Chapter 5. The Sensorimotor System
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Ewen Callaway Ringo, a golden retriever born in 2003 in a Brazilian kennel, was never expected to live long. Researchers bred him and his littermates to inherit a gene mutation that causes severe muscular dystrophy. They hoped that the puppies would provide insight into Duchenne muscular dystrophy (DMD), an untreatable and ultimately fatal human disease caused by inactivation of the same gene. But Ringo’s muscles didn't waste away like his littermates', and researchers have now determined why: he was born with another mutation that seems to have protected him from the disease, according to a paper published in Cell1. Scientists hope that by studying Ringo’s mutation — which has never before been linked to muscular dystrophy — they can find new treatments for the disease. As many as 1 in 3,500 boys inherit mutations that produce a broken version of a protein called dystrophin, causing DMD. (The disease appears in boys because the dystrophin gene sits on the X chromosome, so girls must inherit two copies of the mutated gene to develop DMD.) The protein helps to hold muscle fibres together, and its absence disrupts the regenerative cycle that rebuilds muscle tissue. Eventually, fat and connective tissue replace muscle, and people with DMD often become reliant on a wheelchair before their teens. Few survive past their thirties. Some golden retriever females carry dystrophin mutations that cause a similar disease when passed onto male puppies. Dog breeders can prevent this through genetic screening. But Mayana Zatz, a geneticist at the University of São Paulo in Brazil, and her colleagues set out to breed puppies with the mutation to model the human disease. © 2015 Nature Publishing Group,
By Emily Underwood Researchers have found a way to increase how fast, and for how long, four paralyzed people can type using just their thoughts. The advance has to do with brain-machine interfaces (BCI), which are implanted in brain tissue and record hundreds of neurons firing as people imagine moving a computer cursor. The devices then use a computer algorithm to decode those signals and direct a real cursor toward words and letters on a computer screen. One of the biggest problems with BCIs is the brain itself: When the soft, squishy organ shifts in the skull, as it frequently does, it can displace the electrode implants. As a result, the movement signal extracted from neuronal firing is constantly being distorted, making it impossible for a patient to keep the cursor from drifting off course without a researcher recalibrating the instrument every 10 minutes or so. In the new study, part of a clinical trial of BCIs called BrainGate, researchers performed several software tweaks that allow the devices to self-correct in real time by calculating the writer’s intention based on the words they’ve already written. The devices can now also correct for neuronal background noise whenever a person stops typing. These improvements, demonstrated in the video above, allow BCI users to type faster and for longer periods of time, up to hours or days, the team reports today in Science Translational Medicine. Though the technology still needs to be miniaturized and wireless before it can be used outside of the lab, the new work is a big step towards BCIs that paralyzed people can use on their own at home, the scientists say. © 2015 American Association for the Advancement of Science
Link ID: 21626 - Posted: 11.12.2015
By Virginia Morell Plunge a live crab into a pot of boiling water, and it’s likely to try to scramble out. Is the crab’s behavior simply a reflex, or is it a sign of pain? Many scientists doubt that any invertebrate (or fish) feels pain because they lack the areas in the brain associated with human pain. Others argue this is an unfair comparison, noting that despite the major differences between vertebrate and invertebrate brains, their functions (such as seeing) are much the same. To get around this problem, researchers in 2014 argued that an animal could be classified as experiencing pain if, among other things, it changes its behavior in a way that indicates it’s trying to prevent further injury, such as through increased wariness, and if it shows a physiological change, such as elevated stress hormones. To find out whether crabs meet these criteria, scientists collected 40 European shore crabs (Carcinus maenas), shown in the photo above, in Northern Ireland. They placed the animals into individual tanks, and gave half 200-millisecond electrical shocks every 10 seconds for 2 minutes in their right and left legs. The other 20 crabs served as controls. Sixteen of the shocked crabs began walking in their tanks, and four tried to climb out. None of the control crabs attempted to clamber up the walls, but 14 walked, whereas six didn’t move at all. There was, however, one big physiological difference between the 16 shocked, walking crabs and the 14 control walkers, the scientists report in today’s issue of Biology Letters: Those that received electrical jolts had almost three times the amount of lactic acid in their haemolymph, a fluid that’s analogous to the blood of vertebrates—a clear sign of stress. Thus, crabs pass the bar scientists set for showing that an animal feels pain. © 2015 American Association for the Advancement of Science.
By Arlene Karidis Several years ago, Peggy Chenoweth began having excruciating cramping in her ankle. It felt severely sprained and as if her toe were twisting to the point where it was being ripped off her foot. “The pain is right here,” she told an orthopedic surgeon, “in my ankle and foot.” But the 41-year-old Gainesville, Va., resident no longer had that ankle and foot. Her leg had been amputated below the knee after a large piece of computer equipment fell off a cart, crushed her foot and caused nerve damage. Further, she insisted that since the amputation, she could feel her missing toes move. Chenoweth’s surgeon knew exactly what was going on: phantom pain. Lynn Webster, an anesthesiologist and past president of the American Academy of Pain Medicine, explains the phenomenon: “With ‘phantom pain,’ nerves that transmitted information from the brain to the now-missing body part continue to send impulses, which relay the message of pain.” It feels as if the removed part is still there and hurting, but pain is actually in the brain. The sensation ranges from annoying itching to red-hot burning. Physicians wrote about phantom pain as early as the 1860s, but U.S. research on this condition has increased recently, spurred by the surge of amputees returning from warfare in Iraq and Afghanistan and by increasing rates of diabetes. (Since 2003, nearly 1,650 service members have lost limbs, according to the Congressional Research Service. In 2010, about 73,000 amputations were performed on diabetics in the United States, according to the Centers for Disease Control and Prevention.)
Keyword: Pain & Touch
Link ID: 21620 - Posted: 11.10.2015
By Jason G. Goldman When a monkey has the sniffles or a headache, it doesn't have the luxury of popping a few painkillers from the medicine cabinet. So how does it deal with the common colds and coughs of the wildlife world? University of Georgia ecologist Ria R. Ghai and her colleagues observed a troop of more than 100 red colobus monkeys in Uganda's Kibale National Park for four years to figure out whether the rain forest provides a Tylenol equivalent. Monkeys infected with a whipworm parasite were found to spend more time resting and less time moving, grooming and having sex. The infected monkeys also ate twice as much tree bark as their healthy counterparts even though they kept the same feeding schedules. The findings were published in September in the journal Proceedings of the Royal Society B. The fibrous snack could help literally sweep the intestinal intruder out of the simians' gastrointestinal tracts, but Ghai suspects a more convincing reason. Seven of the nine species of trees and shrubs preferred by sick monkeys have known pharmacological properties, such as antisepsis and analgesia. Thus, the monkeys could have been self-medicating, although she cannot rule out other possibilities. The sick individuals were, however, using the very same plants that local people use to treat illnesses, including infection by whipworm parasites. And that “just doesn't seem like a coincidence,” Ghai says. © 2015 Scientific American,
by Laura Sanders Babies’ minds are mysterious. Thoughts might be totally different in a brain that lacks words, and sensations might feel alien in a body so new. Are babies’ perceptions like ours, or are they completely different? Even if babies could talk, words would surely fail to convey what it’s like to experience, oh, every single thing for the first time. A recent paper offers a sliver of insight into young babies’ inner lives. The study, published October 19 in Current Biology, finds an example in which 4-month-old babies are happily oblivious to the external world. The research focuses on a perceptual trick that suckers adults and 6-month-old babies alike. When the hands are crossed, people often mistake which hand feels a touch. Let’s say your left hand (now crossed over to the right side of your body) gets a tickle. Your eyes would see a hand on the right side of your body get touched — a place usually claimed by your right hand, but now occupied by your left. Those mismatches between sight, touch and expectation can thwart you from quickly and correctly saying which hand was touched. Here’s the twist: 4-month-old babies don’t fall for this trick, Andrew Bremner of Goldsmiths, University of London and his colleagues found. In the experiment, a researcher would hold infants’ legs in either a crossed position or straight, while one of two remote-controlled buzzers taped to their feet tickled one foot. The researchers then watched which foot or leg wiggled as a result. If the buzzed foot moved, that meant that the baby got it right. © Society for Science & the Public 2000 - 2015.
David Cyranoski A Chinese neuroscientist has been sacked after reporting he had used magnetic fields to control neurons and muscle cells in nematode worms (pictured), using a protein that senses magnetism. Tsinghua University in Beijing has sacked a neuroscientist embroiled in a dispute over work on a long-sought protein that can sense magnetic fields. The university has not given a specific reason for its dismissal, however, and the scientist involved, Zhang Sheng-jia, says that he will contest their action. In September, Zhang reported in the journal Science Bulletin1 that he could manipulate neurons in worms by applying a magnetic field — a process that uses a magnetic-sensing protein. But a biophysicist at neighbouring Peking University, Xie Can, who claims to have discovered the protein’s magnetic-sensing capacity and to have a paper detailing his research under review, complained that Zhang should not have published his paper before Xie’s own work appeared. Xie said that by publishing, Zhang violated an agreement that the pair had reached — although the two scientists tell different versions about the terms of their agreement, and have different explanations of how Zhang came to be working with the protein. © 2015 Nature Publishing Group
Keyword: Animal Migration
Link ID: 21608 - Posted: 11.06.2015
By SINDYA N. BHANOO Some kinds of itching can be caused by the lightest of touches, a barely felt graze that rustles tiny hairs on the skin’s surface. This type of itch is created via a dedicated neural pathway, a new study suggests. The finding, which appears in the journal Science, could help researchers better understand chronic itchiness in conditions like eczema, diabetic neuropathy, multiple sclerosis and some cancers. The study also may help researchers determine why certain patients do not respond well to antihistamine drugs. “In the future, we may have some way to manipulate neuron activity to inhibit itching,” said Quifu Ma, a neurobiologist at Harvard University and one of the study’s authors. In the study, Dr. Ma and his colleagues inhibited neurons that express a neuropeptide known as Y or NPY in mice. When these neurons were suppressed and the mice were poked with a tiny filament, they fell into scratching fits. Normally, mice would not even respond to this sort of stimuli. “We start to see skin lesions — they don’t stop scratching,” Dr. Ma said. “It’s pretty traumatic.” The neurons only seem related to itches prompted by light touching, known as mechanically induced itches. Chemical itches, like those caused by a mosquito bite or an allergic reaction, are not transmitted by the same neurons. © 2015 The New York Times Company
Keyword: Pain & Touch
Link ID: 21593 - Posted: 11.03.2015
By Hanae Armitage Fake fingerprints might sound like just another ploy to fool the feds. But the world’s first artificial prints—reported today—have even cooler applications. The electronic material, which mimics the swirling designs imprinted on every finger, can sense pressure, temperature, and even sound. Though the technology has yet to be tested outside the lab, researchers say it could be key to adding sensation to artificial limbs or even enhancing the senses we already have. “It’s an interesting piece of work,” says John Rogers, materials scientist at the University of Illinois, Urbana-Champaign, who was not involved in the study. “It really adds to the toolbox of sensor types that can be integrated with the skin.” Electronic skins, known as e-skins, have been in development for years. There are several technologies used to mimic the sensations of real human skin, including sensors that can monitor health factors like pulse or temperature. But previous e-skins have been able to “feel” only two sensations: temperature and pressure. And there are additional challenges when it comes to replicating fingertips, especially when it comes to mimicking their ability to sense even miniscule changes in texture, says Hyunhyub Ko, a chemical engineer at Ulsan National Institute of Science and Technology in South Korea. So in the new study, Ko and colleagues started with a thin, flexible material with ridges and grooves much like natural fingerprints. This allowed them to create what they call a “microstructured ferroelectric skin” The e-skin’s perception of pressure, texture, and temperature all come from a highly sensitive structure called an interlocked microdome array—the tiny domes sandwiched in the bottom two layers of the e-skin, also shown in the figure below. © 2015 American Association for the Advancement of Science
Laura Sanders A fly tickling your arm hair can spark a maddening itch. Now, scientists have spotted nerve cells in mice that curb this light twiddling sensation. If humans possess similar itch-busters, the results, published in the Oct. 30 Science, could lead to treatments for the millions of people who suffer from intractable, chronic itch. For many of these people, there are currently no good options. “This is a major problem,” says clinician Gil Yosipovitch of Temple University School of Medicine in Philadelphia and director of the Temple Itch Center. The new study shows that mice handle an itch caused by a fluttery touch differently than other kinds of itch. This distinction “seems to have clinical applications that clearly open our field,” Yosipovitch says. In recent years, scientists have made progress teasing apart the pathways that carry itchy signals from skin to spinal cord to brain (SN: 11/22/2008, p. 16). But those itch signals often originate from chemicals, such as those delivered by mosquitoes. All that’s needed to spark a different sort of itch, called mechanical itch, is a light touch on the skin. The existence of this kind of itch is no surprise, Yosipovitch says. Mechanical itch may help explain why clothes or even dry, scaly skin can be itchy. The new finding came from itchy mice engineered to lack a type of nerve cell in their spinal cords. Without prompting, these mice scratched so often that they developed sore bald patches on their skin. © Society for Science & the Public 2000 - 2015
Keyword: Pain & Touch
Link ID: 21587 - Posted: 10.31.2015
Adam Cole Watch a scary movie and your skin crawls. Goose bumps have become so associated with fear that the word is synonymous with thrills and chills. But what on earth does scary have do to with chicken-skin bumps? For a long time, it wasn't well understood. Physiologically, it's fairly simple. Adrenaline stimulates tiny muscles to pull on the roots of our hairs, making them stand out from our skin. That distorts the skin, causing bumps to form. Call it horripilation, and you'll be right — bristling from cold or fear. Charles Darwin once investigated goose bumps by scaring zoo animals with a stuffed snake. He argued for the now accepted theory that goose bumps are a vestige of humanity's ancient past. Our ancestors were hairy. Goose bumps would have fluffed up their hair. When they were scared, that would have made them look bigger — and more intimidating to attackers. When they were cold, that would have trapped an insulating layer of air to keep them warm. We modern humans still get goose bumps when we're scared or cold, even though we've lost the advantage of looking scarier or staying warmer ourselves. And researchers have found that listening to classical music (or Phil Collins), seeing pictures of children or drinking a sour drink can also inspire goose bumps. There's clearly a link with emotion and reward, too. © 2015 npr
By Diana Kwon Six years before her husband was diagnosed with Parkinson’s disease, a progressive neurodegenerative disorder marked by tremors and movement difficulties, Joy Milne detected a change in his scent. She later linked the subtle, musky odor to the disease when she joined the charity Parkinson’s UK and met others with the same, distinct smell. Being one of the most common age-related disorders, Parkinson’s affects an estimated seven million to 10 million people worldwide. Although there is currently no definitive diagnostic test, researchers hope that this newly found olfactory signature will lead help create one. Milne, a super-smeller from Perth, Scotland, wanted to share her ability with researchers. So when Tilo Kunath, a neuroscientist at the University of Edinburgh, gave a talk during a Parkinson’s UK event in 2012, she raised her hand during the Q&A session and claimed she was able to smell the disease. “I didn’t take her seriously at first,” Kunath says. “I said, ‘No, I never heard of that, next question please.’” But months later Kunath shared this anecdote with a colleague and received a surprising response. “She told me that that lady wasn’t wrong and that I should find her,” Kunath says. Once the researchers found Milne, they tested her claim by having her sniff 12 T-shirts: six that belonged to people with Parkinson’s and six from healthy individuals. Milne correctly identified 11 out of 12, but miscategorized one of the non-Parkinson’s T-shirts in the disease category. It turned out, however, she was not wrong at all—that person would be diagnosed with Parkinson’s less than a year later. © 2015 Scientific American
By Diana Kwon | In the human form of mad cow disease, called Creutzfeldt-Jakob, a person's brain deteriorates—literally developing holes that cause rapidly progressing dementia. The condition is fatal within one year in 90 percent of cases. The culprits behind the disease are prions—misfolded proteins that can induce normal proteins around them to also misfold and accumulate. Scientists have known that these self-propagating, pathological proteins cause some rare brain disorders, such as kuru in Papua New Guinea. But growing evidence suggests that prions are at play in many, if not all, neurodegenerative disorders, including Alzheimer's, Huntington's and Parkinson's, also marked by aggregations of malformed proteins. Until recently, there was no evidence that the abnormal proteins found in people who suffer from these well-known diseases could be transmitted directly from person to person. The tenor of that discussion suddenly changed this September when newly published research in the journal Nature provided the first hint such human-to-human transmission may be possible. (Scientific American is part of Springer Nature.) For the study, John Collinge, a neurologist at University College London, and his colleagues conducted autopsies on eight patients who died between the ages of 36 and 51 from Creutzfeldt-Jakob. All the subjects had acquired the disease after treatment with growth hormone later found to be contaminated with prions. The surprise came when the researchers discovered that six of the brains also bore telltale signs of Alzheimer's—in the form of clumps of beta-amyloid proteins, diagnostic for the disease—even though the patients should have been too young to exhibit such symptoms. © 2015 Scientific American,
by Helen Thompson Five, six, seven, eight! All together now, let's spread those jazz hands and get moving, because synchronized dancing improves our tolerance of pain and helps us bond as humans, researchers suggest October 28 in Biology Letters. A team of psychologists at the University of Oxford taught high school students varied dance routines — each requiring different levels of exertion and synchronized movement — and then tested their pain tolerance with the sharp squeeze of a blood pressure cuff. Statistically, routines with more coordinated choreography and full body movement produced higher pain thresholds and sunny attitudes toward others in the group. Coordinated dancing with a group and exerting more energy may independently promote the release of pain-blocking endorphins as well as increase social bonding, the team writes. |© Society for Science & the Public 2000 - 2015
Keyword: Pain & Touch
Link ID: 21575 - Posted: 10.28.2015
By Hanae Armitage CHICAGO, ILLINOIS—Huntingtons disease, a neurological condition caused by brain-destroying mutant proteins, starts with mood swings and twitching and ends in dementia and death. The condition, which afflicts about 30,000 Americans, has no cure. But now, a new gene-editing method that many believe will lead to a Nobel Prize has been shown to effectively halt production of the defective proteins in mice, leading to hope that a potent therapy for Huntingtons is on the distant horizon. That new method is CRISPR, which uses RNA-guided enzymes to snip out or add segments of DNA to a cell. In the first time it has been applied to Huntingtons disease, CRISPR’s results are “remarkably encouraging,” says neuroscientist Nicole Déglon of the University of Lausanne in Switzerland, who led the mouse study, results of which she and her co-researcher Nicolas Merienne shared yesterday at the Society for Neuroscience Conference in Chicago, Illinois. As neurological diseases go, Huntingtons is an ideal candidate for CRISPR therapy, because the disease is determined by a single gene, Déglon notes. A mutation in the gene, which codes for a normally helpful brain protein called huntingtin, consists of different numbers of “tandem repeats,” repeating segments of DNA that cause the protein to fold into a shape that is toxic to the brain. Déglon and her team wondered whether CRISPR could halt production of this dangerous molecule. Using a virus as a delivery vehicle, the researchers infected two separate groups of healthy adult mice with a mutant huntingtin gene, but only one group received the therapy: a CRISPR “cassette,” which includes DNA for the gene-editing enzyme Cas9 and the RNA to target the huntingtin gene. © 2015 American Association for the Advancement of Science
Link ID: 21538 - Posted: 10.21.2015
Alan Hoffman says nilotinib has changed his life. Just weeks after he started taking the drug in a clinical trial, he began to feel himself recovering from his Parkinson’s disease. The retired professor of social science first started to show the signs of Parkinson’s in 1997. Over the years, his symptoms worsened. “I couldn’t get out of bed without my wife,” Hoffman says. Once a prolific reader, devouring four or five books a week, Hoffman found himself unable to keep his attention on even a short magazine article. His body became increasingly rigid, and he started to lose his sense of balance. “I fell a lot,” he says. And it affected his social life. The disorder was such a struggle, Hoffman says he considered taking his own life. He tried a range of medications, which eased his symptoms to varying degrees. In 2008, he had surgery to implant an electrode into his brain. The deep brain stimulation that followed helped with the rigidity, he says. But deep brain stimulation doesn’t offer a cure – the brain cells continue to die. So Hoffman agreed to join a six-month clinical trial of nilotinib – a drug typically used to treat leukaemia. Nilotinib blocks a protein that interferes with lysosomes – cell structures that destroy harmful proteins. Researchers behind the trial think that nilotinib can free up lysosomes to do a better job of clearing out proteins associated with Parkinson’s disease. (For a full report on the effect of the drug see “People with Parkinson’s walk again after promising drug trial”.) © Copyright Reed Business Information Ltd.
Link ID: 21537 - Posted: 10.21.2015
Mr Tickle can’t bamboozle a baby. Unlike grown-ups, young infants don’t let the positioning of their bodies confuse their sense of touch. If adults who can see are touched on each hand in quick succession while their hands are crossed, they can find it hard to name which hand was touched first. Adults who have been blind from birth don’t have this difficulty, but people who become blind later in life have the same trouble as those who can still see. “That suggests that early on in life, something to do with visual experience is crucial in setting up a typical way of perceiving touch,” says Andrew Bremner at Goldsmiths, University of London. To investigate how this develops in infancy, Bremner and his colleagues compared how babies reacted to having one foot tickled. With their legs crossed over, babies aged 6 months moved the foot being tickled half of the time. But 4-month-olds did better, moving the tickled foot 70 per cent of the time – as often as they did with their legs uncrossed. The team concludes that at 4 months, babies haven’t yet learned to relate what they touch to the physical space that their body occupies. For many adults, the concept might be difficult to envision. “It’s like imagining that you feel a touch on your body, but not really knowing how that’s related to what you’re looking at,” says Bremner. “It’s almost like you have multiple sensory worlds: a visual world, an auditory world and a tactile world, which are separate and not combined in space.” © Copyright Reed Business Information Ltd.
An expensive cancer drug may reverse late-stage Parkinson’s disease, enabling participants in a small clinical trial to speak and walk again for the first time in years. While there are several treatments for the symptoms of Parkinson’s, if confirmed this would be the first time a drug has worked on the causes of the disease. “We’ve seen patients at end stages of the disease coming back to life,” says Charbel Moussa of Georgetown University Medical Center in Washington DC, who led the trial. The drug, called nilotinib, works by boosting the brain’s own “garbage disposal system” to clear proteins that accumulate in the brains of people with Parkinson’s disease, says Moussa. These proteins are thought to trigger the death of brain cells that make molecules like dopamine that are needed for movement and other functions. Nilotinib is already approved to treat cancer – it blocks a protein that drives chronic myeloid leukaemia. It also blocks another protein that interferes with lysosomes – cell structures that destroy harmful proteins. Moussa thinks that nilotinib can free up lysosomes to do a better job of clearing out proteins associated with Parkinson’s disease. Tests in animals showed promise, so Moussa, his colleague Fernando Pagan and their team set up a small trial of 12 volunteers with Parkinson’s disease or a similar condition called dementia with Lewy bodies. The trial was designed to test only the safety of the oral drug, which was given as a daily dose for six months. © Copyright Reed Business Information Ltd.
Link ID: 21528 - Posted: 10.20.2015
Three teams of scientists supported by the National Institutes of Health showed that a genetic mutation linked to some forms of amyotrophic lateral sclerosis (ALS) and frontotemporal degeneration (FTD) may destroy neurons by disrupting the movement of materials in and out of the cell’s nucleus, or command center where most of its DNA is stored. The results, published in the journals Nature and NatureNeuroscience, provide a possible strategy for treating the two diseases. “This research shines a spotlight on the role of nuclear transport in the health of neurons,” said Amelie Gubitz, Ph.D., program director at the NIH’s National Institute of Neurological Disorders and Stroke (NINDS). “The results provide new insights into how this mutation derails an essential process in neurons and opens new avenues for therapy development.” Both ALS and FTD are caused by the death of specific neurons. In ALS, this leads to movement difficulties and eventually paralysis, while in FTD, patients experience problems with language and decision making. Past research has connected a specific mutation in the C9orf72 gene to 40 percent of inherited ALS cases and 25 percent of inherited FTD cases, as well as nearly 10 percent of non-inherited cases of each disorder. The recent experiments, conducted in yeast, fruit flies, and neurons from patients, found that the mutation prevents proteins and genetic material called RNA from moving between the nucleus and the cytoplasm that surrounds it. “At the end of the day, this culminates in a defect in the flow of genetic information, which leads to problems expressing genes in the right place at the right time,” said J. Paul Taylor, M.D., Ph.D., a researcher at St. Jude’s Children’s Research Hospital in Memphis, Tennessee, and the senior author of one of the papers.
Keyword: ALS-Lou Gehrig's Disease
Link ID: 21524 - Posted: 10.17.2015
By Robert F. Service Prosthetic limbs may work wonders for restoring lost function in some amputees, but one thing they can’t do is restore an accurate sense of touch. Now, researchers report that one day in the not too distant future, those artificial arms and legs may have a sense of touch closely resembling the real thing. Using a two-ply of flexible, thin plastic, scientists have created novel electronic sensors that send signals to the brain tissue of mice that closely mimic the nerve messages of touch sensors in human skin. Multiple research teams have long worked on restoring touch to people with prosthetic limbs. 2 years ago, for example, a group at Case Western Reserve University in Cleveland, Ohio, reported giving people with prosthetic hands a sense of touch by wiring pressure sensors on the hands to peripheral nerves in their arms. Yet although these advances have restored a rudimentary sense of touch, the sensors and signals are very different from those sent by mechanoreceptors, natural touch sensors in the skin. For starters, natural mechanoreceptors put out what amounts to a digital signal. When they sense pressure, they fire a stream of nerve impulses; the more pressure, the higher the frequency of pulses. But previous tactile sensors have been analogue devices, where more pressure produces a stronger electrical signal, rather than a more frequent stream of pulses. The electrical signals must then be sent to another processing chip that converts the strength of the signals to a digital stream of pulses that is only then sent on to peripheral nerves or brain tissue. © 2015 American Association for the Advancement of Science.