Chapter 10. Vision: From Eye to Brain

Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.


Links 1 - 20 of 1261

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.

Keyword: Vision; Prions
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

Keyword: Vision; Stem Cells
Link ID: 26045 - Posted: 03.18.2019

Liam Drew A mouse scurries down a hallway, past walls lined with shifting monochrome stripes and checks. But the hallway isn’t real. It’s part of a simulation that the mouse is driving as it runs on a foam wheel, mounted inside a domed projection screen. While the mouse explores its virtual world, neuroscientist Aman Saleem watches its brain cells at work. Light striking the mouse’s retinas triggers electrical pulses that travel to neurons in its primary visual cortex, where Saleem has implanted electrodes. Textbooks say that these neurons each respond to a specific stimulus, such as a horizontal or vertical line, so that identical patterns of inputs should induce an identical response. But that’s not what happens. When the mouse encounters a repeat of an earlier scene, its neurons fire in a different pattern. “Five years ago, if you’d told me that, I’d have been like, ‘No, that’s not true. That’s not possible’,” says Saleem, in whose laboratory at University College London we are standing. His results, published last September1, show that cells in the hippocampus that track where the mouse has run along the hallway are somehow changing how cells in the visual cortex fire. In other words, the mouse’s neural representation of two identical scenes differs, depending on where it perceives itself to be. It’s no surprise that an animal’s experiences change how it sees the world: all brains learn from experience and combine multiple streams of information to construct perceptions of reality. But researchers once thought that at least some areas in the brain — those that are the first to process inputs from the sense organs — create relatively faithful representations of the outside world. According to this model, these representations then travel to ‘association’ areas, where they combine with memories and expectations to produce perceptions.

Keyword: Learning & Memory; Vision
Link ID: 26039 - Posted: 03.15.2019

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.

Keyword: Vision
Link ID: 25999 - Posted: 03.01.2019

By Tom Avril Smoking cigarettes has long been known for its ability to damage eyesight, on top of the harm it causes to the lungs, heart and other organs. But a new study suggests that smoking can impair vision far earlier than is commonly thought. Heavy smokers with an average age of 35 were markedly worse than nonsmokers at distinguishing colors as well as the contrast between different shades of gray, the study authors said. Previous research has linked smoking with macular degeneration and cataracts, which tend to occur decades later. The new results, published in Psychiatry Research, do not indicate how smoking damages perception of color and contrast. But the broad nature of the impairment suggests that it is not the result of damage to specific kinds of light-sensitive cells, such as rods or cones, said co-author Steven Silverstein, a professor of psychiatry and ophthalmology at Rutgers Robert Wood Johnson Medical School. Instead, cigarette use probably harms a more general aspect of vision biology, such as blood vessels or nerve cells. “There is probably some more widespread problem like overall blood flow in the eye that is compromised due to all the toxic chemicals in cigarettes,” said Silverstein, who collaborated with authors from the Perception, Neuroscience and Behavior Laboratory in Joao Pessoa, Brazil. © 1996-2019 The Washington Post

Keyword: Drug Abuse; Vision
Link ID: 25985 - Posted: 02.26.2019

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

Keyword: Vision; Evolution
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.

Keyword: Vision
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

Keyword: Vision
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.

Keyword: Vision
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.

Keyword: Vision
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

Keyword: Vision
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.

Keyword: Vision
Link ID: 25723 - Posted: 11.27.2018

National Institutes of Health scientists and their colleagues have found evidence of the infectious agent of sporadic Creutzfeldt-Jakob disease (CJD) in the eyes of deceased CJD patients. The finding suggests that the eye may be a source for early CJD diagnosis and raises questions about the safety of routine eye exams and corneal transplants. Sporadic CJD, a fatal neurodegenerative prion disease of humans, is untreatable and difficult to diagnose. Prion diseases originate when normally harmless prion protein molecules become abnormal and gather in clusters and filaments in the body and brain. Scientists hope that early diagnosis of prion and related diseases—such as Alzheimer’s, Parkinson’s and dementia with Lewy bodies—could lead to effective treatments that slow or prevent these diseases. Scientists from NIH’s National Institute of Allergy and Infectious Diseases (NIAID) collaborated on the research with colleagues from the University of California at San Diego and UC-San Francisco. About 40 percent of sporadic CJD patients develop eye problems that could lead to an eye exam, meaning the potential exists for the contamination of eye exam equipment designed for repeat use. Further, cadaveric corneal transplants from undiagnosed CJD patients have led to two probable and three possible cases of disease transmission, the researchers say. Previous studies have shown that the eyes of CJD patients contain infectious prions, though the distribution of prions among the various components of the eye was not known. To address this question, the scientists recruited 11 CJD patients who agreed to donate their eyes upon death. The researchers found evidence of prion infection throughout the eyes of all 11 deceased patients using real time quaking-induced conversion (RT-QuIC), a highly sensitive test NIAID scientists developed that detects prion seeding activity in a sample as evidence of infection.

Keyword: Prions; Vision
Link ID: 25706 - Posted: 11.21.2018

By Michael Price Patient BAA, who is 35, lost her sight when she was 27. She can still detect light and dark, but for all intents and purposes, she is blind. Now, she—and other formerly sighted people—may one day regain a limited form of vision using electrodes implanted in the brain. In a new study, such electrodes caused parts of BAA’s and other people’s visual cortexes to light up in specific patterns, allowing them to see shapes of letters in their mind’s eyes. The work is a step forward in a field that emerged more than 40 years ago but has made relatively little progress. The findings suggest technical ways to stimulate images in the brain “are now within reach,” says Pieter Roelfsema, a neuroscientist who directs the Netherlands Institute for Neuroscience in Amsterdam and wasn’t involved in the work. Research to electrically spur blind people’s brains to see shapes began in the 1970s, when biomedical researcher William Dobelle, then at The University of Utah in Salt Lake City, first implanted electrodes in the brain to stimulate the visual cortex. Typically, the rods and cones in retinas translate light waves into neural impulses that travel to the brain. Specialized layers of cells there, known as the visual cortex, process that information for the rest of the brain to use. Dobelle’s implants took advantage of a phenomenon known as retinal mapping. The visual field—the plane of space you see when you look out into the world—roughly maps onto a segment of the visual cortex. By electrically stimulating parts of this brain map, Dobelle could cause flashes of light called phosphenes to appear in the minds of people who were blind, but who had experienced at least a few years of vision. By stimulating different electrodes, he could get phosphenes to flash in different parts of a person’s visual field. © 2018 American Association for the Advancement of Science

Keyword: Vision; Robotics
Link ID: 25697 - Posted: 11.17.2018

Nicola Davis Children should be encouraged to spend time outdoors to reduce their risk of becoming shortsighted, experts have said. Shortsightedness is rising around the world, with the condition said to have reached epidemic proportions in east Asia: estimates suggest about 90% of teenagers and young adults in China have the condition. While genetics are thought to play a large role in who ends up shortsighted – a condition that is down to having an overly long eyeball – research also suggests environmental factors are important. Several studies have found children who spend more time outdoors have a lower risk of myopia. While some report that looking into the distance could be important, others say exposure to outdoor light is key. Experts say they have found new factors, and confirmed others, which could affect a child’s risk of becoming shortsighted. These include playing computer games, being born in the summer and having a more highly educated mother. “There is not much you can do about when your child is born … but periods indoors doing indoor activities does increase your risk of myopia,” said Katie Williams, an author of the study by King’s College London. “A healthy balance of time outdoors and a balance during early education is important.” Writing in the British Journal of Ophthalmology, Williams and her colleagues report how they used data from the twins early development study, which followed children born in England and Wales between 1994 and 1996. The project tracked their development, behaviour and education through questionnaires and tests, and studied their genetics. © 2018 Guardian News and Media Limited

Keyword: Vision; Development of the Brain
Link ID: 25653 - Posted: 11.07.2018

By James Gorman If you love spiders, you will really love jumping spiders. (If you hate spiders, try reading this article on dandelions.) O.K., if you’re still here, jumping spiders are predators that stalk their prey and leap on them, like a cat. They are smart, agile and have terrific eyesight. It has been clear for a long time that their vision is critical to the way they hunt, and to the accuracy of their leaps. But a lot has remained unknown about the way their eyes work together. To find out more, Elizabeth Jakob, a spider biologist at the University of Massachusetts, led a team of researchers from the United States, Kenya and New Zealand in an investigation of spider vision. The first step was getting a custom-built spider eye tracker, similar to ones used on humans, to follow a spider’s gaze. Actually, Dr. Jakob had two made, probably the only two in the world. She has one and her colleagues in New Zealand have the other. Jumping spiders have eight eyes. Two big eyes, right in the center of what you might call the spider’s forehead, are the principal ones, and they pick up detail and color. Of the other three pairs, a rear set looks backward, a middle set is as yet a bit of a mystery, and the foremost detect motion. The lenses of the main eyes are attached by flexible tubes to retinas. A camera was set up to look down those tubes and see the activity of the retinas, which look a bit like boomerangs. The inside of the spider’s head was lit by ultraviolet light, which penetrates the outer carapace. But as accurate as the main eyes are, they only see what is in front of them. If they had to find prey, it would be like using a narrow flashlight beam to explore a dark room. Not very efficient. The researchers found that the front pair of secondary eyes, the motion detectors, tell the main pair of eyes where to look. When they were painted over temporarily and the spider was presented with moving images, it had no idea where to look. © 2018 The New York Times Company

Keyword: Vision; Evolution
Link ID: 25648 - Posted: 11.06.2018

Amanda B. Keener If Leonardo da Vinci had a good eye doctor, he might not have become such a great artist. At least that’s what an analysis of paintings and sculptures believed to be modeled after da Vinci suggests. Visual neuroscientist Christopher Tyler of the City University of London examined six pieces of art, including Salvator Mundi and Vitruvian Man. Five of the pieces depict an eye misalignment consistent with a disorder called exotropia that can interfere with three-dimensional vision, Tyler reports online October 18 in JAMA Ophthalmology. Exotropia, in which one eye turns slightly outward, is one of several eye disorders collectively called strabismus. Today, strabismus, which affects 4 percent of people in the United States, is treated with special glasses, eye patches or surgery. Tyler calculated the differences in eye alignment using the same sorts of measurements that an optometrist does when tailoring a pair of glasses. Most of the portraits showed the eyes misaligned, but Vitruvian Man by da Vinci himself did not. As a result, da Vinci may have had intermittent exotropia, present only some of the time and perhaps controllable, Tyler suspects. “The person [with intermittent exotropia] can align their eyes and see in 3-D, but if they’re inattentive or tired, the eye may droop,” he says. If da Vinci could control his exotropia, Tyler speculates that it would have been an artistic advantage. “The artist’s job is to paint on a 2-D surface,” he says. “This can be difficult when you view the world three-dimensionally.” Both eyes need to focus on the same subject for 3-D vision. Many artists shut one eye when viewing their subjects to more easily translate details into two dimensions. But with intermittent exotropia, da Vinci could have switched from 3-D to 2-D and back again with ease. |© Society for Science & the Public 2000 - 201

Keyword: Vision
Link ID: 25596 - Posted: 10.22.2018

Sara Reardon Cuttlefish are masters at altering their appearance to blend into their surroundings. But the cephalopods can no longer hide their inner thoughts, thanks to a technique that infers a cuttlefish’s brain activity by tracking the ever-changing patterns on its skin. The findings, published in Nature on 17 October1, could help researchers to better understand how the brain controls behaviour. The cuttlefish (Sepia officinalis) camouflages itself by contracting the muscles around tiny, coloured skin cells called chromatophores. The cells come in several colours and act as pixels across the cuttlefish’s body, changing their size to alter the pattern on the animal’s skin. The cuttlefish doesn’t always conjure up an exact match for its background. It can also blanket itself in stripes, rings, mottles or other complex patterns to make itself less noticeable to predators. “On any background, especially a coral reef, it can’t look like a thousand things,” says Roger Hanlon, a cephalopod biologist at the Marine Biological Laboratory in Chicago, Illinois. “Camouflage is about deceiving the visual system.” To better understand how cuttlefish create these patterns across their bodies, neuroscientist Gilles Laurent at the Max Planck Institute for Brain Research in Frankfurt, Germany, and his collaborators built a system of 20 video cameras to film cuttlefish at 60 frames per second as they swam around their enclosures. The cameras captured the cuttlefish changing colour as they passed by backgrounds such as gravel or printed images that the researchers placed in the tanks. © 2018 Springer Nature Limited.

Keyword: Vision; Brain imaging
Link ID: 25589 - Posted: 10.18.2018

By Carolyn Y. Johnson Kiara Eldred sometimes compares her nine-month-long scientific experiments, growing tiny human retinas in a laboratory dish, to raising children. Eldred, a graduate student at Johns Hopkins University, starts by growing thousands of stem cells and feeding them nutrients and chemicals that will steer them to develop into the retina, the part of the eye that translates light into the signals that lead to vision. After two weeks of painstaking cultivation, those cells typically generate 20 to 60 tiny balls of cells, called retinal organoids. As they mature, these nascent retinas get dirty and slough off lots of cells, so they also need to be washed off when they’re fed every other day — at least for the first month and a half. After nine months of assiduous care, Eldred has a batch of miniature human retinas that respond to light, are about two millimeters in diameter and are shaped like a tennis ball cut in half. But growing the organoids is only the first step. In a new study in the journal Science, Eldred and colleagues described using this system to understand a fundamental question about vision that has remained surprisingly mysterious: How does color vision develop? © 1996-2018 The Washington Post

Keyword: Vision; Development of the Brain
Link ID: 25565 - Posted: 10.12.2018

Doris Tsao is a neuroscientist who uses brain imaging technology, electrical recording techniques, and mathematical modeling. Though Tsao has explored several aspects of visual processing, such as the perception of depth and color, her most notable line of research has focused on uncovering the fundamental neural principles that underlie one of the brain’s most highly specialized and socially important tasks: recognizing a face. Prior neuroscientific research has identified regions in the inferior temporal cortex of monkeys that are particularly responsive to faces. These earlier studies, however, shed little light on how face-responsive cells within these regions might be organized and integrated into a system. Early in her career, Tsao confirmed with functional magnetic resonance imaging (fMRI) that the visual cortex of the macaque monkey shows face-selective activation in six small “patches” in each hemisphere of the brain. She then used data from fMRI brain scans as a map to guide the placement of single-neuron, electrical recording probes, which demonstrated that certain neurons display highly attuned sensitivity to faces, but not to other categories of objects, and that different patches across the brain’s cortex are integrated in a network dedicated to the visual processing of faces. Through other elegantly designed experiments, Tsao showed that the sensitivity of specific neurons can be further analyzed by measuring their responses to cartoon representations of faces with subtle variations in features and that certain features, such as facial shape and inter-eye distance, elicit particularly frequent and robust responses. © 2018 John D. and Catherine T. MacArthur Foundation

Keyword: Vision
Link ID: 25532 - Posted: 10.05.2018