, the café wall illusion (Pierce, 1898) demonstrates that parallel horizontal lines are perceived as different angles to each other.

Related chapters from BN8e: Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 7: Vision: From Eye to Brain
Link ID: 25827 - Posted: 12.28.2018

By Nicole Wetsman If a sign tells you To follow the purple skull to your destination, the answer seems simple: Veer left. But isolate the stripes that make up the skulls, and you’ll find neither skull has purple bones; in fact, all the bones are the same color. Slot them back into the banded setting, and they shift to purple and orange. The pigments morph because of the ­Munker-​White illusion, which shifts the perception of two identical color tones when they’re placed against different surrounding hues. No one knows for sure, but the illusion probably results from what David Novick, a computer scientist at the University of Texas at El Paso, calls the color-completion effect. The phenomenon causes an image to skew toward the color of the objects that surround it. In a black-and-white image, a gray element would appear lighter when it’s striped with white, and darker when banded with black. Many neuroscientists think that neural ­signals in charge of relaying information about the pigments in our visual field get averaged—creating a color somewhere in the middle. Here, one skull is covered by blue stripes in the foreground and the other with yellow ones. When the original skulls take on the characteristics of the separate surroundings, they look like different colors entirely. Don’t be fooled: Follow both skulls by going straight. Copyright © 2018 Popular 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: 25806 - Posted: 12.21.2018

Scientists at the National Eye Institute (NEI) have found that neurons in the superior colliculus, an ancient midbrain structure found in all vertebrates, are key players in allowing us to detect visual objects and events. This structure doesn’t help us recognize what the specific object or event is; instead, it’s the part of the brain that decides something is there at all. By comparing brain activity recorded from the right and left superior colliculi at the same time, the researchers were able to predict whether an animal was seeing an event. The findings were published today in the journal Nature Neuroscience. NEI is part of the National Institutes of Health. Perceiving objects in our environment requires not just the eyes, but also the brain’s ability to filter information, classify it, and then understand or decide that an object is actually there. Each step is handled by different parts of the brain, from the eye’s light-sensing retina to the visual cortex and the superior colliculus. For events or objects that are difficult to see (a gray chair in a dark room, for example), small changes in the amount of visual information available and recorded in the brain can be the difference between tripping over the chair or successfully avoiding it. This new study shows that this process – deciding that an object is present or that an event has occurred in the visual field – is handled by the superior colliculus. “While we’ve known for a long time that the superior colliculus is involved in perception, we really wanted to know exactly how this part of the brain controls the perceptual choice, and find a way to describe that mechanism with a mathematical model,” said James Herman, Ph.D., lead author of the study.

Related chapters from BN8e: Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 7: Vision: From Eye to Brain
Link ID: 25723 - Posted: 11.27.2018