Chapter 11. Motor Control and Plasticity
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By GRETCHEN REYNOLDS Before you skip another workout, you might think about your brain. A provocative new study finds that some of the benefits of exercise for brain health may evaporate if we take to the couch and stop being active, even just for a week or so. I have frequently written about how physical activity, especially endurance exercise like running, aids our brains and minds. Studies with animals and people show that working out can lead to the creation of new neurons, blood vessels and synapses and greater overall volume in areas of the brain related to memory and higher-level thinking. Presumably as a result, people and animals that exercise tend to have sturdier memories and cognitive skills than their sedentary counterparts. Exercise prompts these changes in large part by increasing blood flow to the brain, many exercise scientists believe. Blood carries fuel and oxygen to brain cells, along with other substances that help to jump-start desirable biochemical processes there, so more blood circulating in the brain is generally a good thing. Exercise is particularly important for brain health because it appears to ramp up blood flow through the skull not only during the actual activity, but throughout the rest of the day. In past neurological studies, when sedentary people began an exercise program, they soon developed augmented blood flow to their brains, even when they were resting and not running or otherwise moving. But whether those improvements in blood flow are permanent or how long they might last was not clear. So for the new study, which was published in August in Frontiers in Aging Neuroscience, researchers from the department of kinesiology at the University of Maryland in College Park decided to ask a group of exceedingly fit older men and women to stop exercising for awhile. © 2016 The New York Times Company
By Alison F. Takemura Bodies like to keep their pH close to 7.4, whether that means hyperventilating to make the blood alkaline, or burning energy, shifting to anaerobic metabolism, and producing lactate to make the blood acidic. The lungs and kidneys can regulate pH changes systemically, but they may not act quickly on a local scale. Because even small pH changes can dramatically affect the nervous system, a study led by Sten Grillner of Karolinska Institute in Sweden looked for a mechanism for pH homeostasis in the spinal cord. Using the lamprey as a model system, the researchers observed that a type of spinal canal neuron, called CSF-c, fired more rapidly when they bathed it with high pH (7.7) or low pH (7.1) media. They could suspend the elevated activity by blocking two ion channels: PKD2L1 channels, which stimulate neurons in alkaline conditions, or ASIC3 channels, which, the team showed previously, do the same in acidic states. As the neurons fired, they released the hormone somatostatin, which inhibited the lamprey’s locomotor network. These results suggest that, whichever direction pH deviates, “the response of the system is just to reduce activity as much as possible,” Grillner says. The pH-regulating role of CSF-c neurons is likely conserved among animals, the authors suspect, given the presence of these neurons across vertebrate taxa. © 1986-2016 The Scientist
Keyword: Movement Disorders
Link ID: 22688 - Posted: 09.24.2016
By Michael Price A soft brush that feels like prickly thorns. A vibrating tuning fork that produces no vibration. Not being able to tell which direction body joints are moving without looking at them. Those are some of the bizarre sensations reported by a 9-year-old girl and 19-year-old woman in a new study. The duo, researchers say, shares an extremely rare genetic mutation that may shed light on a so-called “sixth sense” in humans: proprioception, or the body’s awareness of where it is in space. The new work may even explain why some of us are klutzier than others. The patients’ affliction doesn’t have a name. It was discovered by one of the study’s lead authors, pediatric neurologist Carsten Bönnemann at the National Institutes of Health (NIH) in Bethesda, Maryland, who specializes in diagnosing unknown genetic illnesses in young people. He noticed that the girl and the woman shared a suite of physical symptoms, including hips, fingers, and feet that bent at unusual angles. They also had scoliosis, an unusual curvature of the spine. And, significantly, they had difficulty walking, showed an extreme lack of coordination, and couldn’t physically feel objects against their skin. Bönnemann screened their genomes and looked for mutations that they might have in common. One in particular stood out: a catastrophic mutation in PIEZO2, a gene that has been linked to the body’s sense of touch and its ability to perform coordinated movements. At about the same time, in a “very lucky accident,” Bönnemann attended a lecture by Alexander Chesler, a neurologist also at NIH, on PIEZO2. Bönnemann invited Chesler to help study his newly identified patients. © 2016 American Association for the Advancement of Science.
By SABRINA TAVERNISE WASHINGTON — The Food and Drug Administration approved the first drug to treat patients with the most common childhood form of muscular dystrophy, a vivid example of the growing power that patients and their advocates wield over the federal government’s evaluation of drugs. The agency’s approval went against the recommendation of its experts. The main clinical trial of the drug was small, involving only 12 boys with the disease known as Duchenne muscular dystrophy, and did not have an adequate control group of boys who had the disease but did not take the drug. A group of independent experts convened by the agency this spring said there was not enough evidence that it was effective. But the vote was close. Large and impassioned groups of patients, including boys in wheelchairs, and their advocates, weighed in. The muscular dystrophy community is well organized and has lobbied for years to win approval for the drug, getting members of Congress to write letters to the agency. A decision on the drug had been delayed for months. The approval was so controversial that F.D.A. employees fought over it, a dispute that was taken to the agency’s commissioner, Dr. Robert M. Califf, who ultimately decided that it would stand. The approval delighted the drug’s advocates and sent the share price of the drug’s maker, Sarepta Therapeutics, soaring. But it was taken as a deeply troubling sign among drug policy experts who believe the F.D.A. has been far too influenced by patient advocates and drug companies, and has allowed the delicate balance in drug approvals to tilt toward speedy decisions based on preliminary data and away from more conclusive evidence of effectiveness and safety. © 2016 The New York Times Company
Carrie Arnold Could a protein that originated in a virus explain why men are more muscular than women? Viruses are notorious for their ability to cause disease, but they also shape human biology in less obvious ways. Retroviruses, which insert their genetic material into our genomes to copy themselves, have left behind genes that help to steer our immune systems and mold the development of embryos and the placenta. Now researchers report in PLOS Genetics that syncytin, a viral protein that enables placenta formation, also helps to increase muscle mass in male mice1. These results could partially explain a lingering mystery in biology: why the males of many mammalian species tend to be more muscular than females. “As soon as I read it, my mind started racing with the potential implications,” says evolutionary virologist Aris Katzourakis of the University of Oxford, UK. About 8% of the 3 billion pairs of As, Ts, Gs and Cs that make up our DNA are viral detritus. Many of those viral hand-me-downs have degraded into useless junk — but not all, as a series of discoveries over the past 15 years has revealed. In 2000, scientists discovered that syncytin, a protein that enables the formation of the placenta, actually originated as a viral protein that humans subsequently ‘borrowed’2. That original viral protein enables the retrovirus to fuse with host cells, depositing its entire genome into the safe harbour of the cytoplasm. Syncytin has changed little from this ancestral protein form; it directs certain placental cells to fuse with cells in the mother’s uterus, forming the outer layer of the placenta. © 2016 Macmillan Publishers Limited
By Karen Weintraub Researchers have long believed that problems with mitochondria—the power plants of cells—underlie some cases of Parkinson’s disease. Now a new study details those problems, and suggests that they may form a common thread linking previously unexplained cases of the disease with those caused by different genetic anomalies or toxins. Finding a common mechanism behind different suspected causes of Parkinson’s suggests that there might also be a common means to measure, treat or cure it, says Marco Baptista, research director at the nonprofit Michael J. Fox Foundation, a leading center for study and advocacy in the fight against Parkinson’s. The study, published Thursday in Cell Stem Cell, did identify a possible way to reverse the damage of Parkinson’s—but only in individual cells and fruit flies. Finding a treatment that does the same thing in people will be challenging, Baptista says. Roughly one million Americans have Parkinson’s disease, which is characterized by motor problems and can cause other symptoms including cognitive and gastrointestinal difficulties. About 1 to 2 percent of cases are linked to mutations in the LRRK2 gene, with far fewer associated with genes known as PINK1 and Parkin. Exposure to environmental factors such as toxic chemicals can also lead to Parkinson’s, although most cases have no obvious cause. In the new paper Xinnan Wang, an assistant professor of neurosurgery at Stanford University, and her colleagues show that mitochondria are underpowered in several types of Parkinson’s and that these mitochondria also release toxic chemicals. Looking at fly models of the disease as well as cells taken from patients, the researchers found that they could correct these problems and reverse neurodegeneration if they reduced levels of a protein involved in mitochondrial activity. © 2016 Scientific American
Link ID: 22642 - Posted: 09.10.2016
By Abby Olena Mammalian prions are notoriously difficult as structural biology subjects, given their insolubility and tendency to aggregate. Researchers have now overcome these challenges to figure out the preliminary structure of a shortened form of infectious prion (PrPSc), which they report today (September 8) in PLOS Pathogens. “For the first time, we have a structure of an infectious mammalian prion,” said Giuseppe Legname of Scuola Internazionale Superiore di Studi Avanzati in Trieste, Italy, who was not involved in this study. “It’s a very important paper,” he added. “What we have done is to obtain a very simple, very preliminary idea of what the structure of these mammalian prions are,” said study coauthor Jesús Requena of the University of Santiago de Compostela in Spain. Requena and colleagues generated a shortened form of PrPSc by injecting a laboratory strain of prions into transgenic mice that express a truncated form of normal cellular prion protein (PrPC), which lacks the attachment of a membrane anchor present in full-length PrPSc. In nature, PrPC transforms into full-length PrPSc, which causes Creutzfeldt-Jakob disease in humans, scrapie in sheep, and mad cow disease. The absence of the membrane anchor in shortened PrPSc from the transgenic mice allowed the researchers to isolate a fairly homogeneous population of PrPSc. They confirmed that this population was infectious by inoculating wild-type mice, which then developed symptoms of prion disease. © 1986-2016 The Scientist
Link ID: 22638 - Posted: 09.10.2016
By The Scientist Staff Growing up, we learn that there are five senses: sight, smell, touch, taste, and hearing. For the past five years, The Scientist has taken deep dives into each of those senses, explorations that revealed diverse mechanisms of perception and the impressive range of these senses in humans and diverse other animals. But as any biologist knows, there are more than just five senses, and it’s difficult to put a number on how many others there are. Humans’ vestibular sense, for example, detects gravity and balance through special organs in the bony labyrinth of the inner ear. Receptors in our muscles and joints inform our sense of body position. (See “Proprioception: The Sense Within.”) And around the animal kingdom, numerous other sense organs aid the perception of their worlds. The comb jelly’s single statocyst sits at the animal’s uppermost tip, under a transparent dome of fused cilia. A mass of cells called lithocytes, each containing a large, membrane-bound concretion of minerals, forms a statolith, which sits atop four columns called balancers, each made up of 150–200 sensory cilia. As the organism tilts, the statolith falls towards the Earth’s core, bending the balancers. Each balancer is linked to two rows of the ctenophore’s eight comb plates, from which extend hundreds of thousands of cilia that beat together as a unit to propel the animal. As the balancers bend, they adjust the frequency of ciliary beating in their associated comb plates. “They’re the pacemakers for the beating of the locomotor cilia,” says Sidney Tamm, a researcher at the Marine Biological Laboratory in Woods Hole, Massachusetts, who has detailed the structure and function of the ctenophore statocyst (Biol Bull, 227:7-18, 2014; Biol Bull, 229:173-84, 2015). © 1986-2016 The Scientist
By CATHERINE SAINT LOUIS In seven countries that recently experienced Zika outbreaks, there were also sharp increases in the numbers of people suffering from a form of temporary paralysis, researchers reported Wednesday. The analysis, published online in The New England Journal of Medicine, adds to substantial evidence that Zika infections — even asymptomatic ones — may bring on a paralysis called Guillain-Barré syndrome. The syndrome can be caused by a number of other factors, including infection with other viruses. Researchers studying the Zika epidemic in French Polynesia had estimated that roughly 1 in 4,000 people infected with the virus could develop the syndrome. The Centers for Disease Control and Prevention has said that the Zika virus is “strongly associated” with Guillain-Barré, but has stopped short of declaring it a cause of the condition. The new data suggest a telling pattern: Each country in the study saw unusual increases in Guillain-Barré that coincided with peaks in Zika infections, the researchers concluded. “It’s pretty obvious that in all seven sites there is a clear relationship,” said Dr. Marcos A. Espinal, the study’s lead author and the director of communicable diseases at the Pan American Health Organization, which collected data on confirmed and suspected cases of Zika infection and on the incidence of Guillain-Barré. “Something is going on.” In Venezuela, officials expected roughly 70 cases of Guillain-Barré from December 2015 to the end of March 2016, as mosquitoes were spreading the virus. Instead, there were 684 cases. Similarly, during five months in which the Zika virus was circulating in Colombia, officials recorded 320 cases of Guillain-Barré when there should have been about 100. From September 2015 to March 2016, while Zika infections peaked in El Salvador, cases of Guillain-Barré doubled to 184 from 92. © 2016 The New York Times Company
Keyword: Movement Disorders
Link ID: 22618 - Posted: 09.01.2016
By Kas Roussy, In a room at Sunnybrook Health Sciences Centre in Toronto, Brian Smith gives one last hug to his wife, Noreen. "You're doing really well, sweetheart," he says to her. Doctors have finished prepping the 76-year-old patient. She's clad in a blue hospital gown, her head has been shaved and metallic headgear is attached to her skull. Google's latest a spoon that steadies tremors New technology could help seniors stay independent longer She's ready to be wheeled into an MRI room, where she'll undergo a procedure that her doctors believe will revolutionize the way brain diseases are treated. Before that happens, Noreen leans into her husband for a kiss. "Best buddy," she whispers. Noreen Smith is among the three per cent of the Canadian population who suffer from a nervous system disorder called essential tremor. It causes uncontrollable shaking, most often in a person's hands. Smith noticed the first signs when she was 33. "It started developing in my dominant hand, which is my right hand," she said the day before her medical procedure from her home in Bobcaygeon, Ont. She went to a specialist who delivered the diagnosis: essential tremor. Media placeholder Smith ‘really, really excited’ about treatment’s potential0:48 Just as shocking was what he said next, alluding to a high-profile actor who had the condition. "This particular person wasn't terribly helpful because he said: 'Do you happen to know Katharine Hepburn? I'm going to give you some medication, and you can go home and get used to the idea that eventually you're going to end up looking like Katharine Hepburn.' I was devastated," says Smith. Medication helped for the first few years. But Smith's tremor was still severe and like others who suffer from this disorder, the shaking worsened with simple movements or everyday tasks like applying makeup or pouring a glass of water. ©2016 CBC/Radio-Canada.
Keyword: Movement Disorders
Link ID: 22603 - Posted: 08.25.2016
Researchers may have discovered a method of detecting changes in the eye which could identify Parkinson's disease before its symptoms develop. Scientists at University College London (UCL) say their early animal tests could lead to a cheap and non-invasive way to spot the disease. Parkinson's affects 1 in 500 people and is the second most common neurodegenerative disease worldwide. The charity Parkinson's UK welcomed the research as a "significant step". The researchers examined rats and found that changes could be seen at the back of their eyes before visible symptoms occurred. Professor Francesca Cordeiro who led the research said it was a "potentially revolutionary breakthrough in the early diagnosis and treatment of one of the world's most debilitating diseases". "These tests mean we might be able to intervene much earlier and more effectively treat people with this devastating condition." Symptoms of Parkinson's include tremors and muscle stiffness, slowness of movement and a reduced quality of life. These symptoms usually only emerge after brain cells have been damaged. But there is currently no brain scan, or blood test, that can definitively diagnose Parkinson's disease. Parkinson's does not directly cause people to die, but symptoms do get worse over time. © 2016 BBC
Link ID: 22577 - Posted: 08.20.2016
Dean Burnett A lot of people, when they travel by car, ship, plane or whatever, end up feeling sick. They’re fine before they get into the vehicle, they’re typically fine when they get out. But whilst in transit, they feel sick. Particularly, it seems, in self-driving cars. Why? One theory is that it’s due to a weird glitch that means your brain gets confused and thinks it’s being poisoned. This may seem surprising; not even the shoddiest low-budget airline would get away with pumping toxins into the passengers (airline food doesn’t count, and that joke is out of date). So where does the brain get this idea that it’s being poisoned? Despite being a very “mobile” species, humans have evolved for certain types of movement. Specifically, walking, or running. Walking has a specific set of neurological processes tied into it, so we’ve had millions of years to adapt to it. Think of all the things going on in your body when you’re walking, and how the brain would pick up on these. There’s the steady thud-thud-thud and pressure on your feet and lower legs. There’s all the signals from your muscles and the movement of your body, meaning the motor cortex (which controls conscious movement of muscles) and proprioception (the sense of the arrangement of your body in space, hence you can know, for example, where your arm is behind your back without looking at it directly) are all supplying particular signals. © 2016 Guardian News and Media Limited
By Robin Wylie Scientists have been searching for a genetic explanation for athletic ability for decades. So far their efforts have focused largely on genes related to physical attributes, such as muscular function and aerobic efficiency. But geneticists have also started to investigate the neurologicalbasis behind what makes someone excel in sports—and new findings implicate dopamine, a neurotransmitter responsible for the feelings of reward and pleasure. Dopamine is also involved in a host of other mental functions, including the ability to deal with stress and endure pain. Consequently, the new research supports the idea that the mental—not just the physical—is what sets elite athletes above the rest. In an effort to piece together what makes a great athlete great, researchers at the University of Parma in Italy collected DNA from 50 elite athletes (ones who had achieved top scores at an Olympic Games or other international competition) and 100 nonprofessional athletes (ones who played sports regularly, but below competitive level). They then compared four genes across the two groups that had previously been suggested as linked to athletic ability: one related to muscle development, one involved with transporting dopamine in the brain, another that regulates levels of cerebral serotonin and one involved in breaking down neurotransmitters. The researchers found a significant genetic difference between the two groups in only one of the genes: the one involved in transporting dopamine. Two particular variants of this gene (called the dopamine active transporter, or DAT) were significantly more common among the elite athletes than in the control group. One variant was almost five times more prevalent in the elite group (occurring in 24 percent of the elites versus 5 percent of the rest); the other variant was approximately 1.7 times more prevalent (51 percent versus 30 percent). The results were published in Journal of Biosciences. © 2016 Scientific American
Neuroscientists peered into the brains of patients with Parkinson’s disease and two similar conditions to see how their neural responses changed over time. The study, funded by the NIH’s Parkinson’s Disease Biomarkers Program and published in Neurology, may provide a new tool for testing experimental medications aimed at alleviating symptoms and slowing the rate at which the diseases damage the brain. “If you know that in Parkinson’s disease the activity in a specific brain region is decreasing over the course of a year, it opens the door to evaluating a therapeutic to see if it can slow that reduction,” said senior author David Vaillancourt, Ph.D., a professor in the University of Florida’s Department of Applied Physiology and Kinesiology. “It provides a marker for evaluating how treatments alter the chronic changes in brain physiology caused by Parkinson’s.” Parkinson’s disease is a neurodegenerative disorder that destroys neurons in the brain that are essential for controlling movement. While many medications exist that lessen the consequences of this neuronal loss, none can prevent the destruction of those cells. Clinical trials for Parkinson’s disease have long relied on observing whether a therapy improves patients’ symptoms, but such studies reveal little about how the treatment affects the underlying progressive neurodegeneration. As a result, while there are treatments that improve symptoms, they become less effective as the neurodegeneration advances. The new study could remedy this issue by providing researchers with measurable targets, called biomarkers, to assess whether a drug slows or even stops the progression of the disease in the brain. “For decades, the field has been searching for an effective biomarker for Parkinson’s disease,” said Debra Babcock, M.D., Ph.D., program director at the NIH’s National Institute of Neurological Disorders and Stroke (NINDS).
By Helen Thomson Take a walk while I look inside your brain. Scientists have developed the first wearable PET scanner – allowing them to capture the inner workings of the brain while a person is on the move. The team plans to use it to investigate the exceptional talents of savants, such as perfect memory or exceptional mathematical skill. All available techniques for scanning the deeper regions of our brains require a person to be perfectly still. This limits the kinds of activities we can observe the brain doing, but the new scanner will enable researchers to study brain behaviour in normal life, as well providing a better understanding of the tremors of Parkinson’s disease, and the effectiveness of treatments for stroke. Positron emission tomography scanners track radioactive tracers, injected into the blood, that typically bind to glucose, the molecule that our cells use for energy. In this way, the scanners build 3D images of our bodies, enabling us to see which brain areas are particularly active, or where tumours are guzzling glucose in the body. To adapt this technique for people who are moving around, Stan Majewski at West Virginia University in Morgantown and his colleagues have constructed a ring of 12 radiation detectors that can be placed around a person’s head. This scanner is attached to the ceiling by a bungee-cord contraption, so that the wearer doesn’t feel the extra weight of the scanner. © Copyright Reed Business Information Ltd
Keyword: Brain imaging
Link ID: 22557 - Posted: 08.13.2016
David R. Jacobs, We all know that exercise improves our physical fitness, but staying in shape can also boost our brainpower. We are not entirely sure how, but evidence points to several explanations. First, to maintain normal cognitive function, the brain requires a constant supply of oxygen and other chemicals, delivered via its abundant blood vessels. Physical exercise—and even just simple activities such as washing dishes or vacuuming—helps to circulate nutrient-rich blood efficiently throughout the body and keeps the blood vessels healthy. Exercise increases the creation of mitochondria—the cellular structures that generate and maintain our energy—both in our muscles and in our brain, which may explain the mental edge we often experience after a workout. Studies also show that getting the heart rate up enhances neurogenesis—the ability to grow new brain cells—in adults. Regardless of the mechanism, mounting evidence is revealing a robust relation between physical fitness and cognitive function. In our 2014 study, published in Neurology, we found that physical activity has an extensive, long-lasting influence on cognitive performance. We followed 2,747 healthy people between the ages of 18 and 30 for 25 years. In 1985 we evaluated their physical fitness using a treadmill test: the participants walked up an incline that became increasingly steep every two minutes. On average, they walked for about 10 minutes, reaching 3.4 miles per hour at an 18 percent incline (a fairly steep hill). Low performers lasted for only seven minutes and high performers for about 13 minutes. A second treadmill test in 2005 revealed that our participants' fitness levels had declined with age, as would be expected, but those who were in better shape in 1985 were also more likely to be fit 20 years later. © 2016 Scientific American
Link ID: 22555 - Posted: 08.13.2016
Tim Radford Eight paraplegics – some of them paralysed for more than a decade by severe spinal cord injury – have been able to move their legs and feel sensation, after help from an artificial exoskeleton, sessions using virtual reality (VR) technology and a non-invasive system that links the brain with a computer. In effect, after just 10 months of what their Brazilian medical team call “brain training” they have been able to make a conscious decision to move and then get a response from muscles that have not been used for a decade. Of the octet, one has been able to leave her house and drive a car. Another has conceived and delivered a child, feeling the contractions as she did so. The extent of the improvements was unexpected. The scientists had intended to exploit advanced computing and robotic technology to help paraplegics recover a sense of control in their lives. But their patients recovered some feeling and direct command as well. The implication is that even apparently complete spinal cord injury might leave some connected nerve tissue that could be reawakened after years of inaction. The patients responded unevenly, but all have reported partial restoration of muscle movement or skin sensation. Some have even recovered visceral function and are now able to tell when they need the lavatory. And although none of them can walk unaided, one woman has been able to make walking movements with her legs, while suspended in a harness, and generate enough force to make a robot exoskeleton move. © 2016 Guardian News and Media Limited
In a global study of myasthenia gravis, an autoimmune disease that causes muscle weakness and fatigue, researchers found that surgical removal of an organ called the thymus reduced patients’ weakness, and their need for immunosuppressive drugs. The study, published in the New England Journal of Medicine, was partially funded by the National Institutes of Health. “Our results support the idea that thymectomy is a valid treatment option for a major form of myasthenia gravis,” said Gil Wolfe, M.D., Professor and Irvin and Rosemary Smith Chair of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, New York, and a leader of the study. The Thymectomy Trial in Non-Thymomatous Myasthenia Gravis Patients Receiving Prednisone (MGTX) was a randomized, controlled study conducted on 126 patients aged 18-65 between 2006 and 2012. The researchers compared the combination of surgery and immunosuppression with the drug prednisone with prednisone treatment alone. They performed extended transternal thymectomies on 57 patients. This major surgical procedure aims to remove most of the thymus, which requires opening of a patient’s chest. On average the researchers found that the combination of surgery and prednisone treatment reduced overall muscle weakness more than prednisone treatment alone. After 36 months of prednisone treatment, both groups of patients had better QMG scores, a measure of muscle strength. Scores for the patients who had thymectomies and prednisone were 2.84 points better than patients who were on prednisone alone.
Meghan Rosen Exercise may not erase old memories, as some studies in animals have previously suggested. Running on an exercise wheel doesn’t make rats forgetprevious trips through an underwater maze, Ashok Shetty and colleagues report August 2 in the Journal of Neuroscience. Exercise or not, four weeks after learning how to find a hidden platform, rats seem to remember the location just fine, the team found. The results conflict with two earlier papers that show that running triggers memory loss in some rodents by boosting the birth of new brain cells. Making new brain cells rejiggers memory circuits, and that can make it hard for animals to remember what they’ve learned, says Paul Frankland, a neuroscientist at the Hospital for Sick Children in Toronto. He has reported this phenomenon in mice, guinea pigs and degus (SN: 6/14/14, p. 7). Maybe rats are the exception, he says, “but I’m not convinced.” In 2014, Frankland and colleagues reported that brain cell genesis clears out fearful memories in three different kinds of rodents. Two years later, Frankland’s team found similar results with spatial memories. After exercising, mice had trouble remembering the location of a hidden platform in a water maze, the team reported in February in Nature Communications. Again, Frankland and colleagues pinned the memory wipeout on brain cell creation — like a chalkboard eraser that brushes away old information. The wipe seemed to clear the way for new memories to form. Shetty, a neuroscientist at Texas A&M Health Science Center in Temple, wondered if the results held true in rats, too. “Rats are quite different from mice,” he says. “Their biology is similar to humans.” |© Society for Science & the Public 2000 - 2016. All rights reserved.
Keyword: Learning & Memory
Link ID: 22510 - Posted: 08.03.2016
By Libby Copeland Don’t get him wrong: Dean Burnett loves the brain as much as the next neuroscientist. But if he’s being honest, it’s “really quite rubbish in a lot of ways,” he says. In his new book, Idiot Brain, Burnett aims to take our most prized organ down a peg or two. Burnett is most fascinated by the brain’s tendency to trip us up when it’s just trying to help. His book explores many of these quirks: How we edit our own memories to make ourselves look better without knowing it; how anger persuades us we can take on a bully twice our size; and what may cause us to feel like we’re falling and jerk awake just as we’re falling asleep. (It could have something to do with our ancestors sleeping in trees.) We caught up with Burnett, who is also a science blogger for The Guardian and a stand-up comic, to ask him some of our everyday questions and frustrations with neuroscience. Why is it that we get motion sickness when we’re traveling in a plane or a car? We haven’t evolved, obviously, to ride in vehicles; that’s a very new thing in evolutionary terms. So the main theory as to why we get motion sickness is that it’s essentially a conflict in the senses that are being relayed to the subcortical part of the brain where the senses are integrated together. The body and the muscles are saying we are still. Your eyes are saying the environment is still. The balance sense in the ears are detecting movement. The brain is getting conflicting messages from the fundamental senses, and in evolutionary terms there’s only one thing that can cause that, which is a neurotoxin. And as a result the brain thinks it’s been poisoned and what do you do when you’ve been poisoned? Throw up.
Link ID: 22508 - Posted: 08.03.2016