Chapter 8. General Principles of Sensory Processing, Touch, and Pain
Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.
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.
Nicola Davis Tyrannosaur, Breaking the Waves and Schindler’s List might make you reach for the tissues, but psychologists say they have found a reason why traumatic films are so appealing. Researchers at Oxford University say that watching traumatic films boosts feelings of group bonding, as well as increasing pain tolerance by upping levels of feel-good, pain-killing chemicals produced in the brain. “The argument here is that actually, maybe the emotional wringing you get from tragedy triggers the endorphin system,” said Robin Dunbar, a co-author of the study and professor of evolutionary psychology at the University of Oxford. Previous research has found that laughing together, dancing together and working in a team can increase social bonding and heighten pain tolerance through an endorphin boost. “All of those things, including singing and dancing and jogging and laughter, all produce an endorphin kick for the same reason - they are putting the musculature of the body under stress,” said Dunbar. Being harrowed, he adds, could have a similar effect. “It has turned out that the same areas in the brain that deal with physical pain also handle psychological pain,” said Dunbar. Writing in the journal Royal Society Open Science, Dunbar and colleagues describe how they set out to unpick whether our love of storytelling, a device used to share knowledge and cultivate a sense of identity within a group, is underpinned by an endorphin-related bonding mechanism. © 2016 Guardian News and Media Limited
By JACK HEALY CINCINNATI — On the day he almost died, John Hatmaker bought a packet of Oreos and some ruby-red Swedish Fish at the corner store for his 5-year-old son. He was walking home when he spotted a man who used to sell him heroin. Mr. Hatmaker, 29, had overdosed seven times in the four years he had been addicted to pain pills and heroin. But he hoped he was past all that. He had planned to spend that Saturday afternoon, Aug. 27, showing his son the motorcycles and enjoying the music at a prayer rally for Hope Over Heroin in this region stricken by soaring rates of drug overdoses and opioid deaths. But first, he decided as he palmed a sample folded into a square of paper, he would snort this. As he crumpled to the sidewalk, Mr. Hatmaker became one of more than 200 people to overdose in the Cincinnati area in the past two weeks, leaving three people dead in what the officials here called an unprecedented spike. Similar increases in overdoses have rippled recently through Indiana, Kentucky and West Virginia, overwhelming ambulance crews and emergency rooms and stunning some antidrug advocates. Addiction specialists said the sharp increases in overdoses were a grim symptom of America’s heroin epidemic, and of the growing prevalence of powerful synthetic opiates like fentanyl. The synthetics are often mixed into batches of heroin, or sprinkled into mixtures of caffeine, antihistamines and other fillers. In Cincinnati, some medical and law enforcement officials said they believed the overdoses were largely caused by a synthetic drug called carfentanil, an animal tranquilizer used on livestock and elephants with no practical uses for humans. Fentanyl can be 50 times stronger than heroin, and carfentanil is as much as 100 times more potent than fentanyl. Experts said an amount smaller than a snowflake could kill a person. © 2016 The New York Times Company
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
Laura Sanders Scientists have identified the “refrigerator” nerve cells that hum along in the brains of mice and keep the body cool. These cells kick on to drastically cool mice’s bodies and may prevent high fevers, scientists report online August 25 in Science. The results “are totally new and very important,” says physiologist Andrej Romanovsky of the Barrow Neurological Institute in Phoenix. "The implications are far-reaching." By illuminating how bodies stay at the right temperature, the discovery may offer insights into the relationship between body temperature and metabolism. Scientists had good reasons to think that nerve cells controlling body temperature are tucked into the hypothalamus, a small patch of neural tissue in the middle of the brain. Temperature fluctuations in a part of the hypothalamus called the preoptic area prompt the body to get back to baseline by conserving or throwing off heat. But the actual identify of the heat sensors remained mysterious. The new study reveals the cells to be those that possess a protein called TRPM2. “Overall, this is a major discovery in the field of thermoregulation,” says Shaun Morrison of Oregon Health & Science University in Portland. Jan Siemens, a neurobiologist at the University of Heidelberg in Germany, and colleagues tested an array of molecules called TRP channels, proteins that sit on cell membranes and help sense a variety of stimuli, including painful tear gas and cool menthol. In tests of nerve cells in lab dishes, one candidate, the protein TRPM2, seemed to respond to heat. |© Society for Science & the Public 2000 - 201
Keyword: Pain & Touch
Link ID: 22605 - Posted: 08.27.2016
Neuroscience News Researchers have identified a brain mechanism that could be a drug target to help prevent tolerance and addiction to opioid pain medication, such as morphine, according to a study by Georgia State University and Emory University. The findings, published in the Nature journal Neuropsychopharmacology in August, show for the first time that morphine tolerance is due to an inflammatory response produced in the brain. This brain inflammation is caused by the release of cytokines, chemical messengers in the body that trigger an immune response, similar to a viral infection. Researchers’ results show blocking a particular cytokine eliminated morphine tolerance, and they were able to reduce the dose of morphine required to alleviate pain by half. “These results have important clinical implications for the treatment of pain and also addiction,” said Lori Eidson, lead author and a graduate student in the laboratory of Dr. Anne Murphy in the Neuroscience Institute of Georgia State. “Until now, the precise underlying mechanism for opioid tolerance and its prevention have remained unknown.” Over 67 percent of the United States population will experience chronic pain at some point in their lives. Morphine is the primary drug used to manage severe and chronic pain, with 3 to 4 percent of adults in the U.S. receiving long-term opioid therapy. However, tolerance to morphine, defined as a decrease in pain relief over time, significantly impedes treatment for about 60 percent of patients. Long-term treatment with opioids is associated with increased risk of abuse, dependence and fatal overdoses.
Laura Sanders For some people, fentanyl can be a life-saver, easing profound pain. But outside of a doctor’s office, the powerful opioid drug is also a covert killer. In the last several years, clandestine drugmakers have begun experimenting with this ingredient, baking it into drugs sold on the streets, most notably heroin. Fentanyl and closely related compounds have “literally invaded the entire heroin supply,” says medical toxicologist Lewis Nelson of New York University Langone Medical Center. Fentanyl is showing up in other drugs, too. In San Francisco’s Bay Area in March, high doses of fentanyl were laced into counterfeit versions of the pain pill Norco. In January, fentanyl was found in illegal pills sold as oxycodone in New Jersey. And in late 2015, fentanyl turned up in fake Xanax pills in California. This ubiquitous recipe-tinkering makes it impossible for users to know whether they’re about to take drugs mixed with fentanyl. And that uncertainty has proved deadly. Fentanyl-related deaths are rising sharply in multiple areas. National numbers are hard to come by, but in many regions around the United States, fentanyl-related fatalities have soared in recent years. Maryland is one of the hardest-hit states. From 2007 to 2012, the number of fentanyl-related deaths hovered around 30 per year. By 2015, that number had grown to 340. A similar rise is obvious in Connecticut, where in 2012, there were 14 fentanyl-related deaths. In 2015, that number was 188. |© Society for Science & the Public 2000 - 2016.
Angus Chen Once people realized that opioid drugs could cause addiction and deadly overdoses, they tried to use newer forms of opioids to treat the addiction to its parent. Morphine, about 10 times the strength of opium, was used to curb opium cravings in the early 19th century. Codeine, too, was touted as a nonaddictive drug for pain relief, as was heroin. Those attempts were doomed to failure because all opioid drugs interact with the brain in the same way. They dock to a specific neural receptor, the mu-opioid receptor, which controls the effects of pleasure, pain relief and need. Now scientists are trying to create opioid painkillers that give relief from pain without triggering the euphoria, dependence and life-threatening respiratory suppression that causes deadly overdoses. That wasn't thought possible until 2000, when a scientist named Laura Bohn found out something about a protein called beta-arrestin, which sticks to the opioid receptor when something like morphine activates it. When she gave morphine to mice that couldn't make beta-arrestin, they were still numb to pain, but a lot of the negative side effects of the drug were missing. They didn't build tolerance to the drug. At certain dosages, they had less withdrawal. Their breathing was more regular, and they weren't as constipated as normal mice on morphine. Before that experiment, scientists thought the mu-opioid receptor was a simple switch that flicked all the effects of opioids on or off together. Now it seems they could be untied. © 2016 npr
By ABBY GOODNOUGH TUSCALOOSA, Ala. — Roslyn Lewis was at work at a dollar store here in Tuscaloosa, pushing a heavy cart of dog food, when something popped in her back: an explosion of pain. At the emergency room the next day, doctors gave her Motrin and sent her home. Her employer paid for a nerve block that helped temporarily, numbing her lower back, but she could not afford more injections or physical therapy. A decade later, the pain radiates to her right knee and remains largely unaddressed, so deep and searing that on a recent day she sat stiffly on her couch, her curtains drawn, for hours. The experience of African-Americans, like Ms. Lewis, and other minorities illustrates a problem as persistent as it is complex: Minorities tend to receive less treatment for pain than whites, and suffer more disability as a result. While an epidemic of prescription opioid abuse has swept across the United States, African-Americans and Hispanics have been affected at much lower rates than whites. Researchers say minority patients use fewer opioids, and they offer a thicket of possible explanations, including a lack of insurance coverage and a greater reluctance among members of minority groups to take opioid painkillers even if they are prescribed. But the researchers have also found evidence of racial bias and stereotyping in recognizing and treating pain among minorities, particularly black patients. “We’ve done a good job documenting that these disparities exist,” said Salimah Meghani, a pain researcher at the University of Pennsylvania. “We have not done a good job doing something about them.” Dr. Meghani’s 2012 analysis of 20 years of published research found that blacks were 34 percent less likely than whites to be prescribed opioids for conditions such as backaches, abdominal pain and migraines, and 14 percent less likely to receive opioids for pain from traumatic injuries or surgery. © 2016 The New York Times Company
By KATHARINE Q. SEELYE PORTLAND, Me. — A woman in her 30s was sitting in a car in a parking lot here last month, shooting up heroin, when she overdosed. Even after the men she was with injected her with naloxone, the drug that reverses opioid overdoses, she remained unconscious. They called 911. Firefighters arrived and administered oxygen to improve her breathing, but her skin had grown gray and her lips had turned blue. As she lay on the asphalt, the paramedics slipped a needle into her arm and injected another dose of naloxone. In a moment, her eyes popped open. Her pupils were pinpricks. She was woozy and disoriented, but eventually got her bearings as paramedics put her on a stretcher and whisked her to a hospital. Every day across the country, hundreds, if not thousands, of people who overdose on opioids are being brought back to life with naloxone. Hailed as a miracle drug by many, it carries no health risk; it cannot be abused and, if given mistakenly to someone who has not overdosed on opioids, does no harm. More likely, it saves a life. As a virulent opioid epidemic continues to ravage the country, with 78 people in the United States dying of overdoses every day, naloxone’s use has increasingly moved out of medical settings, where it has been available since the 1970s, and into the homes and hands of the general public. But naloxone, also known by the brand name Narcan, has also had unintended consequences. Critics say that it gives drug users a safety net, allowing them to take more risks as they seek higher highs. Indeed, many users overdose more than once, some multiple times, and each time, naloxone brings them back. © 2016 The New York Times Company
By Maia Szalavitz When a family member, spouse or other loved one develops an opioid addiction — whether to pain relievers like Vicodin or to heroin — few people know what to do. Faced with someone who appears to be driving heedlessly into the abyss, families often fight, freeze or flee, unable to figure out how to help. Families are sometimes overwhelmed with conflicting advice about what should come next. Much of the advice given by treatment groups and programs ignores what the data says in a similar way that anti-vaccination or climate skeptic websites ignore science. The addictions field is neither adequately regulated nor effectively overseen. There are no federal standards for counseling practices or rehab programs. In many states, becoming an addiction counselor doesn’t require a high school degree or any standardized training. “There’s nothing professional about it, and it’s not evidence-based,” said Dr. Mark Willenbring, the former director of treatment research at the National Institute on Alcohol Abuse and Alcoholism, who now runs a clinic that treats addictions. Consequently, families are often given guidance that bears no resemblance to what the research evidence shows — and patients are commonly subjected to treatment that is known to do harm. People who are treated as experts firmly proclaim that they know what they are doing, but often turn out to base their care entirely on their own personal and clinical experience, not data. “Celebrity Rehab with Dr. Drew,” which many people see as an example of the best care available, for instance, used an approach that is not known to be effective for opioid addiction. More than 13 percent of its participants died after treatment,1 mainly of overdoses that could potentially have been prevented with evidence-based care. Unethical practices such as taking kickbacks for patient referrals are also rampant.
By Diana Kwon Few things feel worse than not knowing when your next paycheck is coming. Economic insecurity has been shown to have a whole host of negative effects, including low self-esteem and impaired cognitive functioning. It turns out financial stress can also physically hurt, according to a paper published in February in Psychological Science. Eileen Chou, a public policy professor at the University of Virginia, and her collaborators began by analyzing a data set of 33,720 U.S. households and found that those with higher levels of unemployment were more likely to purchase over-the-counter painkillers. Then, using a series of experiments, the team discovered that simply thinking about the prospect of financial insecurity was enough to increase pain. For example, people reported feeling almost double the amount of physical pain in their body after recalling a financially unstable time in their life as compared with those who thought about a secure period. In another experiment, university students who were primed to feel anxious about future employment prospects removed their hand from an ice bucket more quickly (showing less pain tolerance) than those who were not. The researchers also found that economic insecurity reduced people's sense of control, which, in turn, increased feelings of pain. Chou and her colleagues suggest that because of this link between financial insecurity and decreased pain tolerance, the recent recession may have been a factor in fueling the prescription painkiller epidemic. Other experts are cautious about taking the findings that far. “I think the hypothesis [that financial stress causes pain] has a lot of merit, but it would be helpful to see additional rigorous evidence in a real-world environment,” says Heather Schofield, an economist at the University of Pennsylvania who was not involved in the study. © 2016 Scientific American,
DAVID GREENE, HOST: Nearly one-quarter of all Americans reach for a bottle of acetaminophen every single week. Many of you might know this drug as Tylenol. It's a pain killer that can take the edge off a headache or treat you when you have a fever. It also might have another effect. And let's talk about this with NPR social science correspondent Shankar Vedantam. And, Shankar, straight out, is this going to make me not want to take Tylenol, what you're about to tell me? VEDANTAM: It might make you not want to take Tylenol when you're talking with me, David. GREENE: Oh, even more interesting. VEDANTAM: (Laughter) I was speaking with Dominik Mischkowski. He's currently a researcher at the National Institutes of Health. He recently conducted a couple of double blind experiments. These are experiments where the volunteers are given either sugar pills or Tylenol, but neither the volunteers nor the researchers know which volunteers are getting which pill. Mischkowski and his advisers at Ohio State University, Jennifer Crocker and Baldwin Way, they played loud noises for the volunteers. Not surprisingly, volunteers given Tylenol experienced less physical discomfort than volunteers given the placebo. © 2016 npr
Keyword: Pain & Touch
Link ID: 22403 - Posted: 07.07.2016
By Damian Garde, A boy in Pakistan became a local legend as a street performer in recent years by traversing hot coals and lancing his arms with knives without so much as a wince. A thousand miles away, in China, lived a family wracked by excruciating bouts of inexplicable pain, passed down generation after generation. Scientists eventually determined what the boy and the family had in common: mutations in a gene that functions like an on-off switch for agony. Now, a bevy of biotech companies, including Genentech and Biogen, are staking big money on the idea that they can develop drugs that toggle that switch to relieve pain without the risk of addiction. The gene in question is SCN9A, which is responsible for producing a pain-related protein called Nav1.7. In patients who feel nothing, SCN9A is pretty much broken. In those who feel searing random pain, the gene is cranking out far too much Nav1.7. That discovery raises an obvious question: Can blocking Nav1.7 provide relief for many types of pain—and someday, perhaps, replace dangerous opioid therapies? “That’s the dream,” said David Hackos, a senior scientist at Genentech, which has two Nav1.7 treatments in the first stage of clinical development. It’s too early make any sweeping predictions—and, indeed, a Pfizer pill targeting Nav1.7 has already stumbled—but the pharma industry clearly sees the potential for a blockbuster. © 2016 Scientific American
Keyword: Pain & Touch
Link ID: 22400 - Posted: 07.06.2016
By Jessica Hamzelou Imagine if each of the words in this article had their own taste, or the music you’re listening to played out as visual scene in your mind. For synaesthetes – a small proportion of people whose senses intertwine – this is the stuff of the every day. “Most people describe it as a gift,” says Jamie Ward, a neuroscientist at the University of Sussex in the UK. Now, he and his colleagues have found a new form of synaesthesia – one that moves beyond written language to sign language. It is the first time the phenomenon has been observed. “People with synaesthesia experience the ordinary world in extraordinary ways,” says Ward. In theory, any two senses can overlap. Some synaesthetes connect textures with words, while others can taste them. More commonly, written letters seem to have corresponding colours. An individual synaesthete may always associate the letter A with the colour pink, for instance. This type of synaesthesia has been found across many written languages, prompting Ward’s team to wonder if it can also apply to sign language. They recruited 50 volunteers with the type of synaesthesia that means they experience colours with letters, around half of whom were fluent in sign language too. All the participants watched a video of sign language and were asked if it triggered any colours. © Copyright Reed Business Information Ltd.
Link ID: 22390 - Posted: 07.02.2016
By Rachel Rabkin Peachman It began with a simple roller-skating accident three years ago. Taylor Aschenbrenner, then 8 years old, lost her balance amid a jumble of classmates, tumbled to the floor and felt someone else’s skate roll over her left foot. The searing pain hit her immediately. The diagnosis, however, would take much longer. An X-ray, M.R.I.s, a CT scan and blood tests over several months revealed no evidence of a break, sprain or other significant problem. Taylor’s primary symptom was pain — so severe that she could not put weight on the foot. “Our family doctor first told us to give it some time,” said Taylor’s mother, Jodi Aschenbrenner, of Hudson, Wis. But time didn’t heal the pain. After about a month, an orthopedist recommended physical therapy. That didn’t end the problem, either. “I couldn’t walk or play outside or do anything,” Taylor said. After she had spent a year and a half on crutches, her orthopedist suggested she see Dr. Stefan Friedrichsdorf, the medical director ofpain medicine, palliative care and integrative medicine at Children’s Hospitals and Clinics of Minnesota. He and his team promptly recognized Taylor’s condition as complex regional pain syndrome, a misfiring within the peripheral and central nervous systems that causes pain signals to go into overdrive and stay turned on even after an initial injury or trauma has healed. He came up with a treatment plan for Taylor that included cognitive behavioral therapy, physical therapy, mind-body techniques, stress-reduction strategies, topical pain-relief patches and a focus on returning to her normal life and sleep routine, among other things. © 2016 The New York Times Company
Emily Conover Sharks have a sixth sense that helps them locate prey in murky ocean waters. They rely on special pores on their heads and snouts, called ampullae of Lorenzini, that can sense electric fields generated when nearby prey move. The pores were first described in 1678, but scientists haven’t been sure how they work. Now, the answer is a bit closer. The pores, which connect to electrosensing cells, are filled with a mysterious clear jelly. This jelly is a highly efficient proton conductor, researchers report May 13 in Science Advances. In the jelly, positively charged particles move and transmit current. Marco Rolandi of the University of California, Santa Cruz and colleagues squeezed jelly from the pores of one kind of shark and two kinds of skate and tested how well protons could flow through the substance. Good proton conductors, including a protein found in squid skin, occur in nature. But the jelly is the best biological proton conductor discovered so far. In fact, even humankind’s best technology isn’t wildly better. The most efficient proton conductor devised by people — a polymer known as Nafion — is a mere 40 times better than the stuff sharks are born with. Citations E.E. Josberger et al. Proton conductivity in ampullae of Lorenzini jelly. Science Advances. Published online May 13, 2016. doi:10.1126/sciadv.1600112. Further Reading |© Society for Science & the Public 2000 - 2016.
Keyword: Pain & Touch
Link ID: 22366 - Posted: 06.28.2016
By Eric Hand That many animals sense and respond to Earth’s magnetic field is no longer in doubt, and people, too, may have a magnetic sense. But how this sixth sense might work remains a mystery. Some researchers say it relies on an iron mineral, magnetite; others invoke a protein in the retina called cryptochrome. Magnetite has turned up in bird beaks and fish noses and even in the human brain, as Joe Kirschvink of the California Institute for Technology in Pasadena reported in 1992, and it is extremely sensitive to magnetic fields. As a result, Kirschvink and other fans say, it can tell an animal not only which way it is heading (compass sense) but also where it is. “A compass cannot explain how a sea turtle can migrate all the way around the ocean and return to the same specific stretch of beach where it started out,” says neurobiologist Kenneth Lohmann of the University of North Carolina, Chapel Hill. A compass sense is enough for an animal to figure out latitude, based on changes in the inclination of magnetic field lines (flat at the equator, plunging into the earth at the poles). But longitude requires detecting subtle variations in field strength from place to place—an extra map or signpost sense that magnetite could supply, Lohmann says. Except in bacteria, however, no one has seen magnetite crystals serving as a magnetic sensor. The crystals could be something else—say, waste products of iron metabolism, or a way for the body to sequester carcinogenic heavy metals. In the early 2000s, scientists found magnetite-bearing cells in the beaks of pigeons. But a follow-up study found that the supposed magnetoreceptors were in fact scavenger immune cells that had nothing to do with the neural system. And because there is no unique stain or marker for magnetite, false sightings are easy to make. © 2016 American Association for the Advancement of Science
Keyword: Pain & Touch
Link ID: 22357 - Posted: 06.24.2016
By Eric Hand Birds do it. Bees do it. But the human subject, standing here in a hoodie—can he do it? Joe Kirschvink is determined to find out. For decades, he has shown how critters across the animal kingdom navigate using magnetoreception, or a sense of Earth’s magnetic field. Now, the geophysicist at the California Institute of Technology (Caltech) in Pasadena is testing humans to see if they too have this subconscious sixth sense. Kirschvink is pretty sure they do. But he has to prove it. He takes out his iPhone and waves it over Keisuke Matsuda, a neuroengineering graduate student from the University of Tokyo. On this day in October, he is Kirschvink’s guinea pig. A magnetometer app on the phone would detect magnetic dust on Matsuda—or any hidden magnets that might foil the experiment. “I want to make sure we don’t have a cheater,” Kirschvink jokes. They are two floors underground at Caltech, in a clean room with magnetically shielded walls. In a corner, a liquid helium pump throbs and hisses, cooling a superconducting instrument that Kirschvink has used to measure tiny magnetic fields in everything from bird beaks to martian meteorites. On a lab bench lie knives—made of ceramic and soaked in acid to eliminate magnetic contamination—with which he has sliced up human brains in search of magnetic particles. Matsuda looks a little nervous, but he will not be going under the knife. With a syringe, a technician injects electrolyte gel onto Matsuda’s scalp through a skullcap studded with electrodes. He is about to be exposed to custom magnetic fields generated by an array of electrical coils, while an electroencephalogram (EEG) machine records his brain waves. © 2016 American Association for the Advancement of Science.
Keyword: Pain & Touch
Link ID: 22356 - Posted: 06.24.2016