Chapter 5. The Sensorimotor System

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By DAVID C. ROBERTS Five years ago, I still lived a double life. I was 35, looking out over the Gulf of Thailand and a few weathered beach tenders. Inside, where dark suits filled the conference room, I could feel the eyes of my fellow diplomats. No doubt they were wondering why I was sitting on my briefcase. I joked to no one in particular “My nuclear codes,” trying to deflect awkwardness. The case actually concealed an orthotic sitting cushion that muffled the pain in my lower back; without it, silent shrieking was all I heard. Or maybe they had noticed I was the only one sweating. The air-conditioning tempered the tropical heat, but it was no match for the corset heat wrap that lay discreetly under my tailored suit. Over the previous decade I had become adept at hiding the unexplained pain that racked my back and joints. To all appearances, I was a fit 6-foot-3 man with an easy gait. No one in that conference room knew my suit pants disguised a lace-up ankle brace and a strap velcroed around my left knee. Nor did they know that during breaks I would sneak back to my hotel room where my wife, an artist who moonlighted as my one-person pit crew, waited to press my quadratus lumborum muscle back into submission. I lasted through that meeting as I had through countless others. But in the months that followed, sitting and walking became increasingly difficult. I started to stand during meetings, avoid plane travel, and take motorcycle taxis to go just a couple of buildings’ distance. Eventually, I let the doctors at the embassy in on my secret. They deemed me unfit for work and medevac’ed me from Bangkok back to the United States for treatment. I left quickly, without awkward explanations or goodbyes. © 2017 The New York Times Company

Keyword: Pain & Touch
Link ID: 23908 - Posted: 08.02.2017

Ashlie Stevens Ah, the brain freeze — the signature pain of summer experienced by anyone who has eaten an ice cream cone with too much enthusiasm or slurped down a slushie a little too quickly. But have you ever stopped mid-freeze to think about why our bodies react like this? Well, researchers who study pain have, and some, like Dr. Kris Rau of the University of Louisville in Kentucky, say it's a good way to understand the basics of how we process damaging stimuli. But first, a lesson in terminology. "There's a scientific medical term for ice cream headaches which is sphenopalatine ganglion neuralgia," Rau says. Try breaking that out at your next ice cream social. Anyway, to understand how brain freeze happens, it helps to think of your body and brain as a big computer where everything is hooked together. In this case, you see an ice cream truck. You get some ice cream. And then your brain gives you the go-ahead and you dive face-first into a double-scoop of mint chocolate chip. "Now on the roof of your mouth there are a lot of little blood vessels, capillaries," Rau says. "And there's a lot of nerve fibers called nociceptors that detect painful or noxious stimuli." The rush of cold causes those vessels to constrict. "And when that happens, it happens so quickly that all of those little pain fibers in the roof of your mouth — they interpret that as being a painful stimulus," Rau says. A message is then shot up to your brain via the trigeminal nerve, one of the major nerves of the facial area. The brain itself doesn't have any pain sensing fibers, but its covering — called the meninges — does. © 2017 npr

Keyword: Pain & Touch
Link ID: 23901 - Posted: 08.01.2017

By Diana Kwon Like humans, some golden retrievers develop Duchenne muscular dystrophy (DMD), a hereditary muscle wasting condition that begins early in life. Using gene therapy, scientists were able to restore muscle function in dogs with the disease, according to a study published today (July 25) in Nature Communications. Researchers injected microdystrophin, a shortened version of the dystrophin gene that individuals with DMD lack, into 12 dogs with the disease. The treatment led to improved muscle function in those animals for more than two years. “This preclinical study demonstrates the safety and efficacy of microdystrophin, and makes it possible to consider developing a clinical trial in patients,” study coauthor Caroline Le Guiner of the Université de Nantes in France, says in a statement. “Indeed, this is the first time that it has been possible to treat the whole body of a large-sized animal with this protein.” Scientists have also used CRISPR to correct the disease-causing mutations in mouse models of DMD and in the cells of a human patient with the condition. “This [study] is very encouraging, as current treatments for muscular dystrophy are merely palliative and patients are under constant medical care throughout their life,” John Counsell, a research associate at University College London who was not involved in the study, in a statement published by the Science Media Center. “Further preclinical trials will be required to show that this treatment can be effective in patients.” © 1986-2017 The Scientist

Keyword: Movement Disorders; Muscles
Link ID: 23883 - Posted: 07.27.2017

By Andrew Wagner Although it’s a far cry from the exosuits of science fiction, researchers have developed a robotic exoskeleton that can help stroke victims regain use of their legs. Nine out of 10 stroke patients are afflicted with partial paralysis, leaving some with an abnormal gait. The exosuit works by pulling cords attached to a shoe insole, providing torque to the ankle and correcting the abnormal walking motion. With the suit providing assistance to their joints, the stroke victims are able to maintain their balance, and walk similarly to the way they had prior to their paralysis, the team reports today in Science Translational Medicine. The exosuit is an adaptation of a previous design developed for the Defense Advanced Research Projects Agency Warrior Web program, a Department of Defense plan to develop assistive exosuits for military applications. Although similar mechanical devices have been built in the past to assist in gait therapy, these were bulky and had to be kept tethered to a power source. This new suit is light enough that with a decent battery, it could be used to help patients walk over terrain as well, not just on a treadmill. The researchers say that although the technology needs long-term testing, it could start to decrease the time it takes for stroke patients to recover in the near future. © 2017 American Association for the Advancement of Science

Keyword: Robotics
Link ID: 23881 - Posted: 07.27.2017

By Aylin Woodward Keep your head up. Today, navigating the urban jungle can be challenging, with uneven sidewalks and errant kerbs presenting obstacles to easy walking. So why do we rarely trip up even though we hardly ever give walking our full attention? It seems that all we need is a brief glimpse of what’s coming next on the road in front of us, just one step ahead of time, to keep up upright. Humans have a unique kind of locomotion – we’re bipedal, meaning we move around on two legs rather than four. Scientists are still struggling to unravel the mystery behind our shift to two legs – for instance, some suggest it freed up our hands to carry food. Others point out that our human gait is much more energetically efficient. Our walking style exploits external forces like gravity and inertia to use as little muscular energy as possible so that we actually fall forward onto the lifted foot with each step. Jonathan Samir Matthis at the University of Texas at Austin wanted to know how we aim and control this forward motion – particularly since the way ahead is rarely level and obstacle-free. “We have to be much more careful about where we place our feet than we would if we had four legs on the ground,” he says. “Because if we do it wrong, there’s serious consequences like breaking your leg.” © Copyright New Scientist Ltd.

Keyword: Movement Disorders; Attention
Link ID: 23872 - Posted: 07.25.2017

By Diana Kwon Using CRISPR, researchers have successfully treated congenital muscular dystrophy type 1A (MDC1A), a rare disease that can lead to severe muscle wasting and paralysis, in mice. The team was able to restore muscle function by correcting a splicing site mutation that causes the disorder, according to a study published today (July 17) in Nature Medicine. “Instead of inserting the corrected piece of information, we used CRISPR to cut DNA in two strategic places,” study coauthor Dwi Kemaladewi, a research fellow at the Hospital for Sick Children (Sick Kids) in Toronto, explains in a statement. “This tricked the two ends of the gene to come back together and create a normal splice site.” By targeting both the skeletal muscles and peripheral nerves, the team was able to improve the animals’ motor function and mobility. “This is important because the development of therapeutic strategies for muscular dystrophies have largely focused on improving the muscle conditions,” Kemaladewi says in the release. “Experts know the peripheral nerves are important, but the skeletal muscles have been perceived as the main culprit in MDC1A and have traditionally been the focus of treatment options.” “The robustness of the correction we see in animal models to me is very encouraging,” Amy Wagers, a biologist at Harvard University who was not involved in this study, tells the Toronto Star. © 1986-2017 The Scientist

Keyword: Muscles
Link ID: 23851 - Posted: 07.19.2017

Robin McKie Observer science editor Scientists at Cambridge University have co-opted an unusual ally in their battle to find treatments for an incurable degenerative ailment that affects thousands of people in the UK. They have taken charge of a flock of merino sheep that have been genetically modified to carry the gene for Huntington’s disease. The research, led by neuroscientist Professor Jenny Morton, aims to understand how to pinpoint early symptoms of the brain condition, which affects more than 6,700 people in the UK. The gene responsible for Huntington’s was isolated more then 30 years ago but scientists have yet to develop drugs that might halt or even slow its development in patients. The brain’s complexity has defied attempts to understand how the condition develops. “Until now, much of our effort has been based on research on mice or rats,” said Morton. “But sheep should make better research subjects. Not only do they live much longer than rodents, their brains are larger and closer in size and structure to humans.” Huntington’s disease, which affects men and women equally, is an inherited neurological condition whose symptoms manifest themselves in adulthood, usually between 35 and 55. Initially mood, personality, coordination and memory are affected but, as the disease progresses, speech, swallowing and motor function deteriorate until death occurs 10 to 25 years after symptoms first appear. There is no known cure for Huntington’s disease although there are treatments to manage symptoms. © 2017 Guardian News and Media Limited

Keyword: Huntingtons
Link ID: 23816 - Posted: 07.09.2017

By Meredith Wadman The hallmark brain damage in Parkinson’s disease is thought to be the work of a misfolded, rogue protein that spreads from brain cell to brain cell like an infection. Now, researchers have found that the normal form of the protein—α-synuclein (αS)—may actually defend the intestines against invaders by marshaling key immune cells. But chronic intestinal infections could ultimately cause Parkinson’s, the scientists suggest, if αS migrates from overloaded nerves in the gut wall to the brain. “The gut-brain immune axis seems to be on a cusp of an explosion of new insights, and this work offers an exceptionally exciting new hypothesis,” says Charles Bevins, an expert in intestinal immunity at the University of California, Davis, who was not involved with the study. The normal function of αS has long been a mystery. Though the protein is known to accumulate in toxic clumps in the brain and the nerves of the gut wall in patients with Parkinson’s disease, no one was sure what it did in healthy people. Noting that a region of the αS molecule behaves similarly to small, microbe-targeting proteins that are part of the body’s immune defenses, Michael Zasloff, an immunologist at Georgetown University Medical Center in Washington, D.C., set out to find whether αS, too, might help fend off microbial invaders. © 2017 American Association for the Advancement of Science

Keyword: Parkinsons
Link ID: 23784 - Posted: 06.28.2017

By Michael Price Contrary to popular lore that portrays chimpanzees as having “super strength,” studies have only found modest differences with humans. But our closest relatives are slightly stronger by several measures, and now a study comparing the muscle fibers of different primates reveals a potential explanation: Humans may have traded strength for endurance, allowing us to travel farther for food. To determine why chimpanzees are stronger than humans—at least on a pound-for-pound basis—Matthew O’Neill, an anatomy and evolution researcher at the University of Arizona College of Medicine in Phoenix, and colleagues biopsied the thigh and calf muscles of three chimps housed at the State University of New York at Stony Brook. They dissected the samples into individual fibers and stimulated them to figure out how much force they could generate. Comparing their measurements to known data from humans, the team found that, at the individual fiber level, muscle output was about the same. Given that different fibers throughout the muscle might make a difference, the researchers conducted a more thorough analysis of tissue samples from pelvic and hind limb muscles of three chimpanzee cadavers from various zoos and research institutes around the United States. Previous studies in mammals have found that muscle composition between trunk, forelimb, and hind limb muscles is largely the same, O’Neill says, so he’s confident the samples are representative across most of the chimp’s musculature. The team used a technique called gel electrophoresis to break down the muscles into individual muscle fibers, and compared this breakdown to human muscle fiber data. © 2017 American Association for the Advancement of Science.

Keyword: Muscles; Evolution
Link ID: 23782 - Posted: 06.27.2017

Carl Zimmer Mark D. Zabel wants to set some fires. Dr. Zabel and his colleagues are developing plans to burn plots of National Park Service land in Arkansas and Colorado. If the experiments turn out as the researchers hope, they will spare some elk and deer a gruesome death. Across a growing swath of North America, these animals are dying from a mysterious disorder called chronic wasting disease. It’s caused not by a virus or bacterium, but a deformed protein called a prion. When ingested, prions force normal proteins in the animal’s body to become deformed as well. Over the course of months, prions can gradually wreck the animal’s nervous system, ultimately killing it. This year is the 50th anniversary of the discovery of chronic wasting disease. In the September issue of Microbiology and Molecular Biology Reviews, Dr. Zabel, an immunologist at Colorado State University, and his former graduate student Aimee Ortega survey what scientists have learned about the slow-spreading plague. It makes for ominous reading. “There’s a lot that we still don’t know and don’t understand about the disease,” Dr. Zabel said in an interview. Once chronic wasting disease gets a foothold, it can spread relentlessly. It’s now documented in 24 states, and continues to expand into new ranges. In some herds, as many as half of the animals carry prions. It’s only been in recent years that scientists have gained crucial clues to how the disease spreads. Direct contact, it turns out, isn’t the only way that the prions get from one animal to another. © 2017 The New York Times Company

Keyword: Prions
Link ID: 23781 - Posted: 06.27.2017

By Natalie Grover (Reuters) - A handful of drugmakers are taking their first steps toward developing marijuana-based painkillers, alternatives to opioids that have led to widespread abuse and caused the U.S. health regulator to ask for a withdrawal of a popular drug this month. The cannabis plant has been used for decades to manage pain and there are increasingly sophisticated marijuana products available across 29 U.S. states, as well as in the District of Columbia, where medical marijuana is legal. There are no U.S. Food and Drug Administration (FDA)-approved painkillers derived from marijuana, but companies such as Axim Biotechnologies Inc, Nemus Bioscience Inc and Intec Pharma Ltd have drugs in various stages of development. The companies are targeting the more than 100 million Americans who suffer from chronic pain, and are dependent on opioid painkillers such as Vicodin, or addicted to street opiates including heroin. Opioid overdose, which claimed celebrities including Prince and Heath Ledger as victims, contributed to more than 33,000 deaths in 2015, according to the Centers for Disease Control and Prevention. Earlier this month, the FDA asked Endo International Plc to withdraw its Opana ER painkiller from the market, the first time the agency has called for the removal of an opioid painkiller for public health reasons. The FDA concluded that the drug's benefits no longer outweighed its risks. Multiple studies have shown that pro-medical marijuana states have reported fewer opiate deaths and there are no deaths related to marijuana overdose on record.(http://reut.rs/2r74Sbe) © 2017 Scientific American

Keyword: Pain & Touch; Drug Abuse
Link ID: 23774 - Posted: 06.26.2017

By Sam Wong People who have had amputations can control a virtual avatar using their imagination alone, thanks to a system that uses a brain scanner. Brain-computer interfaces, which translate neuron activity into computer signals, have been advancing rapidly, raising hopes that such technology can help people overcome disabilities such as paralysis or lost limbs. But it has been unclear how well this might work for people who have had limbs removed some time ago, as the brain areas that previously controlled these may become less active or repurposed for other uses over time. Ori Cohen at IDC Herzliya, in Israel, and colleagues have developed a system that uses an fMRI brain scanner to read the brain signals associated with imagining a movement. To see if it can work a while after someone has had a limb removed, they recruited three volunteers who had had an arm removed between 18 months and two years earlier, and four people who have not had an amputation. While lying in the fMRI scanner, the volunteers were shown an avatar on a screen with a path ahead of it, and instructed to move the avatar along this path by imagining moving their feet to move forward, or their hands to turn left or right. The people who had had arm amputations were able to do this just as well with their missing hand as they were with their intact hand. Their overall performance on the task was almost as good as of those people who had not had an amputation. © Copyright New Scientist Ltd.

Keyword: Robotics
Link ID: 23770 - Posted: 06.24.2017

By KATIE THOMAS Nolan and Jack Willis, twins from upstate New York, and just 10 other boys took part in a clinical trial that led to the approval last fall of the very first drug to treat their rare, deadly muscle disease. Now the Willis boys are again test cases as a different type of medical question comes to the fore: whether insurers will cover the controversial drug, Exondys 51, which can cost more than $1 million a year even though it’s still unclear if it works. The boys’ insurer, Excellus BlueCross BlueShield, refused to cover the cost of the drug because the twins, who are 15, can no longer walk. Their disease, Duchenne muscular dystrophy, overwhelmingly affects boys and causes muscles to deteriorate, killing many of them by the end of their 20s. “I’m cycling between rage and just sadness,” their mother, Alison Willis Hoke, said recently, on the day she learned that an appeal for coverage had been denied. For now, the company that sells the drug, Sarepta Therapeutics, is covering the treatment’s costs, but Mrs. Hoke does not know how long that will last. The desperation in Mrs. Hoke’s voice reflects a sobering reality for families of boys with the disease since their elation last fall over the drug’s approval. Because the Food and Drug Administration overruled its own experts — who weren’t convinced the Exondys 51 had shown sufficiently good results — and gave the drug conditional approval, many insurers are now declining to cover it or are imposing severe restrictions that render patients ineligible. The story of Exondys 51 raises complex and emotionally charged questions about what happens when the F.D.A. approves an expensive drug based on a lower bar of proof. In practice, health insurers have taken over as gatekeeper in determining who will get the drug. © 2017 The New York Times Company

Keyword: Muscles; Movement Disorders
Link ID: 23768 - Posted: 06.23.2017

By Alice Klein EVIDENCE that Parkinson’s disease may be an autoimmune disorder could lead to new ways to treat the illness. Parkinson’s begins with abnormal clumping of a protein called synuclein in the brain. Neighbouring dopamine-producing neurons then die, causing tremors and difficulty moving. The prevailing wisdom has been that these neurons die from a toxic reaction to synuclein deposits. However, Parkinson’s has been linked to some gene variants that affect how the immune system works, leading to an alternative theory that synuclein causes Parkinson’s by triggering the immune system to attack the brain. An argument against this theory has been that brain cells are safe from immune system attack, because most neurons don’t have antigens – the markers immune cells use to recognise a target. But by studying postmortem brain tissue samples, David Sulzer at Columbia University and his team have discovered that dopamine-producing neurons do display antigens. The team has now conducted blood tests to reveal that people with Parkinson’s show an immune response to these antigens, while people who don’t have the condition do not (Nature, DOI: 10.1038/nature22815). These findings suggest Parkinson’s may be an autoimmune disorder, in which the immune system mistakenly attacks part of the body. There have been hints before that the immune system is involved in Parkinson’s, but this is the first evidence that it plays a major pathological role, says Roger Barker at the University of Cambridge. “It would be an attractive target for therapeutic intervention,” he says. However, it isn’t clear yet if the immune response directly causes neuron death, or if it is merely a side effect of the disease. Sulzer’s team plans to try blocking the autoimmune response in Parkinson’s, to see if this can stop the disease progressing. © Copyright New Scientist Ltd.

Keyword: Parkinsons; Neuroimmunology
Link ID: 23760 - Posted: 06.22.2017

Parkinson’s disease is commonly thought of as a movement disorder, but after years of living with the disease, approximately 25 percent of patients also experience deficits in cognition that impair function. A newly developed research tool may help predict a patient’s risk for developing dementia and could enable clinical trials aimed at finding treatments to prevent the cognitive effects of the disease. The research was published in Lancet Neurology and was partially funded by the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health. “This study includes both genetic and clinical assessments from multiple groups of patients, and it represents a significant step forward in our ability to effectively model one of the most troublesome non-motor aspects of Parkinson’s disease,” said Margaret Sutherland, Ph.D., program director at the NINDS. For the study, a team of researchers led by Clemens Scherzer, M.D., combined data from 3,200 people with Parkinson’s disease, representing more than 25,000 individual clinical assessments and evaluated seven known clinical and genetic risk factors associated with developing dementia. From this information, they built a computer-based risk calculator that may predict the chance that an individual with Parkinson’s will develop cognitive deficits. Dr. Scherzer is head of the Neurogenomics Lab and Parkinson Personalized Medicine Program at Harvard Medical School and a member of the Ann Romney Center for Neurologic Diseases at Brigham and Women’s Hospital, Boston.

Keyword: Parkinsons
Link ID: 23759 - Posted: 06.22.2017

By Neuroskeptic A high-profile paper in Cell reports on a new brain stimulation method that’s got many neuroscientists excited. The new technique, called temporal interference (TI) stimulation, is said to be able to reach structures deep inside the brain, using nothing more than scalp electrodes. Currently, the only way to stimulate deep brain structures is by implanting electrodes (wires) into the brain – which is an expensive and potentially dangerous surgical procedure. TI promises to make deep brain stimulation an everyday, non-invasive tool. But will it really work? The paper comes from Nir Grossman et al. from the lab of Edward S. Boyden at MIT. Their technique is based around applying two electrical fields to the subject’s head. Each field is applied using two scalp electrodes. It is the interaction between the two fields that creates brain stimulation. Both fields oscillate at slightly different frequencies, for instance 2 kHz and 2.01 kHz. Where these fields overlap, a pattern of interference is created which oscillates with an ‘envelope’ at a much lower frequency, say 10 Hz. The frequency of the two fields is too high to have any effect on neural activity, but the interference pattern does have an effect. Crucially, while the electric fields are strongest close to the electrodes, the interference pattern is most intense at a remote point – which could be deep in the brain.

Keyword: Brain imaging; Parkinsons
Link ID: 23740 - Posted: 06.14.2017

Jon Hamilton Researchers are working to revive a radical treatment for Parkinson's disease. The treatment involves transplanting healthy brain cells to replace cells killed off by the disease. It's an approach that was tried decades ago and then set aside after disappointing results. Now, groups in Europe, the U.S. and Asia are preparing to try again, using cells they believe are safer and more effective. "There have been massive advances," says Claire Henchcliffe, a neurologist at Weill Cornell Medicine in New York. "I'm optimistic." "We are very optimistic about ability of [the new] cells to improve patients' symptoms," says Viviane Tabar, a neurosurgeon and stem cell biologist at Memorial Sloan Kettering Cancer Center in New York. Henchcliffe and Tabar joined several other prominent scientists to describe plans to revive brain cell transplants during a session Tuesday at the International Society for Stem Cell Research meeting in Boston. Their upbeat message marks a dramatic turnaround for the approach. During the 1980s and 1990s, researchers used cells taken directly from the brains of aborted fetuses to treat hundreds of Parkinson's patients. The goal was to halt the disease. © 2017 npr

Keyword: Parkinsons; Stem Cells
Link ID: 23738 - Posted: 06.14.2017

By Edd Gent There’s been a lot of hype coming out of Silicon Valley about technology that can meld the human brain with machines. But how will this help society, and which companies are leading the charge? Elon Musk, chief executive of Tesla and SpaceX, made waves in March when he announced his latest venture, Neuralink, which would design what are called brain-computer interfaces. Initially, BCIs would be used for medical research, but the ultimate goal would be to prevent humans from becoming obsolete by enabling people to merge with artificial intelligence. Musk is not the only one who’s trying to bring humans closer to machines. Here are five organizations working hard on hacking the brain. According to Musk, the main barrier to human-machine co­operation is communication bandwidth. Because using a touch screen or a keyboard is a slow way to communicate with a computer, Musk’s new venture aims to create a “high-bandwidth” link between the brain and machines. What that system would look like is not entirely clear. Words such as “neural lace” and “neural dust” have been bandied about, but all that has really been revealed is a business model. Neuralink has been registered as a medical research company, and Musk said the firm will produce a product to help people with severe brain injuries within four years. This will lay the groundwork for developing BCIs for healthy people, enabling them to communicate by “consensual telepathy,” possibly within five years, Musk said. Some scientists, particularly those in neuroscience, are skeptical of Musk’s ambitious plans. © 1996-2017 The Washington Post

Keyword: Robotics
Link ID: 23733 - Posted: 06.12.2017

By Clare Wilson Would you have pig cells implanted in your brain? Some people with Parkinson’s disease have, in the hope it will stop their disease progressing. The approach is still in the early stages of testing, but initial results from four people look promising, with all showing some improvement 18 months after surgery. People with Parkinson’s disease, which causes tremors and difficulty moving, usually get worse over time. The disease is caused by the gradual loss of brain cells that make dopamine, a compound that helps control our movements. Current medicines replace the missing dopamine, but their effectiveness wears off over the years. So Living Cell Technologies, based in Auckland, New Zealand, has been developing a treatment that uses cells from the choroid plexus in pigs. This brain structure makes a cocktail of growth factors and signalling molecules known to help keep nerve cells healthy. Last month, surgery was completed on a further 18 people in a placebo-controlled trial, using the choroid plexus cell implants. The hope is that compounds made by these cells will nourish the remaining dopamine-producing cells in the patients’ brains, slowing further loss. © Copyright New Scientist Ltd.

Keyword: Parkinsons; Stem Cells
Link ID: 23731 - Posted: 06.12.2017

By STEPH YIN European eels are born and die in the North Atlantic Ocean, but spend most of their lives in rivers or estuaries across Europe and North Africa. In between, they traverse thousands of miles of ocean, where it’s often unclear which way is up or down. Scientists have therefore long suspected that these critically endangered fish use magnetism to help guide them. A study published Friday in Science Advances shows, for the first time, that European eels might link magnetic cues with the tides to navigate. Studying juveniles during the crucial stage when they move toward land from open ocean, the authors found that eels faced different directions based on whether the tide was flowing in (flood tide) or out (ebb tide). Changing orientation might help eels take advantage of tides to travel from the ocean to the coast, and into fresh water, more efficiently, said Alessandro Cresci, a graduate student at the University of Miami and lead author of the study. Previous studies have shown that eels can detect magnetic fields, but how they use this sixth sense “has remained a matter of speculation” until now, said Michael J. Miller, an eel biologist at Nihon University in Japan who was not involved in the study. When transitioning from sea to coast, European eels are in a stage of their lives where they are about the size of a finger and transparent along their bodies, thus the name “glass eels.” Mr. Cresci’s group studied glass eels from the coast of Norway, observing the animals in the field by putting 54 slippery, see-through eels, one by one, in a drifting chamber equipped with cameras and compasses. When the tide ebbed, these animals generally faced south, but when it flowed in, they showed no consistent orientation. The researchers then studied 49 of the same eels in laboratory tanks. They subjected some of the eels to reoriented magnetic fields, rotating magnetic north to the east, south or west. © 2017 The New York Times Company

Keyword: Animal Migration
Link ID: 23728 - Posted: 06.12.2017