Chapter 5. The Sensorimotor System
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.By JOANNA KLEIN A honey bee gathering pollen on a white flower. Dagmar Sporck/EyeEm, via Getty Images Set your meetings, phone calls and emails aside, at least for the next several minutes. That’s because today you’re a bee. It's time to leave your hive, or your underground burrow, and forage for pollen. Pollen is the stuff that flowers use to reproduce. But it’s also essential grub for you, other bees in your hive and your larvae. Once you’ve gathered pollen to take home, you or another bee will mix it with water and flower nectar that other bees have gathered and stored in the hive. But how do you decide which flowers to approach? What draws you in? In a review published last week in the journal Functional Ecology, researchers asked: What is a flower like from a bee’s perspective, and what does the pollinator experience as it gathers pollen? And that's why we're talking to you in the second person: to help you understand how bees like you, while hunting for pollen, use all of your senses — taste, touch, smell and more — to decide what to pick up and bring home. Maybe you're ready to go find some pollen. But do you even know where to look? © 2016 The New York Times Company
By Clare Wilson WE HAVE been thinking about Parkinson’s disease all wrong. The condition may arise from damage to the gut, not the brain. If the idea is correct, it opens the door to new ways of treating the disease before symptoms occur. “That would be game-changing,” says David Burn at Newcastle University, UK. “There are lots of different mechanisms that could potentially stop the spread.” Parkinson’s disease involves the death of neurons deep within the brain, causing tremors, stiffness and difficulty moving. While there are drugs that ease these symptoms, they become less effective as the disease progresses. One of the hallmarks of the condition is deposits of insoluble fibres of a substance called synuclein. Normally found as small soluble molecules in healthy nerve cells, in people with Parkinson’s, something causes the synuclein molecules to warp into a different shape, making them clump together as fibres. The first clue that this transition may start outside the brain came about a decade ago, when pathologists reported seeing the distinctive synuclein fibres in nerves of the gut during autopsies – both in people with Parkinson’s and in those without symptoms but who had the fibres in their brain. They suggested the trigger was some unknown microbe or toxin. © Copyright Reed Business Information Ltd.
Link ID: 22938 - Posted: 12.01.2016
By Melissa Dahl Considering its origin story, it’s not so surprising that hypnosis and serious medical science have often seemed at odds. The man typically credited with creating hypnosis, albeit in a rather primitive form, is Franz Mesmer, a doctor in 18th-century Vienna. (Mesmer, mesmerize. Get it?) Mesmer developed a general theory of disease he called “animal magnetism,” which held that every living thing carries within it an internal magnetic force, in liquid form. Illness arises when this fluid becomes blocked, and can be cured if it can be coaxed to flow again, or so Mesmer’s thinking went. To get that fluid flowing, as science journalist Jo Marchant describes in her recent book, Cure, Mesmer “simply waved his hands to direct it through his patients’ bodies” — the origin of those melodramatic hand motions that stage hypnotists use today.” After developing a substantial following — “mesmerism” became “the height of fashion” in late 1780s Paris, writes Marchant — Mesmer became the subject of what was essentially the world’s first clinical trial. King Louis XVI pulled together a team of the world’s top scientists, including Benjamin Franklin, who tested mesmerism and found its capacity to “cure” was, essentially, a placebo effect. “Not a shred of evidence exists for any fluid,” Franklin wrote. “The practice … is the art of increasing the imagination by degrees.” Maybe so. But that doesn’t mean it doesn’t work. © 2016, New York Media LLC.
Sara Reardon A new technique might allow researchers and clinicians to stimulate deep regions of the brain, such as those involved in memory and emotion, without opening up a patient’s skull. Brain-stimulation techniques that apply electrodes to a person’s scalp seem to be safe, and proponents say that the method can improve some brain functions, including enhancing intelligence and relieving depression. Some of these claims are much better supported by research than others. But such techniques are limited because they cannot reach deep regions of the brain. By contrast, implants used in deep brain stimulation (DBS) are much more successful at altering the inner brain. The devices can be risky, however, because they involve surgery, and the implants cannot be repaired easily if they malfunction. At the annual Society for Neuroscience conference, held in San Diego, California, last week, neuroengineer Nir Grossman of the Massachusetts Institute of Technology in Cambridge and his colleagues presented their experimental method that adapts transcranial stimulation (TCS) for the deep brain. Their approach involves sending electrical signals through the brain from electrodes placed on the scalp and manipulating the electrical currents in a way that negates the need for surgery. The team used a stimulation device to apply two electric currents to the mouse's skull behind its ears and tuned them to slightly different high frequencies. They angled these two independent currents so that they intersected with each other at the hippocampus. © 2016 Macmillan Publishers Limited,
Tom Goldman Voters in seven more states said "yes" to marijuana this month. Pot now is legal for recreational or medicinal use in more than half the country. It's still against federal law and classified as a Schedule 1 drug, meaning U.S. officials consider marijuana to have a high risk of abuse or harm, and no accepted medical use in treatment. Also, it's still banned in professional sports. Many athletes hope that will change as momentum grows nationwide for legalization. That's especially true in the National Football League, where pain is a constant companion. Advocates say marijuana could offer a safer and better way to manage the pain. Football hurts. As a fan watching from home, that's not always obvious — players collide, fall down, pop back up. They rarely wince or show weakness. That's just not how it's done in football. Kyle Turley hurt plenty during his eight NFL seasons in the 1990s and 2000s. As an offensive lineman, he was involved in jarring collisions nearly every play when his team had the ball. He hurt after his career -– Turley sometimes walks with a cane. And in a recent video, he displayed one by one the bottles of powerful painkillers he used. "Vicodin, Flexeril, Percocets, Vioxx, morphine," Turley recited as he plopped the bottles down on a kitchen counter. © 2016 npr
By R. Douglas Fields SAN DIEGO—A wireless device that decodes brain waves has enabled a woman paralyzed by locked-in syndrome to communicate from the comfort of her home, researchers announced this week at the annual meeting of the Society for Neuroscience. The 59-year-old patient, who prefers to remain anonymous but goes by the initials HB, is “trapped” inside her own body, with full mental acuity but completely paralyzed by a disease that struck in 2008 and attacked the neurons that make her muscles move. Unable to breathe on her own, a tube in her neck pumps air into her lungs and she requires round-the-clock assistance from caretakers. Thanks to the latest advance in brain–computer interfaces, however, HB has at least regained some ability to communicate. The new wireless device enables her to select letters on a computer screen using her mind alone, spelling out words at a rate of one letter every 56 seconds, to share her thoughts. “This is a significant achievement. Other attempts on such an advanced case have failed,” says neuroscientist Andrew Schwartz of the University of Pittsburgh, who was not involved in the study, published in The New England Journal of Medicine. HB’s mind is intact and the part of her brain that controls her bodily movements operates perfectly, but the signals from her brain no longer reach her muscles because the motor neurons that relay them have been damaged by amyotrophic lateral sclerosis (ALS), says neuroscientist Erick Aarnoutse, who designed the new device and was responsible for the technical aspects of the research. He is part of a team of physicians and scientists led by neuroscientist Nick Ramsey at Utrecht University in the Netherlands. Previously, the only way HB could communicate was via a system that uses an infrared camera to track her eye movements. But the device is awkward to set up and use for someone who cannot move, and it does not function well in many situations, such as in bright sunlight. © 2016 Scientific American,
By Alice Klein Alzheimer’s disease can be prevented by stopping a crucial brain protein from turning rogue, a study in mice suggests. Tau protein has long been suspected to play a role in causing the condition. In healthy brains, tau is essential for normal cell functioning. But during Alzheimer’s disease, the protein goes haywire, clumping together to form twisted tangles and, it is thought, releasing toxic chemicals that harm the brain. Now Lars Ittner at the University of New South Wales, Australia, and his colleagues have pinpointed a crucial enzyme that controls how tau proteins behave in the brain. The enzyme, called p38γ kinase, helps keep tau in a healthy, tangle-free state, preventing the onset of memory loss and other symptoms in mice that have been bred to develop Alzheimer’s disease. The enzyme seems to block Alzheimer’s by interfering with the action of another problem protein, called beta-amyloid. Like tau, clumps of this protein accumulate in the brains of people with Alzheimer’s, making it another suspected cause of the disease. When beta-amyloid forms these sticky plaques, it can also modify the structure of tau proteins, causing them to form tangles and release toxic chemicals. But Ittner’s team found that p38γ kinase makes a different kind of structural change to tau. If this change is made first, it prevents beta-amyloid from being able to turn tau bad, and mice do not develop the disease. © Copyright Reed Business Information Ltd.
Link ID: 22883 - Posted: 11.18.2016
Laura Sanders SAN DIEGO — Over the course of months, clumps of a protein implicated in Parkinson’s disease can travel from the gut into the brains of mice, scientists have found. The results, reported November 14 at the annual meeting of the Society for Neuroscience, suggest that in some cases, Parkinson’s may get its start in the gut. That’s an intriguing concept, says neuroscientist John Cryan of the University College Cork in Ireland. The new study “shows how important gut health can be for brain health and behavior.” Collin Challis of Caltech and colleagues injected clumps of synthetic alpha-synuclein, a protein known to accumulate in the brains of people with Parkinson’s, into mice’s stomachs and intestines. The researchers then tracked alpha-synuclein with a technique called CLARITY, which makes parts of the mice’s bodies transparent. Seven days after the injections, researchers saw alpha-synuclein clumps in the gut. Levels there peaked 21 days after the injections. These weren’t the same alpha-synuclein aggregates that were injected, though. These were new clumps, formed from naturally occurring alpha-synuclein, that researchers believe were coaxed into forming by the synthetic versions in their midst. Also 21 days after the injections, alpha-synuclein clumps seemed to have spread to a part of the brain stem containing nerve cells that make up the vagus nerve, a neural highway that connects the gut to the brain. Sixty days after the injections, alpha-synuclein had accumulated in the midbrain, a region packed with nerve cells that make the chemical messenger dopamine. These are the nerve cells that die in people with Parkinson’s, a progressive brain disorder that affects movement. © Society for Science & the Public 2000 - 2016
Link ID: 22881 - Posted: 11.17.2016
Amir Kheradmand, When we spin—on an amusement park ride or the dance floor—we often become disoriented, even dizzy. So how do professional athletes, particularly figure skaters who spin at incredible speeds, avoid losing their balance? The short answer is training, but to really grasp why figure skaters can twirl without getting dizzy requires an understanding of the vestibular system, the apparatus in our inner ear that helps to keep us upright. This system contains special sensory nerve cells that can detect the speed and direction at which our head moves. These sensors are tightly coupled with our eye movements and with our perception of our body's position and motion through space. For instance, if we rotate our head to the right while our eyes remain focused on an object straight ahead, our eyes naturally move to the left at the same speed. This involuntary response allows us to stay focused on a stationary object. Spinning is more complicated. When we move our head during a spin, our eyes start to move in the opposite direction but reach their limit before our head completes a full 360-degree turn. So our eyes flick back to a new starting position midspin, and the motion repeats as we rotate. When our head rotation triggers this automatic, repetitive eye movement, called nystagmus, we get dizzy. © 2016 Scientific American
Link ID: 22878 - Posted: 11.17.2016
By CHRIS BUCKLEY BEIJING — When Flappy McFlapperson and Skybomb Bolt sprang into the sky for their annual migration from wetlands near Beijing, nobody was sure where the two cuckoos were going. They and three other cuckoos had been tagged with sensors to follow them from northern China. But to where? “These birds are not known to be great fliers,” said Terry Townshend, a British amateur bird watcher living in the Chinese capital who helped organize the Beijing Cuckoo Project to track the birds. “Migration is incredibly perilous for birds, and many perish on these journeys.” The answer to the mystery — unfolding in passages recorded by satellite for more than five months — has been a humbling revelation even to many experts. The birds’ journeys have so far covered thousands of miles, across a total of a dozen countries and an ocean. The “common cuckoo,” as the species is called, turns out to be capable of exhilarating odysseys. “It’s impossible not to feel an emotional response,” said Chris Hewson, an ecologist with the British Trust for Ornithology in Thetford, England, who has helped run the tracking project. “There’s something special about feeling connected to one small bird flying across the ocean or desert.” But to follow a cuckoo, you must first seduce it. The common cuckoo is by reputation a cynical freeloader. Mothers outsource parenting by laying their eggs in the nests of smaller birds, and the birds live on grubs, caterpillars and similar soft morsels. British and Chinese bird groups decided to study two cuckoo subspecies found near Beijing, because their winter getaways were a puzzle. In an online poll for the project, nearly half the respondents guessed they went somewhere in Southeast Asia. © 2016 The New York Times Company
By Jessica Hamzelou HB, who is paralysed by amyotrophic lateral sclerosis (ALS), has become the first woman to use a brain implant at home and in her daily life. She told New Scientist about her experiences using an eye-tracking device that takes about a minute to spell a word. What is your life like? All muscles are paralysed. I can only move my eyes. Why did you decide to try the implant? I want to contribute to possible improvements for people like me. What was the surgery like? The first surgery was no problem, but the second had a negative impact for my condition. Can you feel the implant at all? No. How easy is it to use? The hardware is easy to use. The software has been improved enormously by the UNP (Utrecht NeuroProsthesis) team. My part isn’t difficult anymore after these improvements. The most difficult part is timing the clicks. How has the implant changed your life? Now I can communicate outdoors when my eye track computer doesn’t work. I’m more confident and independent now outside. What are the best and worst things about it? The best is to go outside and be able to communicate. The worst were the false-positive clicks. But thanks to the UNP team that is fixed. Now that the study has been completed, would you like to keep the implant, or remove it? Of course I keep it. How do you feel about being the first person to have this implant? It’s special to be the first. Thinking ahead to the future, what else would you like to be able to do with the implant? I would like to change the television channel and my dream is to be able to drive my wheelchair. © Copyright Reed Business Information Ltd.
By STEPH YIN Researchers have designed a system that lets a patient with late-stage Lou Gehrig’s disease type words using brain signals alone. The patient, Hanneke De Bruijne, a doctor of internal medicine from the Netherlands, received a diagnosis of amyotrophic lateral sclerosis, also known as A.L.S. or Lou Gehrig’s disease, in 2008. The neurons controlling her voluntary muscles were dying, and eventually she developed a condition called locked-in syndrome. In this state, she is cognitively aware, but nearly all of her voluntary muscles, except for her eyes, are paralyzed, and she has lost the ability to speak. In 2015, a group of researchers offered an option to help her communicate. Their idea was to surgically implant a brain-computer interface, a system that picks up electrical signals in her brain and relays them to software she can use to type out words. “It’s like a remote control in the brain,” said Nick Ramsey, a professor of cognitive neuroscience at the University Medical Center Utrecht in the Netherlands and one of the researchers leading the study. On Saturday, the research team reported in The New England Journal of Medicine that Ms. De Bruijne independently controlled the computer typing program seven months after surgery. Using the system, she is able to spell two or three words a minute. “This is the world’s first totally implanted brain-computer interface system that someone has used in her daily life with some success,” said Dr. Jonathan R. Wolpaw, the director of the National Center for Adaptive Neurotechnologies in Albany. © 2016 The New York Times Company
David Cyranoski For more than a decade, neuroscientist Grégoire Courtine has been flying every few months from his lab at the Swiss Federal Institute of Technology in Lausanne to another lab in Beijing, China, where he conducts research on monkeys with the aim of treating spinal-cord injuries. The commute is exhausting — on occasion he has even flown to Beijing, done experiments, and returned the same night. But it is worth it, says Courtine, because working with monkeys in China is less burdened by regulation than it is in Europe and the United States. And this week, he and his team report1 the results of experiments in Beijing, in which a wireless brain implant — that stimulates electrodes in the leg by recreating signals recorded from the brain — has enabled monkeys with spinal-cord injuries to walk. “They have demonstrated that the animals can regain not only coordinated but also weight-bearing function, which is important for locomotion. This is great work,” says Gaurav Sharma, a neuroscientist who has worked on restoring arm movement in paralysed patients, at the non-profit research organization Battelle Memorial Institute in Columbus, Ohio. The treatment is a potential boon for immobile patients: Courtine has already started a trial in Switzerland, using a pared-down version of the technology in two people with spinal-cord injury. © 2016 Macmillan Publishers Limited
By Diana Kwon In people who suffer from pain disorders, painful feelings can severely worsen and spread to other regions of the body. Patients who develop chronic pain after surgery, for example, will often feel it coming from the area surrounding the initial injury and even in some parts of the body far from where it originates. New evidence suggests glia, non-neuronal cells in the brain, may be the culprits behind this effect. Glia were once thought to simply be passive, supporting cells for neurons. But scientists now know they are involved in everything from metabolism to neurodegeneration. A growing body of evidence points to their key role in pain. In a study published today in Science, researchers at the Medical University of Vienna report that glia are involved in long-term potentiation (LTP), or the strengthening of synapses, in pain pathways in the spinal cord. Neuroscientists Timothy Bliss and Terje Lømo first described LTP in the hippocampus, a brain area involved in memory, in the 1970s. Since then scientists have been meticulously studying the role this type of synaptic plasticity—the ability of synapses to change in strength—plays in learning and memory. More recently, researchers discovered that LTP could also amplify pain in areas where injuries or inflammation occur. “We sometimes call this a ‘memory trace of pain’ because the painful insult may lead to subsequent hypersensitivity to painful stimuli, and it was clear that synaptic plasticity can play a role here,” says study co-author Jürgen Sandkühler, a neuroscientist also at the Medical University of Vienna. But current models of how LTP works could not explain why discomfort sometimes becomes widespread or experienced in areas a person has never felt it before, he adds. © 2016 Scientific American
Ian Sample Science editor Partially-paralysed monkeys have learned to walk again with a brain implant that uses wireless signals to bypass broken nerves in the spinal cord and reanimate the useless limbs. The implant is the first to restore walking ability in paralysed primates and raises the prospect of radical new therapies for people with devastating spinal injuries. Scientists hope the technology will help people who have lost the use of their legs, by sending movement signals from their brains to electrodes in the spine that activate the leg muscles. One rhesus macaque that was fitted with the new implant regained the ability to walk only six days after it was partially paralysed in a surgical procedure that severed some of the nerves that controlled its right hind leg. “It was a big surprise for us,” said Grégoire Courtine, a neuroscientist who led the research at the Swiss Federal Institute of Technology. “The gait was not perfect, but it was almost like normal walking. The foot was not dragging and it was fully weight bearing.” A second animal in the study that received more serious damage to the nerves controlling its right hind leg recovered the ability to walk two weeks after having the device fitted, according to a report published in the journal, Nature. Both monkeys regained full mobility in three months. The “brain-spine interface” is the latest breakthrough to come from the rapidly-advancing area of neuroprosthetics. Scientists in the field aim to read intentions in the brain’s activity and use it to control computers, robotic arms and even paralysed limbs. © 2016 Guardian News and Media Limited
Nancy Shute Erik Vance didn't go to a doctor until he was 18; he grew up in California in a family that practiced Christian Science. "For the first half of my life, I never questioned the power of God to heal me," Vance writes in his new book, Suggestible You: Placebos, False Memories, Hypnosis, and the Power of Your Astonishing Brain. As a young man, Vance left the faith behind, but as he became a science journalist he didn't stop thinking about how people's beliefs and expectations affect their health, whether it's with placebo pills, mystical practices or treatments like acupuncture. The answer, he found, is in our brains. Erik and I chatted about the book while attending a recent meeting of the National Association of Science Writers. Here are highlights of our conversation, edited for length and clarity. You point out that even though most of us didn't grow up Christian Scientist, we often use belief to manage our health. I've learned from writing this book that there are a lot of people around the world who really rely on expectation and placebos. And I grew up in the most extreme possible group, but it's not that different from seeing a homeopath. You're using faith to manage your body; what a psychologist would call expectation. Having had that experience really prepared me to ask some of these questions. How would your mom take care of you when you were sick? As a kid we might have 7UP with orange juice; we might go that far because it made you feel better. But the treatment was to call a practitioner, to call a healer. © 2016 npr
Keyword: Pain & Touch
Link ID: 22847 - Posted: 11.09.2016
By Simon Oxenham Isy Suttie has felt “head squeezing” since she was young. The comedian, best known for playing Dobbie in the BBC sitcom Peep Show, is one of many people who experience autonomous sensory meridian response (ASMR) – a tingly feeling often elicited by certain videos or particular mundane interactions. Growing up, Suttie says she had always assumed everyone felt it too. Not everyone feels it, but Suttie is by no means alone. On Reddit, a community of more than 100,000 members share videos designed to elicit the pleasurable sensation. The videos, often described as “whisper porn”, typically consist of people role-playing routine tasks, whispering softly into a microphone or making noises by crinkling objects such as crisp packets. The most popular ASMR YouTuber, “Gentle Whispering”, has over 250 million views. To most of us, the videos might seem strange or boring, but the clips frequently garner hundreds of thousands of views. These videos often mimic real-life situations that provoke ASMR in susceptible people. Suttie says her strongest real-world triggers occur during innocuous interactions with strangers, like talking about the weather – “it’s almost as if the more superficial the subject the better,” Suttie says. She feels the sensation particularly strongly when someone brushes past her. For Suttie, the feelings are so powerful that she often feels floored by them, and they even overcome pain and emotional distress. During a trip to the dentist, she still experiences the pleasurable tingles when the assistant brushes past her, she says. © Copyright Reed Business Information Ltd.
By LISA SANDERS, M.D. Yesterday we challenged Well readers to take on the case of a 63-year-old artist who, over the course of several months, developed excruciating headaches, along with changes in his personality, his thinking, even in the way he painted. We provided you with some of the doctor’s notes and medical imaging results that led the doctor who finally made the diagnosis in the right direction. After an extensive evaluation, that doctor asked a single question that led him to make the diagnosis. We asked Well readers to figure out the question the doctor asked and the diagnosis it suggested. It must have been a tough case — or else you were all too worried about the coming election to rise to the challenge — because we got just over 200 responses, fewer than usual. Of those, only six of you figured out the right diagnosis, and only three of you got the question right as well. Despite that, I was very impressed by the thinking of even those who didn’t come up with the right diagnosis. Many of you thought about environmental factors like his recent retirement and his exposure to possible toxins from his painting, and that kind of thinking was, in my opinion, the very essence of thinking like a doctor. Strong work, all of you. The question the doctor asked that led him to the correct diagnosis was: Can you hear your heartbeat in your ears? The patient could. And that suggested the diagnosis: A dural-arteriovenous fistula, or DAVF © 2016 The New York Times Company
Keyword: Pain & Touch
Link ID: 22839 - Posted: 11.07.2016
By Neuroskeptic A new paper could prompt a rethink of a basic tenet of neuroscience. It is widely believed that the motor cortex, a region of the cerebral cortex, is responsible for producing movements, by sending instructions to other brain regions and ultimately to the spinal cord. But according to neuroscientists Christian Laut Ebbesen and colleagues, the truth may be the opposite: the motor cortex may equally well suppress movements. Ebbesen et al. studied the vibrissa motor cortex (VMC) of the rat, an area which is known to be involved in the movement of the whiskers. First, they determined that neurons within the VMC are more active during periods when the rat’s whiskers are resting: for instance, like this: whiskerThe existence of cells whose firing negatively correlates with movement is interesting, but by itself it doesn’t prove that much. Maybe those cells are just doing something else than controlling movement? However, Ebbesen et al. went on to show that electrical stimulation of the VMC caused whiskers to stop moving, while applying a drug (lidocaine) to suppress VMC activity caused the rat’s whiskers to whisk harder. Ebbesen et al. go on to say that the inhibitory role of VMC may extend to other regions of the rat motor cortex, and to other movements beyond the whiskers: Rats can perform long sequences of skilled, learned motor behaviors after motor cortex ablation, but motor cortex is required for them to learn a task of behavioral inhibition (they must learn to postpone lever presses)35. When swimming, intact rats hold their forelimbs still and swim with only their hindlimbs. After forelimb motor cortex lesions, however, rats swim with their forelimbs also36.
Keyword: Movement Disorders
Link ID: 22837 - Posted: 11.07.2016
Laura Sanders A protein that can switch shapes and accumulate inside brain cells helps fruit flies form and retrieve memories, a new study finds. Such shape-shifting is the hallmark move of prions — proteins that can alternate between two forms and aggregate under certain conditions. In fruit flies’ brain cells, clumps of the prionlike protein called Orb2 stores long-lasting memories, report scientists from the Stowers Institute for Medical Research in Kansas City, Mo. Figuring out how the brain forms and calls up memories may ultimately help scientists devise ways to restore that process in people with diseases such as Alzheimer’s. The new finding, described online November 3 in Current Biology, is “absolutely superb,” says neuroscientist Eric Kandel of Columbia University. “It fills in a lot of missing pieces.” People possess a version of the Orb2 protein called CPEB, a commonality that suggests memory might work in a similar way in people, Kandel says. It’s not yet known whether people rely on the prion to store long-term memories. “We can’t be sure, but it’s very suggestive,” Kandel says. When neuroscientist Kausik Si and colleagues used a genetic trick to inactivate Orb2 protein, male flies were worse at remembering rejection. These lovesick males continued to woo a nonreceptive female long past when they should have learned that courtship was futile. In different tests, these flies also had trouble remembering that a certain odor was tied to food. |© Society for Science & the Public 2000 - 2016. All rights reserved.