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Alison Abbott The octopus genome offers clues to how cephalopods evolved intelligence to rival the craftiest vertebrates. With its eight prehensile arms lined with suckers, camera-like eyes, elaborate repertoire of camouflage tricks and spooky intelligence, the octopus is like no other creature on Earth. Added to those distinctions is an unusually large genome, described in Nature1 on 12 August, that helps to explain how a mere mollusc evolved into an otherworldly being. “It’s the first sequenced genome from something like an alien,” jokes neurobiologist Clifton Ragsdale of the University of Chicago in Illinois, who co-led the genetic analysis of the California two-spot octopus (Octopus bimaculoides). The work was carried out by researchers from the University of Chicago, the University of California, Berkeley, the University of Heidelberg in Germany and the Okinawa Institute of Science and Technology in Japan. The scientists also investigated gene expression in twelve different types of octopus tissue. “It’s important for us to know the genome, because it gives us insights into how the sophisticated cognitive skills of octopuses evolved,” says neurobiologist Benny Hochner at the Hebrew University of Jerusalem in Israel, who has studied octopus neurophysiology for 20 years. Researchers want to understand how the cephalopods, a class of free-floating molluscs, produced a creature that is clever enough to navigate highly complex mazes and open jars filled with tasty crabs. © 2015 Nature Publishing Group
A healthy motor neuron needs to transport its damaged components from the nerve-muscle connection all the way back to the cell body in the spinal cord. If it cannot, the defective components pile up and the cell becomes sick and dies. Researchers at the National Institutes of Health’s National Institute of Neurological Disorders and Stroke (NINDS) have learned how a mutation in the gene for superoxide dismutase 1 (SOD1), which causes ALS, leads cells to accumulate damaged materials. The study, published in the journal Neuron, suggests a potential target for treating this familial form of ALS. More than 12,000 Americans have ALS, also known as Lou Gehrig’s disease, and roughly 5-10 percent of them inherited a genetic mutation from a parent. These cases of familial ALS are often caused by mutations in the gene that codes for SOD1, an important enzyme located in the neuron’s mitochondria, the cell’s energy-producing structures. This mutation causes the death of motor neurons that control the patient’s muscles, resulting in progressive paralysis. “About 90 percent of the energy in the brain is generated by mitochondria,” said Zu-Hang Sheng, Ph.D., an NINDS scientist and the study’s senior author. “If the mitochondria aren’t healthy, they produce energy less efficiently; they can also release harmful chemicals called reactive oxygen species that cause cell death. As a consequence, mitochondrial damage can cause neurodegeneration.” In healthy neurons, storage containers called late endosomes collect damaged mitochondria and various destructive chemicals. A motor protein called dynein then transports the endosomes to structures called lysosomes, which use the chemicals to break down the endosomes. Dr. Sheng’s team discovered that this crucial process is faulty in nerve cells with SOD1 mutations because mutant SOD1 interferes with a critical molecule called snapin that hooks the endosome to the dynein motor protein.
Keyword: ALS-Lou Gehrig's Disease
Link ID: 21294 - Posted: 08.13.2015
Richard Harris Hospitals have a free and powerful tool that they could use more often to help reduce the pain that surgery patients experience: music. Scores of studies over the years have looked at the power of music to ease this kind of pain; an analysis published Wednesday in The Lancet that pulls all those findings together builds a strong case. When researchers in London started combing the medical literature for studies about music's soothing power, they found hundreds of small studies suggesting some benefit. The idea goes back to the days of Florence Nightingale, and music was used to ease surgical pain as early as 1914. (My colleague Patricia Neighmond reported on one of these studies just a few months ago). Dr. Catherine Meads at Brunel University focused her attention on 73 rigorous, randomized clinical trials about the role of music among surgery patients. "As they studies themselves were small, they really didn't find all that much," Meads says. "But once we put them all together, we had much more power to find whether music worked or not." She and her colleagues now report that, yes indeed, surgery patients who listened to music, either before, during or after surgery, were better off — in terms of reduced pain, less anxiety and more patient satisfaction. © 2015 NPR
Keyword: Pain & Touch
Link ID: 21293 - Posted: 08.13.2015
by Julia Belluz When neuroscientists stuck a dead salmon in an fMRI machine and watched its brain light up, they knew they had a problem. It wasn't that there was a dead fish in their expensive imaging machine; they'd put it there on purpose, after all. It was that the medical device seemed to be giving these researchers impossible results. Dead fish should not have active brains. The lit of brain of a dead salmon — a cautionary neuroscience tale. (University of California Santa Barbara research poster) The researchers shared their findings in 2009 as a cautionary tale: If you don't run the proper statistical tests on your neuroscience data, you can come up with any number of implausible conclusions — even emotional reactions from a dead fish. In the 1990s, neuroscientists started using the massive, round fMRI (or functional magnetic resonance imaging) machines to peer into their subjects' brains. But since then, the field has suffered from a rash of false positive results and studies that lack enough statistical power — the likelihood of finding a real result when it exists — to deliver insights about the brain. When other scientists try to reproduce the results of original studies, they too often fail. Without better methods, it'll be difficult to develop new treatments for brain disorders and diseases like Alzheimer's and depression — let alone learn anything useful about our most mysterious organ. © 2015 Vox Media, Inc
Keyword: Brain imaging
Link ID: 21292 - Posted: 08.13.2015
Alison Abbott This is the crackle of neural activity that allows a fruit-fly (Drosophila melanogaster) larva to crawl backwards: a flash in the brain and a surge that undulates through the nervous system from the top of the larva’s tiny body to the bottom. When the larva moves forwards, the surge flows the other way. The video — captured almost at the resolution of single neurons — demonstrates the latest development in a technique to film neural activity throughout an entire organism. The original method was invented by Philipp Keller and Misha Ahrens at the Howard Hughes Medical Institute's Janelia Research Campus in Ashburn, Virginia. The researchers genetically modify neurons so that each cell fluoresces when it fires; they then use innovative microscopy that involves firing sheets of light into the brain to record that activity. In 2013, the researchers produced a video of neural activity across the brain of a (transparent) zebrafish larva1. The fruit-fly larva that is mapped in the latest film, published in Nature Communications on 11 August2, is more complicated. The video shows neural activity not just in the brain, but throughout the entire central nervous system (CNS), including the fruit-fly equivalent of a mammalian spinal cord. And unlike the zebrafish, the fruit fly's nervous system is not completely transparent, which makes it harder to image. The researchers stripped the CNS from the larva’s body to examine it. For up to an hour after removal, the CNS continues to spontaneously fire the coordinated patterns of activity that typically drive crawling (and other behaviours). © 2015 Nature Publishing Group
Keyword: Brain imaging
Link ID: 21291 - Posted: 08.12.2015
Your body may be still, but as you dream, your eyes can flicker manically. The rapid eye movement stage of sleep is when we have our most vivid dreams – but do our flickering eyes actually “see” anything? It is a question psychologists have been asking since REM sleep was first described in the 1950s, says Yuval Nir at Tel Aviv University in Israel. “The idea was that we scan an imaginary scene,” says Nir. “It’s an intuitive idea, but it has been very difficult to provide evidence for it.” Until now, much of the evidence has been anecdotal, says Nir. “People who were woken up when their eyes were moving from left to right would say they were dreaming about tennis, for example,” he says. More evidence comes from a previous study that monitored the sleep of people who have a disorder that means they often physically act out their dreams. Their eye movements matched their actions around 80 per cent of the time – a man dreaming about smoking, for example, appeared to look at a dream ashtray as he put out a cigarette. But most of the REM sleep these people had was not accompanied by body movements, making it hard to know for sure. And other researchers have argued that the eye flickers can’t be linked to “seeing” anything because rapid eye movements happen in both fetuses and people who are blind – neither group would have experience of vision and so wouldn’t be expected to move their eyes to follow an object, for example. © Copyright Reed Business Information Ltd.
Link ID: 21290 - Posted: 08.12.2015
Ashley Yeager A mouse scurries across a round table rimmed with Dixie cup–sized holes. Without much hesitation, the rodent heads straight for the hole that drops it into a box lined with cage litter. Any other hole would have led to a quick fall to the floor. But this mouse was more than lucky. It had an advantage — human glial cells were growing in its brain. Glia are thought of as the support staff for the brain’s nerve cells, or neurons, which transmit and receive the brain’s electrical and chemical signals. Named for the Greek term for “glue,” glia have been known for nearly 170 years as the cells that hold the brain’s bits together. Some glial cells help feed neurons. Other glia insulate nerve cell branches with myelin. Still others attack brain invaders responsible for infection or injury. Glial cells perform many of the brain’s most important maintenance jobs. But recent studies suggest they do a lot more. Glia can shape the conversation between neurons, speeding or slowing the electrical signals and strengthening neuron-to-neuron connections. When scientists coaxed human glia to grow in the brains of baby mice, the mice grew up to be supersmart, navigating tabletops full of holes and mastering other tasks much faster than normal mice. This experiment and others suggest that glia may actually orchestrate learning and memory, says neuroscientist R. Douglas Fields. “Glia aren’t doing vibrato. That’s for the neurons,” says Fields, of the National Institute of Child Health and Human Development in Bethesda, Md. “Glia are the conductors.” © Society for Science & the Public 2000 - 2015
There may finally be a way to stop people progressing beyond the first signs of schizophrenia – fish oil. When people with early-stage symptoms took omega-3 supplements for three months, they had much lower rates of progression than those who did not, according to one small-scale trial. People with schizophrenia are usually diagnosed in their teens or 20s, but may experience symptoms for years beforehand, such as minor delusions or paranoid thoughts. Only about a third of people with such symptoms do go on to develop psychosis, however, and antipsychotic drugs can cause nasty side effects, so these are rarely given as a preventative. Fish oil supplements, which contain polyunsaturated fatty acids like omega-3, may be a benign alternative. These fatty acids may normally help dampen inflammation in the brain and protect neurons from damage, and lower levels in the brain have been implicated in several mental illnesses. Tests have found that people with schizophrenia have lower levels of these fatty acids in their blood cells, suggesting the same could be true for their brain cells. Fish oil supplements have been investigated as a treatment for adults with schizophrenia, but so far results have been mixed – four trials found no benefit while another four found a small reduction in symptoms. But a study that gave omega-3 fish oil pills to younger people suggests that what matters is catching the condition in time. The trial followed 81 people aged 13 to 25 with early signs of schizophrenia. Roughly half took fish oil pills and half took placebo tablets for three months. A year later, those given fish oils were less likely to have developed psychosis. © Copyright Reed Business Information Ltd.
Link ID: 21288 - Posted: 08.12.2015
Despite virtual reality’s recent renaissance, the technology still has some obvious problems. One, you look like a dumbass using it. Two, the stomach-churning mismatch between what you see and what you feel contributes to “virtual reality sickness.” But there’s another, less obvious flaw that could add to that off-kilter sensation: an eye-focusing problem called vergence-accommodation conflict. It’s only less obvious because, well, you rarely experience it outside of virtual reality. At SIGGRAPH in Los Angeles this week, Stanford professor Gordon Wetzstein and his colleagues are presenting a new head-mounted display that minimizes the vergence-accommodation conflict. This isn’t just some esoteric academic problem. Leading VR companies like Oculus and Microsoft know all too well their headsets are off, and Magic Leap, the super secret augmented reality company in Florida, is betting the house on finding a solution first. “It’s an exciting area of research,” says Martin Banks, a vision scientist at the University of California, Berkeley. “I think it’s going to be the next big thing in displays.” Okay okay, so what’s the big deal with the vergence-accommodation conflict? Two things happen when you simply “look” at an object. First, you point your eyeballs. If an object is close, your eyes naturally converge on it; if it’s far, they diverge. Hence, vergence. If your eyes don’t line up correctly, you end up seeing double. The second thing that happens is the lenses inside your eyes focus on the object, aka accommodation. Normally, vergence and accommodation are coupled. “The visual system has developed a circuit where the two response talk to each other,” says Banks. “That makes perfect sense in the natural environment. They’re both trying to get to the same distance, so why wouldn’t they talk to one another?” In other words, your meat brain has figured out a handy shortcut for the real world.
Link ID: 21287 - Posted: 08.12.2015
Could taking iodine pills in pregnancy help to raise children’s IQ? Some researchers suggest women in the UK should take such supplements, but others say the evidence is unclear, and that it could even harm development. Iodine is found in dairy foods and fish, and is used in the body to make thyroid hormone, which is vital for brain development in the womb. In some parts of the world, such as inland areas where little fish is consumed or the soil is low in iodine, severe deficiencies can markedly lower intelligence in some people. In most affected areas, iodine is now added to salt. The UK was not thought to need this step, but in 2013 a large study of urine samples from pregnant women found that about two-thirds had mild iodine deficiency, and that the children of those with the lowest levels had the lowest IQs. Now another team has combined data from this study with other data to calculate that if all women in the UK were given iodine supplements from three months before pregnancy until they finished breastfeeding, average IQ would increase by 1.2 points per child. And the children of mothers who were most iodine deficient would probably benefit more, says Kate Jolly of the University of Birmingham, who was involved in the study. “We are talking about very small differences but on a population basis it could mean quite a lot,” she says. The team calculated that providing these iodine supplements would be worth the cost to the UK’s National Health Service because it would boost the country’s productivity. © Copyright Reed Business Information Ltd.
By Dina Fine Maron Don’t stress too much about cutting calories if you want to shed pounds—focus on getting more exercise. That’s the controversial message beverage giant Coca-Cola is backing in its new campaign to curb obesity. Coke is pushing this idea via a new Coke-backed nonprofit called Global Energy Balance Network, The New York Times reported on August 9. Money from Coke, the Times reported, is also financing studies that support the notion that exercise trumps diet. But is there any merit to such a stance? Not much, says Rutgers University–based diet and behavior expert Charlotte Markey. She is the author of an upcoming cover story in Scientific American MIND on this topic, and spoke about the Coke claims with Scientific American on Monday. In your fall Scientific American MIND feature you write “study after study shows that working out is not terribly effective for weight loss on its own.” Why is that? Exercise increases appetite, and most people just make up for whatever they exercised off. There’s a lot of wonderful reasons to exercise and I always suggest it to people who are trying to lose weight—some sort of exercise regimen keeps them focused on their health and doing what is good for them, and it’s psychologically healthy. But in and of itself it won’t usually help people lose weight. Two years ago there was a review study in Frontiers in Psychology that concluded dieting often actually led to weight gain. Why would that happen? When people try to diet, they try to restrict themselves, which often leads to overeating. They cut out food groups which make those food groups more desirable to them. They think too much about short-term goals and don’t think about sustainable changes. But if you are going to lose weight, you have to change your behaviors for the rest of your life or otherwise you gain it back. That’s not a sexy message because it seems daunting. © 2015 Scientific American
Link ID: 21285 - Posted: 08.12.2015
Sarah Schwartz In 2011, science journalist Jon Palfreman saw a doctor about a tremor in his left hand. The doctor diagnosed Palfreman, then 60, with Parkinson’s disease. The disorder, which is newly diagnosed in 60,000 Americans each year, promised a crippling future of tremors, loss of mobility, dementia and more. Palfreman decided to use his reporting expertise to investigate how Parkinson’s disease affects the body and learn about efforts to find a cure. With Brain Storms, Palfreman follows Parkinson’s history from the careful observations of 19th century physicians to today’s cutting-edge research. Palfreman relates complex research studies as gripping medical mysteries. He describes how scientists connected Parkinson’s with the dramatic loss of the brain chemical dopamine and with tenacious protein knots called Lewy bodies that are a hallmark of the disease. Palfreman also explores treatments past and present, including the widely used drug levodopa that restores motion (sometimes uncontrollably), gene therapies, brain surgeries and promising experimental antibody treatments that attack and dissolve misfolded Parkinson’s-related proteins. Ultimately, Brain Storms is about more than Parkinson’s disease; it’s about the people living with the disorder. Palfreman describes patients who must teach themselves to walk without falling over or who freeze in place. He writes about a researcher driven to search for a cure after the disease affects his own father. © Society for Science & the Public 2000 - 2015
Link ID: 21284 - Posted: 08.12.2015
By Anahad O’Connor Coca-Cola, the world’s largest producer of sugary beverages, is backing a new “science-based” solution to the obesity crisis: To maintain a healthy weight, get more exercise and worry less about cutting calories. The beverage giant has teamed up with influential scientists who are advancing this message in medical journals, at conferences and through social media. To help the scientists get the word out, Coke has provided financial and logistical support to a new nonprofit organization called the Global Energy Balance Network, which promotes the argument that weight-conscious Americans are overly fixated on how much they eat and drink while not paying enough attention to exercise. “Most of the focus in the popular media and in the scientific press is, ‘Oh they’re eating too much, eating too much, eating too much’ — blaming fast food, blaming sugary drinks and so on,” the group’s vice president, Steven N. Blair, an exercise scientist, says in a recent video announcing the new organization. “And there’s really virtually no compelling evidence that that, in fact, is the cause.” Health experts say this message is misleading and part of an effort by Coke to deflect criticism about the role sugary drinks have played in the spread of obesity and Type 2 diabetes. They contend that the company is using the new group to convince the public that physical activity can offset a bad diet despite evidence that exercise has only minimal impact on weight compared with what people consume. This clash over the science of obesity comes in a period of rising efforts to tax sugary drinks, remove them from schools and stop companies from marketing them to children. In the last two decades, consumption of full-calorie sodas by the average American has dropped by 25 percent. © 2015 The New York Times Company
Link ID: 21283 - Posted: 08.10.2015
By Janet Davison, CBC News Maddy Huggins would binge drink as a teenager and black out, just like other kids at her high school in Kelowna, B.C. When she went backpacking during her gap year, there were more alcoholic overloads and "really risky" moments when something bad could have transpired. "Nothing too terrible happened, but there was the potential for that," says Huggins, 22, who's just about to start fourth year at the University of Saskatchewan. As she settled into university, however, Huggins did some serious thinking about alcohol in her life. "It was just a gradual progression where I was like, 'OK, enough of this.'" These days, Huggins knows her low-risk alcoholic limits and won't hesitate to order water even if her friends are going for something stronger. But other young Canadian women haven't stepped back like that. Reports suggest the percentage of young women binge drinking — defined now as having at least four drinks per occasion at least once a month — is on the rise and encompasses nearly one in four Canadian women between 20 and 34. Indeed, the trend has become so pronounced that the Paris-based Organization of Economic Co-operation and Development warned in May that binge drinking by young people, including in Canada, has become a "major public health and social concern." Looming problems It's a concern that goes beyond the headline issues like date rape and campus horrors to where health scientists are warning that because of physiology — women generally weigh less than men, have a higher percentage of body fat and smaller livers — excessive drinking by young women is setting them up for a series of health problems down the road. ©2015 CBC/Radio-Canada
Rachel Martin The National Football League held its annual hall of fame induction ceremony Saturday night, in Canton, Ohio. Eight players were given football's highest honor, including a posthumous induction for Junior Seau, the former linebacker for the San Diego Chargers who killed himself in 2012. After his death, Seau's brain showed signs of chronic damage — the same kind of damage that has been found in dozens of other former NFL players. Scientific studies have shown that the kind of repeated hits NFL players take is linked to chronic traumatic encephalopathy, or CTE, a degenerative brain disease. CTE is associated with memory loss, impulse control problems, depression and eventually dementia. Some players are rethinking their careers — like up-and-coming linebacker Chris Borland, who quit after his first season with the 49ers a few months ago — for fear of head injuries. Parents are weighing the risks as well. So when someone like Chicago Bears coach Mike Ditka talks, they listen. When host Bryant Gumbel asked Ditka on HBO's Real Sports earlier this year whether, if he had an 8-year-old now, he would want him to play football. "No," he answered. "That's sad. I wouldn't, and my whole life was football. I think the risk is worse than the reward." Tregg Duerson's father, Dave Duerson, a defensive back who played most of his pro football career with the Chicago Bears, killed himself in 2011 in his Miami home. Duerson was part of the legendary '85 team that won the Superbowl, and five years later helped the New York Giants win their own championship. © 2015 NPR
Keyword: Brain Injury/Concussion
Link ID: 21281 - Posted: 08.10.2015
By PAUL GLIMCHER and MICHAEL A. LIVERMORE THE United States government recently announced an $18.7 billion settlement of claims against the oil giant BP in connection with the Deepwater Horizon oil rig explosion in April 2010, which dumped millions of barrels of oil into the Gulf of Mexico. Though some of the settlement funds are to compensate the region for economic harm, most will go to environmental restoration in affected states. Is BP getting off easy, or being unfairly penalized? This is not easy to answer. Assigning a monetary value to environmental harm is notoriously tricky. There is, after all, no market for intact ecosystems or endangered species. We don’t reveal how much we value these things in a consumer context, as goods or services for which we will or won’t pay a certain amount. Instead, we value them for their mere existence. And it is not obvious how to put a price tag on that. In an attempt to do so, economists and policy makers often rely on a technique called “contingent valuation,” which amounts to asking individuals survey questions about their willingness to pay to protect natural resources. The values generated by contingent valuation studies are frequently used to inform public policy and litigation. (If the government had gone to trial with BP, it most likely would have relied on such studies to argue for a large judgment against the company.) Contingent valuation has always aroused skepticism. Oil companies, unsurprisingly, have criticized the technique. But many economists have also been skeptical, worrying that hypothetical questions posed to ordinary citizens may not really capture their genuine sense of environmental value. Even the Obama administration seems to discount contingent valuation, choosing to exclude data from this technique in 2014 when issuing a new rule to reduce the number of fish killed by power plants. © 2015 The New York Times Company
By John Danaher Discoveries in neuroscience, and the science of behaviour more generally, pose a challenge to the existence of free will. But this all depends on what is meant by ‘free will’. The term means different things to different people. Philosophers focus on two conditions that seem to be necessary for free will: (i) the alternativism condition, according to which having free will requires the ability to do otherwise; and (ii) the sourcehood condition, according to which having free will requires that you (your ‘self’) be the source of your actions. A scientific and deterministic worldview is often said to threaten the first condition. Does it also threaten the second? That is what Christian List and Peter Menzies article “My brain made me do it: The exclusion argument against free will and what’s wrong with it” tries to figure out. As you might guess from the title, the authors think that the scientific worldview, in particular the advances in neuroscience, do not necessarily threaten the sourcehood condition. I discussed their main argument in the previous post. To briefly recap, they critiqued an argument from physicalism against free will. According to this argument, the mental states which constitute the self do not cause our behaviour because they are epiphenomenal: they supervene on the physical brain states that do all the causal work. List and Menzies disputed this by appealing to a difference-making account of causation. This allowed for the possibility of mental states causing behaviour (being the ‘difference makers’) even if they were supervenient upon underlying physical states.
Link ID: 21279 - Posted: 08.10.2015
April Dembosky Developers of a new video game for your brain say theirs is more than just another get-smarter-quick scheme. Akili, a Northern California startup, insists on taking the game through a full battery of clinical trials so it can get approval from the Food and Drug Administration — a process that will take lots of money and several years. So why would a game designer go to all that trouble when there's already a robust market of consumers ready to buy games that claim to make you smarter and improve your memory? Think about all the ads you've heard for brain games. Maybe you've even passed a store selling them. There's one at the mall in downtown San Francisco — just past the cream puff stand and across from Jamba Juice — staffed on my visit by a guy named Dominic Firpo. "I'm a brain coach here at Marbles: The Brain Store," he says. Brain coach? "Sounds better than sales person," Firpo explains. "We have to learn all 200 games in here and become great sales people so we can help enrich peoples' minds." He heads to the "Word and Memory" section of the store and points to one product that says it will improve your focus and reduce stress in just three minutes a day. "We sold out of it within the first month of when we got it," Firpo says. The market for these "brain fitness" games is worth about $1 billion and is expected to grow to $6 billion in the next five years. Game makers appeal to both the young and the older with the common claim that if you exercise your memory, you'll be able to think faster and be less forgetful. Maybe bump up your IQ a few points. "That's absurd," says psychology professor Randall Engle from the Georgia Institute of Technology. © 2015 NPR
Nell Greenfieldboyce Take a close look at a house cat's eyes and you'll see pupils that look like vertical slits. But a tiger has round pupils — like humans do. And the eyes of other animals, like goats and horses, have slits that are horizontal. Scientists have now done the first comprehensive study of these three kinds of pupils. The shape of the animal's pupil, it turns out, is closely related to the animal's size and whether it's a predator or prey. The pupil is the hole that lets light in, and it comes in lots of different shapes. "There are some weird ones out there," says Martin Banks, a vision scientist at the University of California, Berkeley. Cuttlefish have pupils that look like the letter "W," and dolphins have pupils shaped like crescents. Some frogs have heart-shaped pupils, while geckos have pupils that look like pinholes arranged in a vertical line. Needless to say, scientists want to know why all these different shapes evolved. "It's been an active point of debate for quite some time," says Banks, "because it's something you obviously observe. It's the first thing you see about an animal — where their eye is located and what the pupil shape is." For their recent study, Banks and his colleagues decided to keep things simple. They looked at just land animals, and just three kinds of pupils. "We restricted ourselves to just pupils that are elongated or not," Banks explains. "So they're either vertical, horizontal or round." © 2015 NPR
By John Danaher Consider the following passage from Ian McEwan’s novel Atonement. It concerns one of the novel’s characters (Briony) as she philosophically reflects on the mystery of human action: She raised one hand and flexed its fingers and wondered, as she had sometimes done before, how this thing, this machine for gripping, this fleshy spider on the end of her arm, came to be hers, entirely at her command. Or did it have some little life of its own? She bent her finger and straightened it. The mystery was in the instant before it moved, the dividing moment between not moving and moving, when her intention took effect. It was like a wave breaking. If she could only find herself at the crest, she thought, she might find the secret of herself, that part of her that was really in charge. Is Briony’s quest forlorn? Will she ever find herself at the crest of the wave? The contemporary scientific understanding of human action seems to cast this into some doubt. A variety of studies in the neuroscience of action paint an increasingly mechanistic and subconscious picture of human behaviour. According to these studies, our behaviour is not the product of our intentions or desires or anything like that. It is the product of our neural networks and systems, a complex soup of electrochemical interactions, oftentimes operating beneath our conscious awareness. In other words, our brains control our actions; our selves (in the philosophically important sense of the word ‘self’) do not. This discovery — that our brains ‘make us do it’ and that ‘we’ don’t — is thought to have a number of significant social implications, particularly for our practices of blame and punishment.
Link ID: 21276 - Posted: 08.08.2015