Chapter 10. Vision: From Eye to Brain
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by Douglas Heaven Blind people could soon be able to read street signs using an implant that translates the alphabet into Braille and beams an image of the Braille directly to visual neurons at the back of the eye. The implant is a modified version of a class of devices called retinal prostheses, which are used to restore partial sight to people with retinitis pigmentosa. A degenerative eye disease that kills the photoreceptor cells in the retina, RP tends to affect people in early adulthood and can lead to blindness, but leaves intact the neurons that carry visual signals to the brain. Prostheses such as the Argus II, manufactured by Second Sight in Sylmar, California, convert video from a camera mounted on a pair of glasses into electronic signals "displayed" on a 10-by-6 grid of electrodes implanted over a person's retina. This gives users a pixellated view of the world, allowing them to distinguish light and dark regions and even detect features such as doorways. But deciphering letters and words with the prosthesis is slow because of its low resolution. To make this more practical, Thomas Lauritzen of Second Sight and colleagues have come up with a modified version of the Argus II that presents the user with Braille. Since Braille represents letters and numbers as dots in a 3-by-2 grid, it can be displayed using the electrode array of existing Argus implants. The modified implant was tried out on a Braille-reading volunteer who already uses the Argus II. Tested on single letters and words of up to four letters, transmitted in Braille to the retinal implant, he correctly identified the letters 89 per cent of the time and words 60 to 80 per cent of the time. © Copyright Reed Business Information Ltd.
By Alyssa A. Botelho When Jerry Berrier dreams, he hears and touches and smells and talks, but he doesn’t see. Blind since birth, he rarely remembers his dreams, however, because his sleep has been so poor. At 15, Berrier had both of his eyes removed and lost the little light perception he had as a child. Ever since, the Everett resident, now 60, has battled a vicious sleep cycle — a few days of sleep followed by weeks of hardly any. The bouts of sleeplessness come suddenly and subside without warning. When they hit, Berrier can’t sleep more than a couple hours a night, no matter how tired he is. Though physicians haven’t given him a formal diagnosis, scientists believe he suffers from a rare condition called non-24 sleep-wake disorder, or “non-24.” The chronic condition is characterized by a body clock that is out of synch with the 24-hour cycle of the Earth day. Non-24 can affect those with normal vision, but it especially plagues the totally blind who can’t perceive light, the strongest external signal that keeps the brain’s sleep-wake cycle aligned to the pattern of night and day. Of approximately 100,000 totally blind people in the United States, anywhere from 55 percent to 70 percent of them may suffer from non-24, according to Harvard neuroscientist Steven Lockley, one of the lead researchers in an ongoing clinical trial investigating sleep disorders in the blind. With 25 sites around the country, it’s the largest study of non-24 to date. Berrier is a participant in Boston. The toll of having an internal clock in competition with the 24-hour world can be high, adding another layer of challenge to life without sight. © 2012 NY Times Co.
David Cyranoski In December 2010, Robin Ali became suddenly excited by the usually mundane task of reviewing a scientific paper. “I was running around my room, waving the manuscript,” he recalls. The paper described how a clump of embryonic stem cells had grown into a rounded goblet of retinal tissue. The structure, called an optic cup, forms the back of the eye in a growing embryo. But this one was in a dish, and videos accompanying the paper showed the structure slowly sprouting and blossoming. For Ali, an ophthalmologist at University College London who has devoted two decades to repairing vision, the implications were immediate. “It was clear to me it was a landmark paper,” he says. “He has transformed the field.” 'He' is Yoshiki Sasai, a stem-cell biologist at the RIKEN Center for Developmental Biology in Kobe, Japan. Sasai has impressed many researchers with his green-fingered talent for coaxing neural stem cells to grow into elaborate structures. As well as the optic cup1, he has cultivated the delicate tissue layers of the cerebral cortex2 and a rudimentary, hormone-making pituitary gland3. He is now well on the way to growing a cerebellum4 — the brain structure that coordinates movement and balance. “These papers make for the most addictive series of stem-cell papers in recent years,” says Luc Leyns, a stem-cell scientist at the Free University of Brussels. Sasai's work is more than tissue engineering: it tackles questions that have puzzled developmental biologists for decades. How do the proliferating stem cells of an embryo organize themselves seamlessly into the complex structures of the body and brain? And is tissue formation driven by a genetic program intrinsic to cells, or shaped by external cues from neighbouring tissues? © 2012 Nature Publishing Group
By Ben Thomas In the early 1990s, a team of neuroscientists at the University of Parma made a surprising discovery: Certain groups of neurons in the brains of macaque monkeys fired not only when a monkey performed an action – grabbing an apple out of a box, for instance – but also when the monkey watched someone else performing that action; and even when the monkey heard someone performing the action in another room. In short, even though these “mirror neurons” were part of the brain’s motor system, they seemed to be correlated not with specific movements, but with specific goals. Over the next few decades, this “action understanding” theory of mirror neurons blossomed into a wide range of promising speculations. Since most of us think of goals as more abstract than movements, mirror neurons confront us with the distinct possibility that those everyday categories may be missing crucial pieces of the puzzle – thus, some scientists propose that mirror neurons might be involved in feelings of empathy, while others think these cells may play central roles in human abilities like speech. Some doctors even say they’ve discovered new treatments for mental disorders by reexamining diseases through the mirror neuron lens. For instance, UCLA’s Marco Iacoboni and others have put forth what Iacoboni called the “broken mirror hypothesis” of autism – the idea that malfunctioning mirror neurons are likely responsible for the lack of empathy and theory of mind found in severely autistic people. © 2012 Scientific American,
by Rachel Nuwer The dungeon is pitch black—until the dungeon master blazes a torch, confirming your worst fears. A Beholder monster lurches at you, its eyeballs wriggling on tentacular stems. As you prepare to wield your Vorpal sword, where do you focus your gaze: at the monster's head or at its tentacle eyes? Such a quandary from the role-playing game Dungeons & Dragons may seem like a meaningless trifle, but it holds within it the answer to a scientific question. In fact, a father-son team has used images of such monsters to show that most people will look to another creature's eyes, no matter where they are located on the body. "Dungeons & Dragons monsters have eyes all over the place," says Julian Levy, a ninth grader at Lord Byng Secondary School in Vancouver, Canada. Two years ago, Levy's knowledge of the role-playing game led him to a unique solution for solving a basic scientific question: Do people focus their gaze on another person's eyes or on the center of the head, where the eyes just happen to be located? "We were eating dinner and my dad was talking about how, after publishing a paper about gaze tracking, a reviewer said that you could never prove whether people are looking at the eyes or the center of the face," Levy recalls. So he piped up with an idea, offering Dungeons & Dragons characters as an experimental solution. Because many characters have eyes located on their hands, torso, or other areas of the body, a researcher could track viewers' gazes to see what part of the characters they focus on first. © 2010 American Association for the Advancement of Science.
Link ID: 17439 - Posted: 10.31.2012
By Katherine Harmon With a juicy insect dinner perched on a leaf above the water, what is a hungry little archer fish down below to do? Knock it down with a super-powered, super-precise jet of water that packs six times the power the fish could generate with its own muscles, according to new findings published online October 24 in PLoS ONE. The stunning spitting power of the amazing archer fish (Toxotes jaculatrix) was first described in the 18th century. The creature lives in mostly in mangrove forests and estuaries where insects are prevalent—above water, that is. And these tasty treats are not easily knocked off of the plants that hang over the archer fish’s territory. The insects, such as grasshoppers, can hang on with a force some 10 times their own body weight. So the archer fish has developed an impressive strategy for fetching food that not many other fish can reach. Its water jet can target and dislodge a single insect so that it falls into the water for the fish to eat. Just how the fish manages to do this—and in less than a second—had remained a mystery. Many scientists figured that the source must be a special organ in the fish’s body. “The origin of the effectiveness of the jet squirted by the archer fish has been searched for inside of the fish for nearly 250 years,” Alberto Vailati, a physicist at the University of Milan and co-author of the new paper, said in a prepared statement. © 2012 Scientific American
by Clare Wilson Why does making direct eye contact with someone give you that feeling of a special connection? Perhaps because it excites newly discovered "eye cells" in the amygdala, the part of the brain that processes emotions and social interactions. This new type of neuron was discovered in a Rhesus macaque. If humans have these neurons too, it may be that they are impaired in disorders such as autism and schizophrenia, which affect eye contact and social interactions. Katalin Gothard, a neurophysiologist at the University of Arizona in Tucson, and her team placed seven electrodes in the amygdala of a Rhesus macaque. The electrodes, each one-tenth the thickness of a human hair, allowed them to record activity in individual neurons as the macaque watched a video featuring another macaque. All the while, the team also tracked the macaque's gaze. Out of the 151 neurons the researchers could distinguish, 23 fired only when the macaque was looking at the eyes of the monkey in the video. Of these neurons, which the team call "eye cells", four fired more when the monkey in the video appeared to be gazing back at the laboratory macaque, as if the two animals were making eye contact. "These are cells that have been tuned by evolution to look at the eye, and they extract information about who you are, and most importantly, are you making eye contact with me," says Gothard. Other eye cells fired depending on whether the monkey in the video was behaving in a friendly, aggressive or neutral manner, but not in response to eye contact. © Copyright Reed Business Information Ltd.
Link ID: 17377 - Posted: 10.17.2012
by Douglas Heaven I spy, with my mechanical eye. It seems a simple mechanical change plays a role in sensory perception in fruit flies, and possibly in many other animals, including humans. The eyes of the common fruit fly (Drosophila melanogaster) contain clusters of light-sensitive cells organised into rods. When light strikes one of these cells, it triggers a series of chemical reactions. These cause a protein called a transient receptor potential (TRP) ion channel to open. When it's open, the TRP allows charged particles to flow into the cell, causing the cell to send a signal to the fly's brain. TRP channels play a part in sensory perception in many animals, from nematodes to humans. But nobody knew how the chemical signals make the TRP channel open. Shrinking rods "Everyone's been looking for years and years at the chemical messengers," says Roger Hardie of the University of Cambridge, UK. A mechanical trigger was never considered. "No one thought to look," he says. With Kristian Franze, Hardie found that the chemical signals change the surface area of the cell's outer membrane by destroying some of its constituent molecules. When several cells shrink like this, the entire rod contracts by up to 400 nanometres, a margin big enough to be seen with a microscope. "The whole membrane shrinks," says Hardie. "It's like a little muscle twitching." © Copyright Reed Business Information Ltd.
Link ID: 17365 - Posted: 10.13.2012
by Robert F. Service According to George Bernard Shaw: "The most intolerable pain is produced by prolonging the keenest pleasure." Not to be picky George, but actually both sensations result from the activity of a diverse family of proteins on the surface of cells. This year's Nobel Prize in chemistry was awarded to two Americans—Robert Lefkowitz of Duke University in Durham, North Carolina, and Brian Kobilka of Stanford University School of Medicine in Palo Alto, California—who revealed the inner workings of these proteins, which also orchestrate a variety of things such as the way we see, smell, taste, feel, and fight infections. The notion that a single family of proteins was responsible for so many different physiological processes was far from evident early on. One hint came at the end of the 19th century, when scientists studying the effects of the hormone adrenaline discovered that it had different effects in various parts of the body. It made heart rate and blood pressure increase, but it decreased digestive activity and caused pupils to relax. One idea was that proteins called receptors on different cells somehow captured adrenaline molecules and either ferried the hormone into cells or transferred a message inside to trigger a response. In the 1940s, an American biologist named Raymond Ahlquist made enough progress to conclude that there must be two types of adrenaline receptors, one that caused smooth muscle cells to contract, and the other that stimulated the heart. © 2010 American Association for the Advancement of Science
Sandrine Ceurstemont, editor, New Scientist TV Think an object can't be in two places at once? This animation shows how the perceived location of a dot is influenced by what's happening around it. In this video, a flashing dot is surrounded by two diamonds that shift across the screen. When they move horizontally, the dot seems to shift sideways and slightly upwards. In a second version, in which the corners of the diamonds are obscured, the dot appears to move diagonally. In fact, the dot never changes place. The illusion is the work of Peter Kohler from Dartmouth College in Hanover, New Hampshire, and his team. Kohler has been trying to determine if the dot's perceived shift in position is caused by the overall motion of the diamonds or that of its components. For example, although the shapes as a whole are moving sideways, viewing the edges in isolation shows that segments of the diamonds are moving upwards. "Our results show that global motion does influence the shift," he says. "But the fact that even the unoccluded diamond does not yield a purely horizontal shift indicates that local signals are also very important." The team now plans to investigate how quickly our brain perceives the shift. "Integration of local and global motion is known to take about 150 milliseconds," says Kohler. "It would be interesting to see if the effect takes a similar amount of time to kick in." By presenting the illusion for very short amounts of time, the researchers will be able to determine if different versions are initially perceived in the same way. "We also have fMRI work under way to identify brain areas that represent the perceived shifted location rather than the actual location," says Kohler. The illusion was recently presented at the European Conference on Visual Perception in Alghero, Italy. © Copyright Reed Business Information Ltd.
Link ID: 17312 - Posted: 09.29.2012
By Mary Bates It's an oft-repeated idea that blind people can compensate for their lack of sight with enhanced hearing or other abilities. The musical talents of Stevie Wonder and Ray Charles, both blinded at an early age, are cited as examples of blindness conferring an advantage in other areas. Then there's the superhero Daredevil, who is blind but uses his heightened remaining senses to fight crime. It is commonly assumed that the improvement in the remaining senses is a result of learned behavior; in the absence of vision, blind people pay attention to auditory cues and learn how to use them more efficiently. But there is mounting evidence that people missing one sense don't just learn to use the others better. The brain adapts to the loss by giving itself a makeover. If one sense is lost, the areas of the brain normally devoted to handling that sensory information do not go unused — they get rewired and put to work processing other senses. A new study provides evidence of this rewiring in the brains of deaf people. The study, published in The Journal of Neuroscience, shows people who are born deaf use areas of the brain typically devoted to processing sound to instead process touch and vision. Perhaps more interestingly, the researchers found this neural reorganization affects how deaf individuals perceive sensory stimuli, making them susceptible to a perceptual illusion that hearing people do not experience. These new findings are part of the growing research on neuroplasticity, the ability of our brains to change with experience. A large body of evidence shows when the brain is deprived of input in one sensory modality, it is capable of reorganizing itself to support and augment other senses, a phenomenon known as cross-modal neuroplasticity. © 2012 Scientific American
Sandrine Ceurstemont, editor, New Scientist TV It's not yet possible to make Silvio Berlusconi disappear, but now a new illusion can shrink his head. Created by Tim Meese and colleagues at Aston University in Birmingham, UK, the animation tricks our brain with moving circles of different sizes before presenting the mind-altering images of his face. To perceive the effect, fix your eyes on the cross in the center of the video. Once the motion stops and the head pictures are flashed on-screen, the image on the left should appear smaller than the one on the right. If you pause the video, you'll notice that in fact both heads are the same size. According to Daniel Baker, a member of the team, the trick occurs because our brain adapts to the size of the moving circles, tiring out the mechanisms that respond to those sizes. So after viewing the large circle on the left, the head presented in its place looks smaller and vice versa. The same type of effect can also alter an object's orientation after staring at tilted patterns. The team was surprised to find that the illusion takes place with any image, regardless of the pattern it's filled in with. "It's rare for an effect to be so general," says Baker. "You could adapt to pictures of kittens and it would still work." © Copyright Reed Business Information Ltd.
Link ID: 17260 - Posted: 09.15.2012
by Sara Reardon You can run from a crow that you've wronged, but you can't hide. Wild crows remember human faces in the same way that mammals do. Crows can distinguish human faces and remember how different people treated them, says John Marzluff of the University of Washington in Seattle. To work out how the crows process this information, Marzluff had members of his team wear a latex mask as they captured 12 wild American crows (Corvus brachyrhynchos). The crows learned to associate the captor's mask with this traumatic experience. While in captivity, the crows were fed and looked after by people wearing a different mask. After four weeks, the researchers imaged the birds' brains while they were looking at either the captor or feeder mask. The brain patterns looked similar to those seen in mammals: the feeder sparked activity in areas involved in motivation and reward, whereas the captor stimulated regions associated with fear. The result makes sense, says Kevin McGowan of Cornell Lab of Ornithology in Ithaca, New York. Crows don't mind if humans are in their habitat – but they need to keep a close eye on what we do. Journal reference: Proceedings of the National Academy of Sciences, DOI: 10.1073/pnas.1206109109 © Copyright Reed Business Information Ltd.
By Susana Martinez-Conde and Stephen L. Macknik “There are things in that [wall]paper that nobody knows but me, or ever will. Behind that outside pattern the dim shapes get clearer every day. It is always the same shape, only very numerous. And it is like a woman stooping down and creeping about behind that pattern.” —Charlotte Perkins Gilman, “The Yellow Wallpaper,” 1892 The protagonist in Charlotte Perkins Gilman's short story “The Yellow Wallpaper” suffers from the most notable case of pareidolia in fiction. Pareidolia, the misperception of an accidental or vague stimulus as distinct and meaningful, explains many supposedly paranormal and mystical phenomena, including UFO and Bigfoot sightings and other visions. In Gilman's story, the heroine, secluded in her hideously wallpapered bedroom and having nothing with which to occupy herself, is driven to insanity>—full-blown paranoid schizophrenia>—by the woman behind the yellow pattern. As she descends into madness, she comes to believe that she is imprisoned by the wallpaper. Mental disease can aggravate pareidolia, as can fatigue and sleepiness. After a recent surgery, one of us (Martinez-Conde) noticed faces everywhere, in places as unlikely as the ultrasound images of her left arm during an examination of potential postsurgical blood clots. She realized at once that the ubiquitous faces were the product of lack of sleep and the high titer of pain medication in her bloodstream, so she was more fascinated than concerned. Her doctor agreed but made a note in her file for a different drug regime in the future. Just in case. Luckily, the hospital room's walls were bare, and there was no yellow wallpaper in sight. Our brain is wired to find meaning. Our aptitude to identify structure and order around us, combined with our superior talent for face detection, can lead to spectacular cases of pareidolia, with significant effects in society and in culture. © 2012 Scientific American
Link ID: 17241 - Posted: 09.11.2012
Sandrine Ceurstemont, editor, New Scientist TV Impossible objects, like those drawn by artist M. C. Escher, don't seem like they could exist in the real world. But Kokichi Sugihara from Meiji University in Kawasaki, Japan, is well known for building 3D versions of these structures. Now a new video shows his latest construction: a gravity-defying roof that seems to attract and balance balls on its edge. When the house is rotated, its true form is revealed. According to Sugihara, this type of ambiguous shape is interesting because we perceive the illusion again even after we have seen what the object really looks like. After studying a variety of these objects, he concludes that our brain seems to choose the most rectangular configuration when it tries to make sense of features that can have different interpretations. The brain trick was presented this week at the European Conference on Visual Perception in Alghero, Italy. If you would like to build your own impossible objects, check out printable copies of Sugihara's designs. © Copyright Reed Business Information Ltd.
Link ID: 17234 - Posted: 09.10.2012
By CLAUDIA DREIFUS The developmental psychologist Daphne Maurer made headlines this year with research suggesting that people born with cataracts could improve their eyesight by playing Medal of Honor, the “first-person shooter” video game. But her fame goes far beyond the video screen. Dr. Maurer, 56, director of the Visual Development Lab at McMaster University in Ontario, is an author, with her husband, Charles, of the pioneering 1988 book “The World of the Newborn,” an inventory of what babies sense and experience. In recent years she has been directing a study tracking infants born with visual impairments into later life. This longitudinal study is her attempt to learn how early sensory deprivation affects vision over a lifetime. We spoke in person earlier this year and again by telephone last month. An edited and condensed version of the two conversations follows. How did computer games enter your life? Are you a gamer? No, not at all. I’m a reader. My husband and I don’t have children. So computer games wouldn’t be a part of our lives. I’ve never played one. I can’t imagine enjoying playing one. For more than 25 years, I’ve been an investigator on a longitudinal study following the visual development of infants born with cataracts in their eyes. These youngsters went through a period of temporary visual deprivation. They didn’t get any of that early patterning in the world that regularly sighted infants get. As soon as possible, they received surgeries and corrective contact lenses at Toronto’s Hospital for Sick Children, after which their vision improved. © 2012 The New York Times Company
by Gilead Amit The bath of cells in avian eyes could prolong a delicate quantum state that helps to explain how some birds navigate using Earth's magnetic field. It is thought that light reacts with receptors in the birds' eyes to produce two molecules with unpaired electrons, whose spins are linked by a special state called quantum entanglement. If the relative alignment of the spins is affected by Earth's magnetic field, the electron pair can cause chemical changes that the bird can sense. In 2009, researchers at the University of Oxford calculated that such entanglement must last for at least 100 microseconds for the internal compass to work. But how the sensitive state of quantum entanglement could survive that long in the eye was a mystery. Calculations by Zachary Walters of the Max Planck Institute for the Physics of Complex Systems in Dresden, Germany, now show that interactions with cells in the bird's eye allow the electron pairs to stay entangled for longer through a dampening effect. Rather like the way a car with stiff shock absorbers takes longer to stop bouncing after going over a bump, the signal from the electron pair dies away more slowly under strong interactions with the cellular bath. Predicting exactly how long entanglement is sustained won't be possible until the mechanism is better understood, says Walters. But he believes there's a good chance his model could account for the 100 microseconds. © Copyright Reed Business Information Ltd
Link ID: 17190 - Posted: 08.22.2012
Analysis by Jesse Emspak A glass inspired by spider's webs is being used to keep birds from smacking into windows. Birds can't see glass well, and so many of them die when they hit picture windows. Humans can't see glass well either, which might explain why some people try to walk through glass doors. But most people know that the refection of the sky and landscape in a window isn't real -- unfortunately, birds don't. According to the Fatal Light Awareness Program, a building with glass walls or windows can kill up to 10 birds per day, and estimates of worldwide deaths from such collisions reach hundreds of millions of birds each year. On Lindisfarne Island, off the northeastern coast of England, local authorities wanted to do something about it. Hundreds of species of migratory birds pass through every year. So officials decided to cover a lookout tower with glass designed by Arnold Glas, a German company. Called Ornilux, the glass has a spiderweb-like pattern that humans can't see unless they stand very close (see image below, right). But because glass reflects ultraviolet light, birds can see the pattern very well. Spider webs, particularly those of orb weaver spiders, work the same way, reflecting UV and alerting the bird that there is something there. While flying through a web wouldn't hurt a bird, the bird doesn't know that. So they avoid them. The glass was tested in a flight tunnel in the United States. Birds were allowed to fly to one end of the tunnel which was covered with two types of glass, one with the UV-reflective coating. The birds avoided hitting the coated glass up to 68 percent of the time. © 2012 Discovery Communications, LLC.
Link ID: 17166 - Posted: 08.15.2012
By Susan Milius COLLEGE PARK, Md. — A mantis shrimp, which has one of the most elaborate visual systems ever discovered, turns out to be pretty lousy at distinguishing one color from another. The puzzling underachievement may mean that the mantis shrimp brain perceives color in a way new to science, says Hanne Thoen of the University of Queensland in Brisbane, Australia. She presented results from her ongoing study August 6 at the 10th International Congress of Neuroethology. The stalked eyes of mantis shrimp species that live in shallow water can have up to 16 kinds of photoreceptor cells, 12 of which are specialized for different colors. People make do with four kinds, three of which pick up colors. Yet tests with pairs of increasingly similar colors found that the mantis shrimp Haptosquilla trispinosa flunks out when choices narrow to colors 15 nanometers apart in wavelength, Thoen said. At sweet spots in the color spectrum, people can distinguish between colors only 1 or 2 nanometers apart. “Hanne’s results are a bit of a shock to us,” says Thomas Cronin of the University of Maryland, Baltimore County, whose lab also studies mantis shrimp vision. Thoen tested the color vision of mantis shrimp by training them to scoot out of their burrows toward a pair of optical fibers and punch at the one glowing a particular color. As she narrowed the color gap between the two fibers, she could tell when the animals no longer discerned a difference. © Society for Science & the Public 2000 - 2012
Prosthetic retina helps to restore sight in mice Geoff Brumfiel Two neuroscientists have created a prosthesis that can partially restore the sight to blind mice. The device could eventually be developed for use in humans. More than 20 million people worldwide become blind owing to the degeneration of their retina, the thin tissue at the back of the eye that turns light into a neural signal. Only one prosthesis has been approved for treatment of the condition — it consists of an array of surgically implanted electrodes that directly stimulate the optic nerve and allow patients to discern edges and letters. Patients cannot, however, recognize faces or perform many everyday tasks. Sheila Nirenberg, a physiologist at the Weill Medical College at Cornell University in New York thinks that the problem is at least partially down to coding. Even though the retina is as thin as tissue paper, it contains several layers of nerves that seem to encode light into neural signals. "The thing is, nobody knew the code," she says. Without it, Nirenberg believes that visual prostheses will never be able to create images that the brain can easily recognize. Now, she and her student, Chethan Pandarinath, have come up with a code and developed a device that uses it to restore some sight in blind mice. The duo began by injecting nerve cells in the retinas of their mice with a genetically engineered virus. The virus had been designed to insert a gene that causes the cells to produce a light-sensitive protein normally found in algae. When a beam of light was then shown into the eye, the protein triggered the nerve cells to send a signal to the brain, performing a similar function to healthy rod and cone cells. © 2012 Nature Publishing Group