Chapter 16. None
Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.
By Maggie Koerth-Baker Q: I want to hear what the loudest thing in the world is! — Kara Jo, age 5 No. No, you really don’t. See, there’s this thing about sound that even we grown-ups tend to forget — it’s not some glitter rainbow floating around with no connection to the physical world. Sound is mechanical. A sound is a shove — just a little one, a tap on the tightly stretched membrane of your ear drum. The louder the sound, the heavier the knock. If a sound is loud enough, it can rip a hole in your ear drum. If a sound is loud enough, it can plow into you like a linebacker and knock you flat on your butt. When the shock wave from a bomb levels a house, that’s sound tearing apart bricks and splintering glass. Sound can kill you. Consider this piece of history: On the morning of Aug. 27, 1883, ranchers on a sheep camp outside Alice Springs, Australia, heard a sound like two shots from a rifle. At that very moment, the Indonesian volcanic island of Krakatoa was blowing itself to bits 2,233 miles away. Scientists think this is probably the loudest sound humans have ever accurately measured. Not only are there records of people hearing the sound of Krakatoa thousands of miles away, there is also physical evidence that the sound of the volcano’s explosion traveled all the way around the globe multiple times. Now, nobody heard Krakatoa in England or Toronto. There wasn’t a “boom” audible in St. Petersburg. Instead, what those places recorded were spikes in atmospheric pressure — the very air tensing up and then releasing with a sigh, as the waves of sound from Krakatoa passed through. There are two important lessons about sound in there: One, you don’t have to be able to see the loudest thing in the world in order to hear it. Second, just because you can’t hear a sound doesn’t mean it isn’t there. Sound is powerful and pervasive and it surrounds us all the time, whether we’re aware of it or not.
Link ID: 22453 - Posted: 07.19.2016
Paula Span An estimated one zillion older people have a problem like mine. First: We notice age-related hearing loss. A much-anticipated report on hearing health from the National Academies of Sciences, Engineering and Medicine last month put the prevalence at more than 45 percent of those aged 70 to 74, and more than 80 percent among those over 85. Then: We do little or nothing about it. Fewer than 20 percent of those with hearing loss use hearing aids. I’ve written before about the reasons. High prices ($2,500 and up for a decent hearing aid, and most people need two). Lack of Medicare reimbursement, because the original 1965 law creating Medicare prohibits coverage. Time and hassle. Stigma. Both the National Academies and the influential President’s Council of Advisors on Science and Technology have proposed pragmatic steps to make hearing technology more accessible and affordable. But until there’s progress on those, many of us with mild to moderate hearing loss may consider a relatively inexpensive alternative: personal sound amplification products, or P.S.A.P.s. They offer some promise — and some perils, too. Unlike for a hearing aid, you don’t need an audiologist to obtain a P.S.A.P. You see these gizmos advertised on the back pages of magazines or on sale at drugstore chains. You can buy them online. © 2016 The New York Times Company
Link ID: 22449 - Posted: 07.16.2016
By SARAH MASLIN NIR Almost as soon as the young man crouching on a trash-strewed street in Brooklyn pulled out a crumpled dollar bill from his pocket and emptied its contents of dried leaves into a wrapper, he had company. A half-dozen disheveled men and women walked swiftly to where the young man was rolling a cigarette of a synthetic drug known as K2 to wait for a chance to share. The drug has been the source of an alarming and sudden surge in overdoses — over three days this week, 130 people across New York City were treated in hospital emergency rooms after overdosing on K2, almost equaling the total for the entire month of June, according to the city’s health department. About one-fourth of the overdoses, 33, took place on Tuesday along the border of Bedford-Stuyvesant and Bushwick, the same Brooklyn neighborhoods where, despite a heightened presence of police officers, people were again openly smoking the drug on Thursday. In response to the overdoses, the city is sending a health alert to emergency rooms and other health care providers warning about the drug. The outbreak comes after officials this spring lauded what they described as a successful campaign to severely curb the prevalence of K2. On Thursday, Gov. Andrew M. Cuomo announced that the State Police would step up enforcement against the drug and aggressively go after merchants who illegally sell it. The same day, just steps from where people were using the drug, clusters of police officers patrolled beneath the elevated subway tracks along a stretch where, the day before, five bodegas had been raided. K2 is typically sold by convenience stores, though the raids did not turn up any. © 2016 The New York Times Company
Keyword: Drug Abuse
Link ID: 22448 - Posted: 07.16.2016
By JOANNA KLEIN Jet lag may be the worst part of traveling. And it hits many people harder traveling east than west. Why they feel this way is unclear. But scientists recently developed a model that mimics special time-keeping cells in the body and offers a mathematical explanation for why traveling from west to east feels so much worse. It also offers insights on recovering from jet lag. Deep inside the brain, in a region called the hypothalamus (right above where our optic nerves cross) the internal clock is ticking. And approximately every 24 hours, 20,000 special pacemaker cells that inhabit this area, known as the superchiasmatic nucleus, synchronize, signaling to the rest of the body whether it’s night or day. These cells know which signal to send because they receive light input from our environments — bright says wake, dark says sleep. But when you travel across multiple time zones, like flying from New York to Moscow, those little pacemaker cells that thought they knew the routine scramble around confused before they can put on their show. The whole body feels groggy because it’s looking for the time and can’t find it. The result: jet lag. Most of our internal clocks are a little bit slow, and in the absence of consistent light cues — like when you travel across time zones — the pacemaker cells in your body want to have a longer day, said Michelle Girvan, a physicist at the University of Maryland who worked on the model published in the journal Chaos on Tuesday. “This is all because the body’s internal clock has a natural period of slightly longer than 24 hours, which means that it has an easier time traveling west and lengthening the day than traveling east and shortening the day,” Dr. Girvan said. © 2016 The New York Times Company
Keyword: Biological Rhythms
Link ID: 22446 - Posted: 07.16.2016
NOBODY knows how the brain works. But researchers are trying to find out. One of the most eye-catching weapons in their arsenal is functional magnetic-resonance imaging (fMRI). In this, MRI scanners normally employed for diagnosis are used to study volunteers for the purposes of research. By watching people’s brains as they carry out certain tasks, neuroscientists hope to get some idea of which bits of the brain specialise in doing what. The results look impressive. Thousands of papers have been published, from workmanlike investigations of the role of certain brain regions in, say, recalling directions or reading the emotions of others, to spectacular treatises extolling the use of fMRI to detect lies, to work out what people are dreaming about or even to deduce whether someone truly believes in God. But the technology has its critics. Many worry that dramatic conclusions are being drawn from small samples (the faff involved in fMRI makes large studies hard). Others fret about over-interpreting the tiny changes the technique picks up. A deliberately provocative paper published in 2009, for example, found apparent activity in the brain of a dead salmon. Now, researchers in Sweden have added to the doubts. As they reported in the Proceedings of the National Academies of Science, a team led by Anders Eklund at Linkoping University has found that the computer programs used by fMRI researchers to interpret what is going on in their volunteers’ brains appear to be seriously flawed. © The Economist Newspaper Limited 2016
Keyword: Brain imaging
Link ID: 22444 - Posted: 07.15.2016
Rebecca Boyle Eliane Lucassen works the night shift at Leiden University Medical Center in the Netherlands, beginning her day at 6 p.m. Yet her own research has shown that this schedule might cause her health problems. “It’s funny,” the medical resident says. “Here I am, spreading around that it’s actually unhealthy. But it needs to be done.” Lucassen and Johanna Meijer, a neuroscientist at Leiden, report today in Current Biology1 that a constant barrage of bright light prematurely ages mice, playing havoc with their circadian clocks and causing a cascade of health problems. Mice exposed to constant light experienced bone-density loss, skeletal-muscle weakness and inflammation; restoring their health was as simple as turning the lights off. The findings are preliminary, but they suggest that people living in cities flooded with artificial light may face similar health risks. “We came to know that smoking was bad, or that sugar is bad, but light was never an issue,” says Meijer. “Light and darkness matter.” Disrupted patterns Many previous studies have hinted at a connection between artificial light exposure and health problems in animals and people2. Epidemiological analyses have found that shift workers have an increased risk of breast cancer3, metabolic syndrome4 and osteoporosis5, 6. People exposed to bright light at night are more likely to have cardiovascular disease and often don’t get enough sleep. © 2016 Macmillan Publishers Limited,
Keyword: Biological Rhythms
Link ID: 22442 - Posted: 07.15.2016
Michael Egnor The most intractable question in modern neuroscience and philosophy of the mind is often phrased "What is consciousness?" The problem has been summed up nicely by philosopher David Chalmers as what he calls the Hard Problem of consciousness: How is it that we are subjects, and not just objects? Chalmers contrasts this hard question with what he calls the Easy Problem of consciousness: What are the neurobiological substrates underlying such things as wakefulness, alertness, attention, arousal, etc. Chalmers doesn't mean of course that the neurobiology of arousal is easy. He merely means to show that even if we can understand arousal from a neurobiological standpoint, we haven't yet solved the hard problem: the problem of subjective experience. Why am I an I, and not an it? Chalmers's point is a good one, and I think that it has a rather straightforward solution. First, some historical background is necessary. "What is consciousness?" is a modern question. It wasn't asked before the 17th century, because no one before Descartes thought that the mind was particularly mysterious. The problem of consciousness was created by moderns. The scholastic philosophers, following Aristotle and Aquinas, understood the soul as the animating principle of the body. In a human being, the powers of the soul -- intellect, will, memory, perception, appetite, and such -- were no more mysterious than the other powers of the soul, such as respiration, circulation, etc. Of course, biology in the Middle Ages wasn't as advanced as it is today, so there was much they didn't understand about human physiology, but in principle the mind was just another aspect of human biology, not inherently mysterious. In modern parlance, the scholastics saw the mind as the Easy Problem, no more intractable than understanding how breathing or circulation work.
Link ID: 22441 - Posted: 07.15.2016
Laura Sanders If you’ve ever watched a baby purse her lips to hoot for the first time, or flash a big, gummy grin when she sees you, or surprise herself by rolling over, you’ve glimpsed the developing brain in action. A baby’s brain constructs itself into something that controls the body, learns and connects socially. Spending time with an older person, you may notice signs of slippage. An elderly man might forget why he went into the kitchen, or fail to anticipate the cyclist crossing the road, or muddle medications with awkward and unfamiliar names. These are the signs of the gentle yet unrelenting neural erosion that comes with normal aging. These two seemingly distinct processes — development and aging — may actually be linked. Hidden in the brain-building process, some scientists now suspect, are the blueprints for the brain’s demise. The way the brain is built, recent research suggests, informs how it will decline in old age. That the end can be traced to the beginning sounds absurd: A sturdily constructed brain stays strong for decades. During childhood, neural pathways make connections in a carefully choreographed order. But in old age, this sequence plays in reverse, brain scans reveal. In both appearance and behavior, old brains seem to drift backward toward earlier stages of development. What’s more, some of the same cellular tools are involved in both processes. © Society for Science & the Public 2000 - 2016
Keyword: Development of the Brain
Link ID: 22440 - Posted: 07.14.2016
By Tanya Lewis In recent years, research on mammalian navigation has focused on the role of the hippocampus, a banana-shaped structure known to be integral to episodic memory and spatial information processing. The hippocampus’s primary output, a region called CA1, is known to be divided into superficial and deep layers. Now, using two-photon imaging in mice, researchers at Columbia University in New York have found these layers have distinct functions: superficial-layer neurons encode more-stable maps, whereas deep-layer brain cells better represent goal-oriented navigation, according to a study published last week (July 7) in Neuron. “There are lots of catalogued differences in sublayers of pyramidal cells” within the hippocampus, study coauthor Nathan Danielson of Columbia told The Scientist. “The question is, are the principle cells in each subregion doing the same thing? Or is there a finer level of granularity?” For that past few decades, scientists have been chipping away at an explanation of the brain’s “inner GPS.” The 2014 Nobel Prize in Physiology or Medicine honored the discovery of so-called place cells and grid cells in the hippocampus, which keep track of an individual’s location and coordinates in space, respectively. Since then, studies have revealed that neurons in different hippocampal regions have distinct genetic, anatomical, and physiological properties, said Attila Losonczy of Columbia, Danielson’s graduate advisor and a coauthor on the study. © 1986-2016 The Scientist
Keyword: Learning & Memory
Link ID: 22437 - Posted: 07.14.2016
Suzi Gage Ketamine hydrochloride is a synthetic dissociative anaesthetic. It was first synthesized in the 1960s for medical use, and was first used medicinally during the Vietnam war. Recreationally, it is usually consumed by snorting a white crystalline powder, and at lower doses than when it’s used as an anaesthetic. However it can also be injected, or smoked. It is used in a club setting, but also as a psychedelic. Short term effects When ketamine is snorted, it gets in to the blood stream quickly, and intoxication effects occur soon after it’s taken. Although it’s an anaesthetic, at low doses it raises heart rate. It’s also associated with cognitive impairment during intoxication, including to speech and executive function. It can also induce mild psychedelic effects such as perceptual changes and psychotic-like experiences, which are appealing to some users, but can also be distressing. At slightly higher doses, users can experience a dissociative state, where their mind feels separated from their body. This can also manifest as a feeling of depersonalization. At higher doses, the anaesthetic quality of ketamine becomes more pronounced. People may find it difficult to move and may feel numb, and can experience more vivid hallucinations. This is sometimes called the ‘k-hole’ by users. Amnesia can occur at this level of use. This is a particular danger of using ketamine recreationally: users are vulnerable to assault from others in this state, or can put themselves in danger by not being aware of their surroundings (for example being unaware they are outside and it is cold can lead to hypothermia, or being unaware of surroundings could lead to walking in to traffic). © 2016 Guardian News and Media Limited
Keyword: Drug Abuse
Link ID: 22436 - Posted: 07.14.2016
By Virginia Morell Infanticide—the killing of offspring—is generally rare among birds. And when it happens, it’s usually because of outsiders that want the nesting site or territory. But what happens among birds, such as the greater ani (Crotophaga major, pictured), which have a more socialist approach to nesting? Two to four pairs of the Central and South American cuckoos (which are usually unrelated) build a single nest, and then work together to raise their chicks, which generally hatch at the same time. Intriguingly, the adults cannot recognize either their own eggs or chicks, so they care for all of them. To find out why—and if the simultaneous hatching protects the chicks from infanticide—a scientist analyzed data on nestling mortality gathered at 104 communal greater ani nests from 2006 to 2015. Of the 741 nestlings, 321 (43%) fledged and 420 (57%) died. Most of the deaths (78.5%) were due to predation. But another 13.8%, or 58 nestlings, died from infanticide, the scientist reports online today in Evolution. The remaining 32 (7.7%) died from starvation. At most of the nests, the chicks hatched within 1 day of each other. Those that first emerged from their eggs were the most likely to be dispatched by one of the nest founders, not an outsider. Chicks that hatched last were also unlucky; weaker than their older and larger nest-mates, they weren’t able to compete for food and starved. Those two pressures—infanticide and food competition—end up favoring the chicks in the middle and those that hatch on the same day, the researcher reports. © 2016 American Association for the Advancement of Science
By Karen Weintraub Researchers at Stanford University have coaxed brain cells involved in vision to regrow and make functional connections—helping to upend the conventional dogma that mammalian brain cells, once damaged, can never be restored. The work was carried out in visually impaired mice but suggests that human maladies including glaucoma, Alzheimer’s disease and spinal cord injuries might be more repairable than has long been believed. Frogs, fish and chickens are known to regrow brain cells, and previous research has offered clues that it might be possible in mammals. The Stanford scientists say their new study confirms this and shows that, although fewer than 5 percent of the damaged retinal ganglion cells grew back, it was still enough to make a difference in the mice’s vision. “The brain is very good at coping with deprived inputs,” says Andrew Huberman, the Stanford neurobiologist who led the work. “The study also supports the idea that we may not need to regenerate every neuron in a system to get meaningful recovery.” Other researchers praised the study, published Monday in Nature Neuroscience. “I think it’s a significant step forward toward getting to the point where we really can regenerate optic nerves,” says Don Zack, a professor of ophthalmology at Johns Hopkins University who was not involved in the research. He calls it “one more indication that it may be possible to bring that ability back in humans.” © 2016 Scientific American
By Michael Price The blind comic book star Daredevil has a highly developed sense of hearing that allows him to “see” his environment with his ears. But you don’t need to be a superhero to pull a similar stunt, according to a new study. Researchers have identified the neural architecture used by the brain to turn subtle sounds into a mind’s-eye map of your surroundings. The study appears to be “very solid work,” says Lore Thaler, a psychologist at Durham University in the United Kingdom who studies echolocation, the ability of bats and other animals to use sound to locate objects. Everyone has an instinctive sense of the world around them—even if they can’t always see it, says Santani Teng, a postdoctoral researcher at the Massachusetts Institute of Technology (MIT) in Cambridge who studies auditory perception in both blind and sighted people. “We all kind of have that intuition,” says Teng over the phone. “For instance, you can tell I’m not in a gymnasium right now. I’m in a smaller space, like an office.” That office belongs to Aude Oliva, principal research scientist for MIT’s Computational Perception & Cognition laboratory. She and Teng, along with two other colleagues, wanted to quantify how well people can use sounds to judge the size of the room around them, and whether that ability could be detected in the brain. © 2016 American Association for the Advancement of Science.
Link ID: 22427 - Posted: 07.12.2016
By Maggie Koerth-Baker When former Tennessee women’s basketball coach Pat Summitt died Tuesday morning, news outlets, including ESPN, reported the cause of her death as “early-onset dementia, Alzheimer’s type.” That’s more than just a long-winded way of saying “Alzheimer’s.” By using five words instead of one, journalists were trying to point a big, flashing neon arrow at the complex realities of dementia. Dementia is more of a symptom than a diagnosis, and it can be caused by a number of different diseases. Even Alzheimer’s, the most common type of dementia, doesn’t seem to have a single cause. Instead, what ties Summitt to millions of other Alzheimer’s patients all over the world is the physical damage it wrought in her brain. Worldwide, 47.5 million people are living with some kind of dementia. Alzheimer’s represents 60 percent to 70 percent of those cases. Imagine a map of a city — roads branching out, intersecting with other roads, creating a network that allows mail to be delivered, food to be sold and brought home, people to get to their jobs. What would happen to that town if random intersections were suddenly barricaded and impassible? That’s the dystopian chaos Alzheimer’s causes, as damaged proteins clog the neurons and inhibit the flow of information from one neuron to another. Cut off from food, as well as data, the cells die. The brain shrinks. Eventually, the person dies, too. Afterward, doctors can cut into their brain and see the barriers, which are called plaques.
Link ID: 22426 - Posted: 07.12.2016
By Edd Gent, The devastating neurodegenerative condition Alzheimer's disease is incurable, but with early detection, patients can seek treatments to slow the disease's progression, before some major symptoms appear. Now, by applying artificial intelligence algorithms to MRI brain scans, researchers have developed a way to automatically distinguish between patients with Alzheimer's and two early forms of dementia that can be precursors to the memory-robbing disease. The researchers, from the VU University Medical Center in Amsterdam, suggest the approach could eventually allow automated screening and assisted diagnosis of various forms of dementia, particularly in centers that lack experienced neuroradiologists. Additionally, the results, published online July 6 in the journal Radiology, show that the new system was able to classify the form of dementia that patients were suffering from, using previously unseen scans, with up to 90 percent accuracy. [10 Things You Didn't Know About the Brain] "The potential is the possibility of screening with these techniques so people at risk can be intercepted before the disease becomes apparent," said Alle Meije Wink, a senior investigator in the center's radiology and nuclear medicine department. "I think very few patients at the moment will trust an outcome predicted by a machine," Wink told Live Science. "What I envisage is a doctor getting a new scan, and as it is loaded, software would be able to say with a certain amount of confidence [that] this is going to be an Alzheimer's patient or [someone with] another form of dementia." © 2016 Scientific American
Link ID: 22425 - Posted: 07.12.2016
By Shayla Love In 2005, astronaut John Phillips took a break from his work on the International Space Station and looked out the window at Earth. He was about halfway through a mission that had begun in April and would end in October. When he gazed down at the planet, the Earth was blurry. He couldn’t focus on it clearly. That was strange — his vision had always been 20/20. He wondered: Was his eyesight getting worse? “I’m not sure if I reported that to the ground,” he said. “I think I didn’t. I thought it would be something that would just go away, and fix itself when I got to Earth.” It didn’t go away. During Phillips’ post-flight physical, NASA found that his vision had gone from 20/20 to 20/100 in six months. John Phillips began experiencing sight issues during his time on the International Space Station in 2005, but was reluctant to say anything while in space. (NASA) Rigorous testing followed. Phillips got MRIs, retinal scans, neurological tests and a spinal tap. The tests showed that not only had his vision changed, but his eyes had changed as well. The backs of his eyes had gotten flatter, pushing his retinas forward. He had choroidal folds, which are like stretch marks. His optic nerves were inflamed. Phillips case became the first widely recognized one of a mysterious syndrome that affects 80 percent of astronauts on long-duration missions in space. The syndrome could interfere with plans for future crewed space missions, including any trips to Mars.
Link ID: 22422 - Posted: 07.11.2016
By DENISE GRADY Could pernicious anemia, a disease caused by a vitamin B12 deficiency, have explained the many strange behaviors of Mary Todd Lincoln? She was not exactly a model first lady. Historians have had a field day describing her violent temper, wild shopping sprees (she owned 300 pairs of kid gloves), depressed moods and all-consuming fears of burglars, storms and poverty. Late in life, at her son’s urging, she was committed to a mental hospital for several months. Plenty of theories, none proven, have been floated. She was bipolar. She had syphilis or that well known cause of feminine madness, menstrual trouble. She was spoiled and narcissistic. She never recovered from a road accident in which her head hit a rock. She lost her mind grieving the deaths of three of her four sons and her husband’s assassination. The latest addition to the list of possible diagnoses comes from Dr. John G. Sotos, a cardiologist, technology executive at Intel and one of the medical consultants who helped dream up the mystery diseases that afflicted patients on the television show “House.” Dr. Sotos has long been interested in difficult diagnoses, and has written a self-published book suggesting that Abraham Lincoln had a genetic syndrome that caused cancers of the thyroid and adrenal glands. In an interview, Dr. Sotos said that while he was studying President Lincoln, he came across something that intrigued him about Mrs. Lincoln: an 1852 letter mentioning that she had a sore mouth. He knew that vitamin B deficiencies could cause a sore tongue, and he began looking into her health. © 2016 The New York Times Company
Link ID: 22418 - Posted: 07.09.2016
By SUNITA SAH A POPULAR remedy for a conflict of interest is disclosure — informing the buyer (or the patient, etc.) of the potential bias of the seller (or the doctor, etc.). Disclosure is supposed to act as a warning, alerting consumers to their adviser’s stake in the matter so they can process the advice accordingly. But as several recent studies I conducted show, there is an underappreciated problem with disclosure: It often has the opposite of its intended effect, not only increasing bias in advisers but also making advisees more likely to follow biased advice. When I worked as a physician, I witnessed how bias could arise from numerous sources: gifts or sponsorships from the pharmaceutical industry; compensation for performing particular procedures; viewing our own specialties as delivering more effective treatments than others’ specialties. Although most physicians, myself included, tend to believe that we are invulnerable to bias, thus making disclosures unnecessary, regulators insist on them, assuming that they work effectively. To some extent, they do work. Disclosing a conflict of interest — for example, a financial adviser’s commission or a physician’s referral fee for enrolling patients into clinical trials — often reduces trust in the advice. But my research has found that people are still more likely to follow this advice because the disclosure creates increased pressure to follow the adviser’s recommendation. It turns out that people don’t want to signal distrust to their adviser or insinuate that the adviser is biased, and they also feel pressure to help satisfy their adviser’s self-interest. Instead of functioning as a warning, disclosure can become a burden on advisees, increasing pressure to take advice they now trust less. © 2016 The New York Times Company
Link ID: 22416 - Posted: 07.09.2016
by Adriana Heguy, molecular biologist and genomics researcher: Interestingly, tongue-curling ability is not solely genetic, and the genetic component may be very small. Monozygotic (identical) twins are not always concordant for tongue-curling ability, so if there is a genetic component, it’s clearly not Mendelian. In other words, it’s not a trait coded by one single gene, and it’s clearly influenced by the environment—in this case, practice. But for some reason this is one of the “myths” about genetics that gets spread around in high school, where it is used as an example of a simple Mendelian trait with a simple dominant-recessive nature. It’s hard to comment on the evolutionary purpose of an ability so heavily influenced by the environment, and not obviously useful. There are many traits for which we do not have the faintest idea why they exist or what purpose they serve. In the case of tongue-curling, it’s possible that it’s a case of fine motor control of the tongue. We need to be able to move our tongues to not bite them when we eat, for example, and for swirling food around. For unknown reasons, some individuals are better than others at controlling tongue movement. And since the ability can be acquired by practicing (though not everybody apparently succeeds), it does seem likely that it is indeed a question of motor control. Most people are able to do it. It’s quite common. But it could be that evolution had nothing to do with it. Or it could be a spandrel; in other words, a side effect of evolution. Maybe the evolution of dexterity or finer motor control of other muscles resulted in tongue “dexterity.” It’s possible that it is an atavism, something that increased tongue muscle control was once useful for tasting or eating certain kinds of foods millions of years ago, and it has not disappeared because the developmental program for fine muscle control is still there.
By Andy Coghlan It could be that romantic restaurant, or your favourite park bench. A specific part of the brain seems to be responsible for learning and remembering the precise locations of places that are special to us, research in mice has shown for the first time. Place cells are neurons that help us map our surroundings, and both mice and humans have such cells in the hippocampus – a brain region vital for learning, memory and navigation. Nathan Danielson at Columbia University in New York and his colleagues focused on a part of the hippocampus that feeds signals to the rest of the brain, called CA1. They found that in mice, the CA1 layer where general environment maps are learned and stored is different to the one for locations that have an important meaning. Treadmill test They discovered this by recording brain activity in the two distinct layers of CA1, using mice placed on a treadmill. The treadmill rotated between six distinctive surface materials – including silky ribbons, green pom-pom fabric and silver glitter masking tape. At all times, the mice were able to lick a sensor to try to trigger the release of drinking water. During the first phase of the experiment, however, the sensor only worked at random times. The mice formed generalised maps of their experience on the multi-surfaced treadmill, and the team found that these were stored in the superficial layer of CA1. © Copyright Reed Business Information Ltd.
Keyword: Learning & Memory
Link ID: 22414 - Posted: 07.09.2016