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Allison Whitten When our phones and computers run out of power, their glowing screens go dark and they die a sort of digital death. But switch them to low-power mode to conserve energy, and they cut expendable operations to keep basic processes humming along until their batteries can be recharged. Our energy-intensive brain needs to keep its lights on too. Brain cells depend primarily on steady deliveries of the sugar glucose, which they convert to adenosine triphosphate (ATP) to fuel their information processing. When we’re a little hungry, our brain usually doesn’t change its energy consumption much. But given that humans and other animals have historically faced the threat of long periods of starvation, sometimes seasonally, scientists have wondered whether brains might have their own kind of low-power mode for emergencies. Now, in a paper published in Neuron in January, neuroscientists in Nathalie Rochefort’s lab at the University of Edinburgh have revealed an energy-saving strategy in the visual systems of mice. They found that when mice were deprived of sufficient food for weeks at a time — long enough for them to lose 15%-20% of their typical healthy weight — neurons in the visual cortex reduced the amount of ATP used at their synapses by a sizable 29%. But the new mode of processing came with a cost to perception: It impaired how the mice saw details of the world. Because the neurons in low-power mode processed visual signals less precisely, the food-restricted mice performed worse on a challenging visual task. “What you’re getting in this low-power mode is more of a low-resolution image of the world,” said Zahid Padamsey, the first author of the new study. All Rights Reserved © 2022

Related chapters from BN: Chapter 10: Vision: From Eye to Brain; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 7: Vision: From Eye to Brain; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 28376 - Posted: 06.15.2022

Researchers from the National Eye Institute (NEI) have identified a new disease that affects the macula, a small part of the light-sensing retina needed for sharp, central vision. Scientists report their findings on the novel macular dystrophy, which is yet to be named, in JAMA Ophthalmology. NEI is part of the National Institutes of Health. Macular dystrophies are disorders that usually cause central visual loss because of mutations in several genes, including ABCA4, BEST1, PRPH2, and TIMP3. For example, patients with Sorsby Fundus Dystrophy, a genetic eye disease specifically linked to TIMP3 variants, usually develop symptoms in adulthood. They often have sudden changes in visual acuity due to choroidal neovascularization– new, abnormal blood vessels that grow under the retina, leaking fluid and affecting vision. TIMP3 is a protein that helps regulate retinal blood flow and is secreted from the retinal pigment epithelium (RPE), a layer of tissue that nourishes and supports the retina’s light-sensing photoreceptors. All TIMP3 gene mutations reported are in the mature protein after it has been “cut” from RPE cells in a process called cleavage. “We found it surprising that two patients had TIMP3 variants not in the mature protein, but in the short signal sequence the gene uses to ‘cut’ the protein from the cells. We showed these variants prevent cleavage, causing the protein to be stuck in the cell, likely leading to retinal pigment epithelium toxicity,” said Bin Guan, Ph.D., lead author. The research team followed these findings with clinical evaluations and genetic testing of family members to verify that the two new TIMP3 variants are connected to this atypical maculopathy.

Related chapters from BN: Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 7: Vision: From Eye to Brain
Link ID: 28364 - Posted: 06.11.2022

Smriti Mallapaty Live-cell imaging of the eye’s transparent cornea has revealed a surprising resident — specialized immune cells that circle the tissue, ready to attack pathogens. “We thought that the central cornea was devoid of any immune cells,” says Esen Akpek, a clinician-scientist who works on immunological diseases of the cornea at Johns Hopkins University in Baltimore, Maryland. The study, published in Cell Reports1 on 24 May, could help researchers to better understand diseases that affect the eye and to develop therapies that target infections on the eye’s surface, says Tanima Bose, an immunologist at the pharmaceutical company Novartis in Kundl, Austria. Immune response The cornea has a dampened response to infection, in part because aggressive immune cells could damage the clear layer of tissue and obstruct vision, says co-author Scott Mueller, an immunologist at the University of Melbourne, Australia. For this reason, the immune cells that mount a quick but crude response to an infection, such as dendritic cells and macrophages, largely reside in the outer sections of the cornea and emerge only when needed. But in almost every tissue in the body are long-lived immune cells, known as T cells, that swiftly attack pathogens they have previously encountered — a process called ‘immune memory’. Mueller and his colleagues wondered whether such cells lived in the cornea. Using a powerful multiphoton microscope for studying living tissue, the researchers examined the corneas of mice whose eyes had been infected with herpes simplex virus. They saw that cytotoxic T cells and T-helper cells — precursors for immune memory — had infiltrated the cornea and persisted for up to a month after the infection. Further investigations, including more intrusive microscopy techniques, revealed that the cytotoxic T cells had developed into long-lived memory cells that resided in the cornea. © 2022 Springer Nature Limited

Related chapters from BN: Chapter 10: Vision: From Eye to Brain; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 7: Vision: From Eye to Brain; Chapter 11: Emotions, Aggression, and Stress
Link ID: 28357 - Posted: 06.07.2022

By Colleen DeGuzman Jessica Oberoi, 13, cannot remember when her eyesight started getting blurry. All she knows is that she had to squint to see the whiteboard at school. It wasn’t until last fall when her eighth-grade class in Bloomington, Ind., got vision screenings that Jessica’s extreme nearsightedness and amblyopia, or lazy eye, were discovered. She has been going through intense treatment since then, and her optometrist, Katie Connolly, said Jessica has made great improvements — but her lazy eye, which causes depth perception problems, may never go away. The chances of it being completely corrected would have been much higher if her condition had been caught earlier, said Connolly, chief of pediatric and binocular vision service at Indiana University’s School of Optometry. Jessica is one of the countless students falling through the cracks of the nation’s fractured efforts to catch and treat vision problems among children. A mobile clinic is helping low-income students to see clearly — one pair of glasses at a time The Centers for Disease Control and Prevention estimates that more than 600,000 children and teens are blind or have a vision disorder. A recent opinion article published on JAMA Network notes that a large number of these children could be helped simply with glasses, but because of high costs and lack of insurance coverage, many are not getting them. Yet the National Survey of Children’s Health, funded by the U.S. Health Resources and Services Administration, found that in 2016-2017 a quarter of children were not regularly screened for vision problems. And a large majority of those vision impairments could be treated or cured if caught early, Connolly said. “Screenings are important for kids because kids don’t realize what’s abnormal,” Connolly said. “They don’t know what their peers around them — or even their parents — are seeing to realize their experience is different.” © 1996-2022 The Washington Post

Related chapters from BN: Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 7: Vision: From Eye to Brain
Link ID: 28355 - Posted: 06.07.2022

The Age-Related Eye Disease Studies (AREDS and AREDS2) established that dietary supplements can slow progression of age-related macular degeneration (AMD), the most common cause of blindness in older Americans. In a new report, scientists analyzed 10 years of AREDS2 data. They show that the AREDS2 formula, which substituted antioxidants lutein and zeaxanthin for beta-carotene, not only reduces risk of lung cancer due to beta-carotene, but is also more effective at reducing risk of AMD progression, compared to the original formula. A report on the study, funded by the National Institutes of Health, published in JAMA Ophthalmology. “Because beta-carotene increased the risk of lung cancer for current smokers in two NIH-supported studies, our goal with AREDS2 was to create an equally effective supplement formula that could be used by anyone, whether or not they smoke,” said Emily Chew, M.D., director of the Division of Epidemiology and Clinical Application at the National Eye Institute (NEI), and lead author of the study report. “This 10-year data confirms that not only is the new formula safer, it’s actually better at slowing AMD progression.” AMD is a degenerative disease of the retina, the light-sensitive tissue at the back of the eye. Progressive death of retinal cells in the macula, the part of the retina that provides clear central vision, eventually leads to blindness. Treatment can slow or reverse vision loss; however, no cure for AMD exists. The original AREDS study, launched in 1996, showed that a dietary supplement formulation (500 mg vitamin C, 400 international units vitamin E, 2 mg copper, 80 mg zinc, and 15 mg beta-carotene) could significantly slow the progression of AMD from moderate to late disease. However, two concurrent studies also revealed that people who smoked and took beta-carotene had a significantly higher risk of lung cancer than expected.

Related chapters from BN: Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 7: Vision: From Eye to Brain
Link ID: 28348 - Posted: 06.04.2022

Researchers have identified distinct differences among the cells comprising a tissue in the retina that is vital to human visual perception. The scientists from the National Eye Institute (NEI) discovered five subpopulations of retinal pigment epithelium (RPE)—a layer of tissue that nourishes and supports the retina’s light-sensing photoreceptors. Using artificial intelligence, the researchers analyzed images of RPE at single-cell resolution to create a reference map that locates each subpopulation within the eye. A report on the research published in Proceedings of the National Academy of Sciences. “These results provide a first-of-its-kind framework for understanding different RPE cell subpopulations and their vulnerability to retinal diseases, and for developing targeted therapies to treat them,” said Michael F. Chiang, M.D., director of the NEI, part of the National Institutes of Health. “The findings will help us develop more precise cell and gene therapies for specific degenerative eye diseases,” said the study’s lead investigator, Kapil Bharti, Ph.D., who directs the NEI Ocular and Stem Cell Translational Research Section. Vision begins when light hits the rod and cone photoreceptors that line the retina in the back of the eye. Once activated, photoreceptors send signals through a complex network of other retinal neurons that converge at the optic nerve before traveling to various centers in the brain. The RPE sits beneath the photoreceptors as a monolayer, one cell deep. Age and disease can cause metabolic changes in RPE cells that can lead to photoreceptor degeneration. The impact on vision from these RPE changes varies dramatically by severity and where the RPE cells reside within the retina. For example, late-onset retinal degeneration (L-ORD) affects mostly peripheral retina and, therefore, peripheral vision. Age-related macular degeneration (AMD), a leading cause of vision loss, primarily affects RPE cells in the macula, which is crucial for central vision.

Related chapters from BN: Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 7: Vision: From Eye to Brain
Link ID: 28318 - Posted: 05.07.2022

Yasemin Saplakoglu A mosquito watches you through a lattice of microscopic lenses. You stare back, fly swatter in hand, closely tracking the bloodsucker with your humble single-lens eyes. But it turns out that the way you see each other — and the world — may have more in common than you might think. A study published last month in Science Advances found that inside mammalian eyes, mitochondria, the organelles that power cells, may serve a second role as microscopic lenses, helping to focus light on the photoreceptor pigments that convert the light into neural signals for the brain to interpret. The findings, which draw a striking parallel between mammalian eyes and the compound eyes of insects and other arthropods, suggest that our own eyes have hidden levels of optical complexity, and that evolution has found new uses for very old parts of our cellular anatomy. Abstractions navigates promising ideas in science and mathematics. Journey with us and join the conversation. The lens at the very front of the eye focuses light from the environment onto a thin layer of tissue called the retina in the back. There, photoreceptor cells — cones that paint our world in color and rods that help us navigate in low light — absorb the light and translate it into nerve signals that propagate into the brain. But light-sensitive pigments sit at the very ends of photoreceptors, right behind a thick bundle of mitochondria. The odd placement of this bundle turns the mitochondria into seemingly unnecessary, light-scattering obstacles. The mitochondria are the “final hurdle” for the light particles, said Wei Li, a senior investigator at the National Eye Institute and senior author on the paper. For years, vision scientists couldn’t make sense of this odd placement of these organelles — after all, most cells have their mitochondria hugging their center organelle, the nucleus. All Rights Reserved © 2022

Related chapters from BN: Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 7: Vision: From Eye to Brain
Link ID: 28272 - Posted: 04.06.2022

Terry Gross One morning in 2017, New York Times columnist Frank Bruni woke up to find that everything looked blurry and smeared. "There was a fog, a dappled fog over the right side of my field of vision," Bruni says. "And I thought for hours that there must be some gunk in my eye, or maybe I'd had too much to drink the night before. Then I thought, Oh, no, it's my eyeglasses. I just have to clean them. And on and on, until deep into the day, I realized there was something wrong beyond all of that." Bruni, then 52, soon learned that he'd experienced a rare kind of stroke that had irreparably damaged his optic nerve. The prognosis: His vision in that eye would never return. What's more, there was a 20 to 40% chance that another stroke would impact his good eye. The news was devastating. "I had some emotional, psychological and really spiritual work to do to accept this and figure out how to go on in the most productive and constructive fashion," he says. But after going through a period of shock and terror, Bruni saw himself at a decision point: He could fixate on what had been lost, or he could focus on what remained. He chose to do the latter. "I feel like once you've recognized what's happened, ... it is so important and so constructive and so right to focus instead on all the things you can still do, all the blessings that remain," he says. "I ended up determined — determined to show myself that I could adapt to whatever was going to happen." In the memoir, The Beauty of Dusk, Bruni chronicles the changes to his vision and the adaptations he's had to make in his work, personal life and attitude. The book also profiles a number of other people who've survived and thrived in ways that Bruni says are profoundly instructive. © 2022 npr

Related chapters from BN: Chapter 19: Language and Lateralization; Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 15: Language and Lateralization; Chapter 7: Vision: From Eye to Brain
Link ID: 28248 - Posted: 03.23.2022

By Lisa Sanders, M.D. “You can’t see the ceiling, can you?” the man asked his 31-year-old wife. She grimaced, then shook her head. She was lying in bed looking toward the familiar shadows and shapes cast by the wintry morning sun. But she couldn’t see them. It was as if a dense white fog lay between her and those daily shifting patterns. Squinting didn’t help. Opening her eyes as wide as she could didn’t, either. All her life she had perfect vision. It was a secret source of pride. She’d never even seen an eye doctor. But that morning changed everything. She first noticed the trouble in her eyes six months earlier. She is a professional violinist and a teacher and that summer took her students to Italy to experience the sacred music and art. As she gazed up at the frescos decorating the ceiling of a favorite cathedral, a shimmering shape with jagged, irregular edges appeared out of nowhere. The points seemed to twinkle as the starlike image slowly enlarged. Inside the glittering outline, the colors were jumbled, like the crystals in a kaleidoscope. It was beautiful and terrifying. She dropped her head, closed her eyes and rubbed her aching neck. When she opened her eyes, the star burst, with its glimmering edges, was still there, distorting all that lay beyond it. It grew so large that it was almost all she could see. Then slowly it began to fade; after nearly a half-hour, the world started to resume its familiar look and shape. There had been similar, if less severe, experiences: Every now and then, when she would get up quickly after sitting or lying down, she would feel an intense pressure inside her head, and when it released, everything briefly looked faded and pale before returning to normal hues. These spells only lasted a few seconds and happened only a handful of times over the past few years. She wrote it off to fatigue or stress. After that day in Italy, those glistening star bursts appeared weekly, then daily. Stranger still, straight lines developed weird lumps and bumps when she looked at them out of the corner of her eye. Doorways, curbs and table edges seemed to waver, growing bulges and divots. When she looked at the object full on, it would obediently straighten out but resumed its aberration once it was on the sidelines again. © 2022 The New York Times Company

Related chapters from BN: Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 7: Vision: From Eye to Brain
Link ID: 28242 - Posted: 03.19.2022

Researchers at the National Eye Institute (NEI) have discovered that power-producing organelles in the eye’s photoreceptor cells, called mitochondria, function as microlenses that help channel light to these cells’ outer segments where it’s converted into nerve signals. The discovery in ground squirrels provides a more precise picture of the retina’s optical properties and could help detect eye disease earlier. The findings, published today in Science Advances, also shed light on the evolution of vision. NEI is part of the National Institutes of Health. “We were surprised by this fascinating phenomenon that mitochondria appear to have a dual purpose: their well-established metabolic role producing energy, as well as this optical effect,” said the study’s lead investigator, Wei Li, Ph.D./B.M., who leads the NEI Retinal Neurophysiology Section. Using a modified confocal microscope, the researchers observed the optical properties of living cone mitochondria exposed to light. The path of light became concentrated with transmission from the inner to the outer segments of cone photoreceptors. Credit: John Ball, Ph.D., NEI The findings also address a long-standing mystery about the mammalian retina. Despite evolutionary pressure for light to be translated into signals and pass instantly from the retina to the brain, the trip is hardly direct. Once light reaches the retina, it must pass through multiple neural layers before reaching the outer segment of photoreceptors, where phototransduction (the conversion of light’s physical energy into cellular signals) occurs. Photoreceptors are long, tube-like structures divided into inner and outer segments. The last obstacle a photon must traverse before moving from the inner to the outer segment is an unusually dense bundle of mitochondria. Those bundles of mitochondria would seem to work against the process of vision either by scattering light or absorbing it. So, Li’s team set out to investigate their purpose by studying cone photoreceptors from the 13-lined ground squirrel.

Related chapters from BN: Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 7: Vision: From Eye to Brain
Link ID: 28228 - Posted: 03.02.2022

By David A. Kaplan Our cross-country drive last winter from New York to Lake Tahoe was going to be eventful enough, with a pandemic, blizzards and the cancellation of salads at McDonald’s. But by Omaha, when the lanes on Interstate 80 seemed to be bouncing around before my very eyes, we entered unexpected territory. “Are you practicing your slalom turns at 80 miles an hour?” my wife asked. Road conditions were normal. Our S.U.V. had new tires. But the lanes often seemed to blur together. Sometimes the melding of lanes occurred late in the day, sometimes early. Sometimes in blinding sun, sometimes in fog. If I closed one eye, the lanes became separate again. What was happening? I’d worn glasses for nearsightedness since fifth grade; I’d seen my eye doctor within the year; my prescription was current. When we reached Tahoe, I went to an optometrist before even unpacking my skis. She said my eyes were fine, but advised an M.R.I. to rule out a brain bleed or a tumor. Days later, it did. She also told me to see a neuro-ophthalmologist, an increasingly rare subspecialty. Nationally, there are only about 600 of them, and because many do academic research or have general ophthalmic practices, just 250 of them are full-time clinicians. In six states, there are none practicing, according to a paper in the Journal of Neuro-Ophthalmology last year. The Tahoe optometrist warned it could take months to obtain an appointment with one of the few practitioners in the area. But my brother, a surgeon at Stanford, helped me get an appointment at Stanford Medical Center, four hours away, in Palo Alto, Ca., the following week. Dr. Heather Moss conducted the 90-minute examination, taking measurements that included the degree to which my eyes were properly centered. © 2022 The New York Times Company

Related chapters from BN: Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 7: Vision: From Eye to Brain
Link ID: 28220 - Posted: 02.26.2022

By Christina Caron Q: Sometimes my eyelid twitches on and off for days — weeks, even. It’s distracting and irritating. How do I get it to stop? And should I be concerned? Eyelid spasms, while annoying, are “rarely a sign of something serious,” said Stephanie Erwin, an optometrist at Cleveland Clinic’s Cole Eye Institute. The most common type of eye twitch is a series of muscle contractions called eyelid myokymia, which produces involuntary and intermittent contractions of the eyelid, typically the lower one. Only one eye is affected at a time because the twitch originates in the muscle surrounding the eye, and not the nerve that controls the blink reflex, which sends the same message to both eyes simultaneously, Dr. Erwin added. The spasms can last from hours to days to months. “If the twitching persists for a long period of time, or is accompanied by additional symptoms, it is a good idea to be checked by an eye doctor to make sure nothing else is going on,” she said. If the twitching spreads to other muscles in the face or if you notice both eyes are twitching at the same time, those are indications of a more serious problem. Other red flags include a drooping eyelid or a red eye. But if just one eyelid is twitching on and off, it is usually a harmless (and often exasperating) case of eyelid myokymia. As for why it happens: “Nobody knows exactly why,” said Dr. Alice Lorch, an ophthalmologist at Massachusetts Eye and Ear in Boston. But more commonly, it is stress, lack of sleep or excessive caffeine intake that brings on eyelid twitching, the experts said. Dry eye, a common affliction among those who stare at screens most of the day, is another culprit. Studies have indicated that we blink less when looking at digital devices, which makes our eyes feel dry. © 2021 The New York Times Company

Related chapters from BN: Chapter 10: Vision: From Eye to Brain; Chapter 14: Biological Rhythms, Sleep, and Dreaming
Related chapters from MM:Chapter 7: Vision: From Eye to Brain; Chapter 10: Biological Rhythms and Sleep
Link ID: 28131 - Posted: 12.31.2021

By Marlene Cimons Ruth Obadal, 72, a retired firefighter in Eugene, Ore., was tired of having to constantly switch glasses, one major reason she decided to have cataract surgery. “I needed progressive lenses for reading up close and for distance such as driving,” she says. Moreover, as a volunteer track-and-field official working outdoors, “I also needed the sunglasses version,” she says. “I also had separate glasses for computer and piano, as I needed to see up close and straight ahead, not just down.” U.S. coronavirus cases tracker and map In addition to the inconvenience, she found it increasingly difficult to get crisp vision, even when fine-tuning her prescriptions. So she had the procedure in both eyes — each two weeks apart — in May. She is happy with the results. “Now, I don’t use glasses for anything,” she says. Everyone who ages is vulnerable to developing a cataract in one or both eyes, a cloudy area in the eye’s natural lens that can cause vision to become blurry, hazy and less colorful. Cataracts result from normal changes in the eyes as people get older. At about age 40, the proteins in the lens begin to break down and clump together, causing the cloudiness. Over time, it worsens. Sunlight during the day and nighttime glare from streetlights and cars can be uncomfortable, even painful, interfering with the daily tasks of life, such as driving a vehicle, especially after dark. “I tell my patients that the time for surgery is when you can’t see what you need to do, whether it’s driving, reading the sports scores on bottom of your TV screen or seeing your mobile device,” says Amir Khan, an ophthalmologist at the Mayo Clinic. “We let the patient decide.”

Related chapters from BN: Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 7: Vision: From Eye to Brain
Link ID: 28067 - Posted: 11.09.2021

Bill Chappell A former science teacher who's been blind for 16 years became able to see letters, discern objects' edges — and even play a Maggie Simpson video game — thanks to a visual prosthesis that includes a camera and a brain implant, according to American and Spanish researchers who collaborated on the project. The test subject had the implant for six months and experienced no disruptions to her brain activity or other health complications, according to an abstract of the study that was published this week in The Journal of Clinical Investigation. The study furthers what it calls a "long-held dream of scientists," to impart a rudimentary form of sight to blind people by sending information directly to the brain's visual cortex. "These results are very exciting because they demonstrate both safety and efficacy," said one of the lead researchers, Eduardo Fernández of Miguel Hernández University, in a statement. "We have taken a significant step forward, showing the potential of these types of devices to restore functional vision for people who have lost their vision." In the experiment, a neurosurgeon implanted a microelectrode array into the visual cortex of Berna Gómez, a former teacher who has been blind for more than 16 years. The implant was then paired with a video camera mounted in the center of a pair of glasses. After a training period, Gómez was able to decipher visual information that was fed from the camera directly to her brain. The training included a video game that helped Gómez learn how to interpret the signals coming from the electrodes. In the game, a screen suddenly shows an image of Maggie Simpson holding a gun, in either her left or right hand. The player must correctly select which hand holds the weapon; using input from the array, Gómez learned how to succeed in that task. At the time of the study, Gómez was 57 years old. Because of her participation, including her ability to give clinically precise feedback to the scientists, Gómez was named as a co-author of the study. © 2021 npr

Related chapters from BN: Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 7: Vision: From Eye to Brain
Link ID: 28052 - Posted: 10.27.2021

Jon Hamilton The visual impairment known as "lazy eye" can be treated in kids by covering their other eye with a patch. Scientists may have found a way to treat adults with the condition using a pufferfish toxin. MARY LOUISE KELLY, HOST: Children who develop the visual impairment often called lazy eye can be treated by covering their other eye with a patch. Now researchers think they have found a way to treat adults using a toxin found in deadly puffer fish. The approach has only been tried in animals so far, but NPR's Jon Hamilton reports the results are encouraging. JON HAMILTON, BYLINE: A lazy eye isn't really lazy. The term refers to amblyopia, a medical condition that occurs when the brain starts ignoring the signals from one eye. Existing treatments restrict use of the strong eye in order to force the brain to pay attention to the weak one. But Mark Bear, a neuroscientist at MIT, says that approach has limits. MARK BEAR: There are a very significant number of adults with amblyopia where the treatment either didn't work or it was initiated too late. HAMILTON: After a critical period that ends at about age 10, the connections between eye and brain become less malleable. They lose what scientists call plasticity. So for several decades, Bear and a team of researchers have been trying to answer a question. BEAR: How can we rejuvenate these connections? How can they be brought back online? HAMILTON: To find out, Bear's team studied adults with amblyopia who lost their strong eye to a disease or an injury. © 2021 npr

Related chapters from BN: 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 and Learning
Link ID: 27989 - Posted: 09.15.2021

By Talia Ogliore New research from Washington University in St. Louis reveals that neurons in the visual cortex — the part of the brain that processes visual stimuli — change their responses to the same stimulus over time. Although other studies have documented “representational drift” in neurons in the parts of the brain associated with odor and spatial memory, this result is surprising because neural activity in the primary visual cortex is thought to be relatively stable. Xia The study published Aug. 27 in Nature Communications was led by Ji Xia, a recent PhD graduate of the laboratory of Ralf Wessel, professor of physics in Arts & Sciences. Xia is now a postdoctoral fellow at Columbia University. “We know that the brain is a flexible structure because we expect the neural activity in the brain to change over days when we learn, or when we gain experience — even as adults,” Xia said. “What is somewhat unexpected is that even when there is no learning, or no experience changes, neural activity still changes across days in different brain areas.” Researchers in Wessel’s group explore sensory information processing in the brain. Working with collaborators, they use novel data analysis to address questions of dynamics and computation in neural circuits of the visual cortex of the brain. Study co-senior author Michael J. Goard, from the Neuroscience Research Institute at the University of California, Santa Barbara, showed mice a single, short movie clip on a loop. (They used a section of the opening from a classic Orson Welles black-and-white film, de rigueur for today’s mouse vision studies.) While a mouse watched the movie, researchers simultaneously recorded activity in several hundred neurons in the primary visual cortex, using two-photon calcium imaging. ©2021 Washington University in St. Louis

Related chapters from BN: Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 7: Vision: From Eye to Brain
Link ID: 27972 - Posted: 09.01.2021

By Carolyn Wilke Frog and toad pupils come in quite the array, from slits to circles. But overall, there are seven main shapes of these animals’ peepholes, researchers report in the Aug. 25 Proceedings of the Royal Society B. Eyes are “among the most charismatic features of frogs and toads,” says herpetologist Julián Faivovich of the Museo Argentino de Ciencias Naturales “Bernardino Rivadavia” in Buenos Aires. People have long marveled at the animals’ many iris colors and pupil shapes. Yet “there’s almost nothing known about the anatomical basis of that diversity.” Faivovich and colleagues catalogued pupil shapes from photos of 3,261 species, representing 44 percent of known frogs and toads. The team identified seven main shapes: vertical slits, horizontal slits, diamonds, circles, triangles, fans and inverted fans. The most common shape, horizontal slits, appeared in 78 percent of studied species. Mapping pupil shapes onto a tree of evolutionary relationships allowed the scientists to infer how these seven shapes emerged. Though uncommon in other vertebrates, horizontal pupils seem to have given rise to most of the other shapes in frogs and toads. All together, these seven shapes have evolved at least 116 times, the researchers say. Pupil shape affects the amount of light that reaches the retina and its light-receiving cells, says Nadia Cervino, a herpetologist also at the Argentine museum. But how the shape influences what animals actually see isn’t well-known. © Society for Science & the Public 2000–2021.

Related chapters from BN: 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: 27958 - Posted: 08.25.2021

Ruth Williams In the days before a newborn mouse opens its peepers, nerve impulses that have been sweeping randomly across the retina since birth start flowing consistently in one direction, according to a paper published in Science today (July 22). This specific pattern has a critical purpose, the authors say, helping to establish the brain circuitry to be used later in motion detection. “I love this paper. It blew my mind,” says David Berson, who studies the visual system at Brown University and was not involved in the research. “What it implies is that evolution has built a visual system that can simulate the patterns of activity that it will see later when it’s fully mature and the eyes are open, and that [the simulated pattern] in turn shapes the development of the nervous system in a way that makes it better adapted to seeing those patterns. . . . That’s staggering.” The thread of this concept may be looped, but to unravel it, Berson says, it helps to think of the mammalian visual system, or really any neuronal circuitry, as being formed by a combination of evolution and life experiences—in short, nature and nurture. We might expect that life’s visual experiences, the nurture part, would begin when the eyes open. But, much like a human baby in the womb practices breathing and sucking without ever having experienced air or breastfeeding, the eyes of newborn mice appear to practice seeing before they can actually see. Motion detection is important enough to mouse survival that evolution has selected for gene variants that set up this prevision training, says Berson. © 1986–2021 The Scientist.

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 7: Vision: From Eye to Brain
Link ID: 27950 - Posted: 08.18.2021

By Lisa Sanders, M.D. The burning started as soon as the 59-year-old woman put the drops into her eye. She blinked to try to rinse away the medication with her tears. She leaned forward to the mirror. Her left eye was red and angry-looking. She’d been using these eye drops for nearly a year to treat her newly diagnosed glaucoma, adding artificial tears for the dry eyes that appeared a few months later. And while she’d had plenty of problems with her eyes since all this started, this fiery pain was new. The vision in her left eye had been bad for a few years by then, but with an operation nearly two years earlier to remove an abnormal membrane on her retina and more recent cataract surgery, she had hoped she would have her old vision back by now. She was a physician-researcher and spent much of her time reading and writing, so her vision was very important to her livelihood. But despite the efforts of her eye doctors — and at this point she had many — she still couldn’t see well. It was when she was getting ready for the cataract surgery that the patient learned she had glaucoma. After her initial exam, her new eye surgeon told her that the pressure inside her left eye was abnormally high, and she was already showing signs of damage from it. He wanted her to see one of his colleagues, Dr. Amanda Bicket, a glaucoma specialist who was then at the Wilmer Eye Institute at Johns Hopkins. A quick phone call later, she had an appointment to see the doctor that day. It was urgent that this be evaluated and treated before her upcoming surgery. © 2021 The New York Times Company

Related chapters from BN: Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 7: Vision: From Eye to Brain
Link ID: 27938 - Posted: 08.11.2021

Scientists studied the brain activity of school-aged children during development and found that regions that activated upon seeing limbs (hands, legs, etc.) subsequently activated upon seeing faces or words when the children grew older. The research, by scientists at Stanford University, Palo Alto, California, reveals new insights about vision development in the brain and could help inform prevention and treatment strategies for learning disorders. The study was funded by the National Eye Institute and is published in Nature Human Behaviour. “Our study addresses how experiences, such as learning to read, shape the developing brain,” said Kalanit Grill-Spector, Ph.D., a professor at Stanford University’s Wu Tsai Neurosciences Institute. “Further, it sheds light on the initial functional role of brain regions that later in development process written words, before they support this important skill of reading.” Grill-Spector’s team used functional MRI to study areas in the ventral temporal cortex (VTC) that are stimulated by the recognition of images. About 30 children, ages 5 to 12 at their first MRI, participated in the study. While in the MRI scanner, the children viewed images from 10 different categories, including words, body parts, faces, objects, and places. The researchers mapped areas of VTC that exhibited stimulation and measured how they changed in intensity and volume on the children’s subsequent MRI tests over the next one to five years. Results showed that VTC regions corresponding to face and word recognition increased with age. Compared to the 5-9-year-olds, teenagers had twice the volume of the word-selective region in VTC. Notably, as word-selective VTC volume doubled, limb-selective volume in the same region halved. According to the investigators, the decrease in limb-selectivity is directly linked to the increase in word- and face-selectivity, providing the first evidence for cortical recycling during childhood development.

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 7: Vision: From Eye to Brain
Link ID: 27860 - Posted: 06.19.2021