Chapter 13. Memory, Learning, and Development
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by Clare Wilson Figuring out how the brain works is enough to make your head spin. But now we seem to have a handle on how it gets its folded shape. The surface layer of the brain, or cortex, is also referred to as our grey matter. Mammals with larger brains have a more folded cortex, and the human brain is the most wrinkled of all, cramming as much grey matter into our skulls as possible. L. Mahadevan at Harvard University and his colleagues physically modelled how the brain develops in the embryo, using a layer of gel to stand in for the grey matter. This gel adhered to the top of a solid hemisphere of gel representing the white matter beneath. In the embryo, grey matter grows as neurons are created or others migrate to the cortex from the brain's centre. By adding a solvent to make the grey matter gel expand, the team mimicked how the cortex might grow in the developing brain. They didn't model what effect, if any, the skull would have had. Hills and valleys The team varied factors such as the stiffness of the gels and the depth of the upper layer to find a combination that led to similarly shaped wrinkles as those of the human brain, with smooth "hills" and sharply cusped "valleys". There are several theories about how the brain's folds form. These include the possibility that more neurons migrate to the hills, making them rise above the valleys, or that the valleys are pulled down by the axons – fibres that connect neurons to each other – linking highly interconnected parts of the brain together. © Copyright Reed Business Information Ltd.
Keyword: Development of the Brain
Link ID: 19974 - Posted: 08.19.2014
Sara Reardon The National Science Foundation (NSF)’s role in the Brain Research through Advancing Innovative Neurotechnologies (BRAIN) Initiative is starting to take shape. On 18 August, the NSF awarded 36 small grants totalling US$10.8 million to projects studying everything from electrodes that measure chemical and electronic signals to artificial intelligence programs to identify brain structures. The three agencies participating in the BRAIN Initiative have taken markedly different approaches. The Defense Advanced Research Projects Agency, which received $50 million this year for the neuroscience programme, is concentrating on prosthetics and treatments for brain disorders that affect veterans, such as post-traumatic stress disorder. It has already awarded multi-million dollar grants to several teams. The National Institutes of Health, which received $40 million this year, has put together a 146-page plan to map and observe the brain over the next decade, and will announce its first round of grant recipients next month. The NSF, by contrast, has cast a wider net. The agency sent an request in March for informal, two-page project ideas. The only criterion was that the projects somehow address the properties of neural circuits. The response was overwhelming, says James Deshler, deputy director of the NSF’s Division of Biological Infrastructure. The agency had expected to fund about 12 grants, but decided to triple that number after receiving nearly 600 applications. “People started finding money in different pockets,” Deshler says. The wide-ranging list of winning projects includes mathematical models that help computers recognize different parts and patterns in the brain, physical tools such as new types of electrodes, and other tools that integrate and link neural activity to behaviour. © 2014 Nature Publishing Group
Helen Shen For most adults, adding small numbers requires little effort, but for some children, it can take all ten fingers and a lot of time. Research published online on 17 August in Nature Neuroscience1 suggests that changes in the hippocampus — a brain area associated with memory formation — could help to explain how children eventually pick up efficient strategies for mathematics, and why some children learn more quickly than others. Vinod Menon, a developmental cognitive neuroscientist at Stanford University in California, and his colleagues presented single-digit addition problems to 28 children aged 7–9, as well as to 20 adolescents aged 14–17 and 20 young adults. Consistent with previous psychology studies2, the children relied heavily on counting out the sums, whereas adolescents and adults tended to draw on memorized information to calculate the answers. The researchers saw this developmental change begin to unfold when they tested the same children at two time points, about one year apart. As the children aged, they began to move away from counting on fingers towards memory-based strategies, as measured by their own accounts and by decreased lip and finger movements during the task. Using functional magnetic resonance imaging (fMRI) to scan the children's brains, the team observed increased activation of the hippocampus between the first and second time point. Neural activation decreased in parts of the prefrontal and parietal cortices known to be involved in counting, suggesting that the same calculations had begun to engage different neural circuits. © 2014 Nature Publishing Group
by Andy Coghlan Pioneering studies of post-mortem brain tissues have yielded the first evidence of a potential association between Alzheimer's disease and the epigenetic alteration of gene function. The researchers stress, however, that more research is needed to find out if the changes play a causal role in the disease or occur as a result of it. We already have some evidence that the risk of developing Alzheimer's might be elevated by poor diet, lack of exercise, and inflammatory conditions such as diabetes, obesity and clogging of blood vessels with fatty deposits. The new research hints that the lifestyle changes that raise Alzheimer's risk may be taking effect through epigenetic changes. The idea is strengthened by the fact that the brain tissue samples studied in the new work came from hundreds of people, many of whom had Alzheimer's when they died, and that a number of genes identified were found by two teams working independently, one in the UK and one in the US. "The results are compelling and consistent across four cohorts of patients taken across the two studies," says Jonathan Mill at the University of Exeter, who led the UK-based team. "It's illuminated new genetic pathways affecting the disease and, given the lack of success tackling Alzheimer's so far, new leads are going to be vital." "We can now focus our efforts on understanding how these genes are associated with the disease," says Philip De Jager of the Brigham and Women's Hospital in Boston, who headed the US team. © Copyright Reed Business Information Ltd.
|By Christie Nicholson Children who experience neglect, abuse and poverty have a tougher time as adults than do well-cared-for kids. Now there’s evidence that such stress can actually change the size of brain structures responsible for learning, memory and processing emotion. The finding is in the journal Biological Psychiatry. [Jamie L. Hanson et al, Behavioral Problems After Early Life Stress: Contributions of the Hippocampus and Amygdala] Researchers took images of the brains of 12-year-olds who had suffered either physical abuse or neglect or had grown up poor. From the images the scientists were able to measure the size of the amygdala and hippocampus—two structures involved in emotional processing and memory. And they compared the sizes of these structures with those of 12-year-old children who were raised in middle-class families and had not been abused. And they found that the stressed children had significantly smaller amygdalas and hippocampuses than did the kids from the more nurturing environments. Early stress has been associated with depression, anxiety, cancer and lack of career success later on in adulthood. This study on the sizes of brain regions may offer physiological clues to why what happens to toddlers can have such a profound impact decades later. © 2014 Scientific American
by Catherine Brahic Think crayfish and you probably think supper, perhaps with mayo on the side. You probably don't think of their brains. Admittedly, crayfish aren't known for their grey matter, but that might be about to change: they can grow new brain cells from blood. Humans can make new neurons, but only from specialised stem cells. Crayfish, meanwhile, can convert blood to neurons that resupply their eyestalks and smell circuits. Although it's a long way from crayfish to humans, the discovery may one day help us to regenerate our own brain cells. Olfactory nerves are continuously exposed to damage and so naturally regenerate in many animals, from flies to humans, and crustaceans too. It makes sense that crayfish have a way to replenish these nerves. To do so, they utilise what amounts to a "nursery" for baby neurons, a little clump at the base of the brain called the niche. In crayfish, blood cells are attracted to the niche. On any given day, there are a hundred or so cells in this area. Each cell will split into two daughter cells, precursors to full neurons, both of which migrate out of the niche. Those that are destined to be part of the olfactory system head to two clumps of nerves in the brain called clusters 9 and 10. It's there that the final stage of producing new smell neurons is completed. © Copyright Reed Business Information Ltd.
Sara Reardon When the states of Colorado and Washington voted to legalize marijuana in 2012, the abrupt and unprecedented policy switch sent the US National Institute on Drug Abuse (NIDA) into what its director Nora Volkow describes as “red alarm”. Although marijuana remained illegal for people under the age of 21, the drug’s increased availability and growing public acceptance suggested that teenagers might be more likely to try it (see ‘Highs and lows’). Almost nothing is known about whether or how marijuana affects the developing adolescent brain, especially when used with alcohol and other drugs. The new laws, along with advances in brain-imaging technology, convinced Volkow to accelerate the launch of an ambitious effort to follow 10,000 US adolescents for ten years in an attempt to determine whether marijuana, alcohol and nicotine use are associated with changes in brain function and behaviour. At a likely cost of more than US$300 million, it will be the largest longitudinal brain-imaging study of adolescents yet. Researchers are eager to study a poorly understood period of human development — but some question whether it is possible to design a programme that will provide useful information about the effects of drugs. “It’s definitely an idea that’s overdue,” says Deanna Barch, a psychologist at Washington University in St. Louis, Missouri. “The downside is it’s a lot of eggs in one basket.” © 2014 Nature Publishing Group,
Jia You Premature babies are more likely to produce piercing cries than their full-term peers are, researchers report online today in Biology Letters. Scientists have studied infant crying as a noninvasive way to assess how well a baby’s nervous system develops. Previous research of full-term babies indicates that an abnormally high pitch is associated with disturbances in an infant’s metabolism and neurological development. The team recorded spontaneous crying in preterm babies and full-term babies of the same age and compared the pitch of their sobs. They found that preterm babies whimper in a shriller voice, but not because they are smaller in size or grew at a slower rate in their mothers’ wombs. Instead, the researchers suspect the high pitch could reflect lower levels of activities in a premature baby’s vagal nerve, which extends from the brain stem to the abdomen. Vagal nerve activities are believed to decrease tension in the vocal cords, thus producing a lower pitch. Previous studies show that giving preterm babies massage therapies can stimulate their vagal activities, improve their ingestion, and help them gain weight. © 2014 American Association for the Advancement of Science
Keyword: Development of the Brain
Link ID: 19946 - Posted: 08.13.2014
By Rachel Feltman Bioengineers have created the most realistic fake brain tissue ever – and it’s built like a jelly doughnut. The 3-D tissue, described in a paper published Monday in Proceedings of the National Academy of Sciences, is so structurally similar to a real rat brain (a common substitute for human brains in the lab) that it could help scientists answer longstanding questions about brain injuries and disease. Currently, the best way to study brain tissue is to grow neurons in a petri dish, but those neurons can only be grown flat. A real brain contains a complicated structure of 3-D tissue. Simply giving the neurons room to grow in three dimensions didn’t prove successful: While neurons will grow into more complicated structures in the right kind of gel, they don’t survive very long or mimic the structure of a real brain. Led by David Kaplan, the director of the Tissue Engineering Resource Center at Tufts University, researchers developed a new combination of materials to mimic the gray and white matter of the brain. The new model relies on a doughnut-shaped, spongy scaffold made of silk proteins with a collagen-based gel at the center. The outer scaffold layer, which is filled with rat neurons, acts as the grey matter of the brain. As the neurons grew networks throughout the scaffold, they sent branches out across the gel-filled center to connect with neurons on the other side. And that configuration is about as brain-like as lab-grown tissue can get. The basic structure can be reconfigured, too.
By PAM BELLUCK The 40-year-old man showed up in Dr. Mary Malloy’s clinic with sadly disfiguring symptoms. His hands, elbows, ears and feet were blemished with protruding pustules and tuber-like welts, some so painful it was hard for him to walk. He suffered from a rare genetic condition called dysbetalipoproteinemia, which caused his cholesterol levels to soar so high that pools of fatty tissue seemed to bubble up under his skin. But there was something else about this patient. He was missing a gene that, when present in one form, greatly increases the risk of developing Alzheimer’s disease. Dr. Malloy, who co-directs the Adult Lipid Clinic at the University of California, San Francisco, and her colleagues saw an opportunity to answer an important neurological riddle: Does the absence of the gene — named apolipoprotein E, or APOE, after the protein it encodes — hurt the brain? If a person with this rare condition were found to be functioning normally, that would suggest support for a new direction in Alzheimer’s treatment. It would mean that efforts — already being explored by dementia experts — to prevent Alzheimer’s by reducing, eliminating or neutralizing the effects of the most dangerous version of APOE might succeed without causing other problems in the brain. The researchers, who reported their findings on Monday in the journal JAMA Neurology, discovered exactly that. They ran a battery of tests, including cognitive assessments, brain imaging and cerebrospinal fluid analyses. The man’s levels of beta-amyloid and tau proteins, which are markers of Alzheimer’s, gave no indication of neurological disease. His brain size was unaffected, and the white matter was healthy. His thinking and memory skills were generally normal. “This particular case tells us you can actually live without any APOE in the brain,” said Dr. Joachim Herz, a neuroscientist and molecular geneticist at University of Texas Southwestern Medical Center, who was not involved in the research. “So if they were to develop anti-APOE therapies for Alzheimer’s, we would not have to worry about serious neurological side effects.” © 2014 The New York Times Company
Link ID: 19943 - Posted: 08.12.2014
By Smitha Mundasad Health reporter, BBC News Human brains grow most rapidly just after birth and reach half their adult size within three months, according to a study in JAMA Neurology. Using advanced scanning techniques, researchers found male brains grew more quickly than those of female infants. Areas involved in movement developed at the fastest pace. Those associated with memory grew more slowly. Scientists say collating this data may help them identify early signs of developmental disorders such as autism. For centuries doctors have estimated brain growth using measuring tape to chart a baby's head circumference over time. Any changes to normal growth patterns are monitored closely as they can suggest problems with development. But as head shapes vary, these tape measurements are not always accurate. Led by scientists at the University of California, researchers scanned the brains of 87 healthy babies from birth to three months. They saw the most rapid changes immediately after birth - newborn brains grew at an average rate of 1% a day. This slowed to 0.4% per day at the end of the 90-day period. Researchers say recording the normal growth trajectory of individual parts of the brain might help them better understand how early disorders arise. They found the cerebellum, an area of the brain involved in the control of movement, had the highest rate of growth - doubling in size over the 90-day period. BBC © 2014
by Aviva Rutkin What can the human brain do for a computer? There's at least one team of researchers that thinks it might have the answer. Working at IBM Research–Almaden in San Jose, California, they have just released more details of TrueNorth, a computer chip composed of one million digital "neurons". Under way for several years, the project abandons traditional computer architecture for one inspired by biological synapses and axons. The latest results, published in Science, provide a timely reminder of the promise of brain-inspired computing. The human brain still crushes any modern machines when it comes to tasks like vision or voice recognition. What's more, it manages to do so with less energy than it takes to power a light bulb. Building those qualities into a computer is an alluring prospect to many researchers, like Kwabena Boahen of Stanford University in California. "The first time I learned how computers worked, I thought it was ridiculous," he says. "I basically felt there had to be a better way." Aping the brain's structure could help us build computers that are far more powerful and efficient than today's, says TrueNorth team leader Dharmendra Modha. "We want to approximate the anatomy and physiology, the structure and dynamics of the brain, within today's silicon technology," he says. "I think that the chip and the associated ecosystem have the potential to transform science, technology, business, government and society." But how best to go about building a proper artificial brain is a matter of debate. © Copyright Reed Business Information Ltd
Link ID: 19932 - Posted: 08.09.2014
Posted by Ewen Callaway More than 130 leading population geneticists have condemned a book arguing that genetic variation between human populations could underlie global economic, political and social differences. “A Troublesome Inheritance“, by science journalist Nicholas Wade, was published in June by Penguin Press in New York. The 278-page work garnered widespread criticism, much of it from scientists, for suggesting that genetic differences (rather than culture) explain, for instance, why Western governments are more stable than those in African countries. Wade is former staff reporter and editor at the New York Times, Science and Nature. But the letter — signed by a who’s who of population genetics and human evolution researchers, and to be published in the 10 August New York Times — represents a rare unified statement from scientists in the field and includes many whose work was cited by Wade. “It’s just a measure of how unified people are in their disdain for what was done with the field,” says Michael Eisen, a geneticist at the University of California, Berkeley, who co-drafted the letter. “Wade juxtaposes an incomplete and inaccurate explanation of our research on human genetic differences with speculation that recent natural selection has led to worldwide differences in I.Q. test results, political institutions and economic development. We reject Wade’s implication that our findings substantiate his guesswork. They do not,” states the letter, which is a response to a critical review of the book published in the New York Times. “This letter is driven by politics, not science,” Wade said in a statement. “I am confident that most of the signatories have not read my book and are responding to a slanted summary devised by the organizers.” © 2014 Macmillan Publishers Limited
Keyword: Genes & Behavior
Link ID: 19931 - Posted: 08.09.2014
by Bethany Brookshire For most of us, where our birthday falls in the year doesn’t matter much in the grand scheme of things. A July baby doesn’t make more mistakes than a Christmas kid — at least, not because of their birthdays. But for neurons, birth date plays an important role in how these cells find their connections in the brain, a new study finds. Nerve cells that form early in development will make lots of connections — and lots of mistakes. Neurons formed later are much more precise in their targeting. The findings are an important clue to help scientists understand how the brain wires itself during development. And with more information on how the brain forms its network, scientists might begin to see what happens when that network is injured or malformed. Many, many brain cells are born as the brain develops. Each one has to reach out and make connections, sometimes to other cells around them and sometimes to other regions of the brain. To do this, these nerve cells send out axons, long, incredibly thin projections that reach out to other regions. How mammalian axons end up at their final destination in the growing brain remains a mystery. To find out how developing brains get wired up, Jessica Osterhout and colleagues at the University of California, San Diego and colleagues started in the eye. They looked at retinal ganglion cells, neurons that connect the brain and the eye. “It’s easy to access,” explains Andrew Huberman, a neuroscientist at UC San Diego and an author on the paper. “Your retina is basically part of the central nervous system that got squeezed into your eye during development.” Retinal ganglion cells all have the same function: To convey visual information from the eyes to the brain. But they are not all the same. © Society for Science & the Public 2000 - 2013
Ian Sample, science editor Stroke patients who took part in a small pilot study of a stem cell therapy have shown tentative signs of recovery six months after receiving the treatment. Doctors said the condition of all five patients had improved after the therapy, but that larger trials were needed to confirm whether the stem cells played any part in their progress. Scans of the patients' brains found that damage caused by the stroke had reduced over time, but similar improvements are often seen in stroke patients as part of the normal recovery process. At a six-month check-up, all of the patients fared better on standard measures of disability and impairment caused by stroke, but again their improvement may have happened with standard hospital care. The pilot study was designed to assess only the safety of the experimental therapy and with so few patients and no control group to compare them with, it is impossible to draw conclusions about the effectiveness of the treatment. Paul Bentley, a consultant neurologist at Imperial College London, said his group was applying for funding to run a more powerful randomised controlled trial on the therapy, which could see around 50 patients treated next year. "The improvements we saw in these patients are very encouraging, but it's too early to draw definitive conclusions about the effectiveness of the therapy," said Soma Banerjee, a lead author and consultant in stroke medicine at Imperial College Healthcare NHS Trust. "We need to do more tests to work out the best dose and timescale for treatment before starting larger trials." The five patients in the pilot study were treated within seven days of suffering a severe stroke. Each had a bone marrow sample taken, from which the scientists extracted stem cells that give rise to blood cells and blood vessel lining cells. These stem cells were infused into an artery that supplied blood to the brain. © 2014 Guardian News and Media Limited
by Laura Sanders In their first year, babies grow and change in all sorts of obvious and astonishing ways. As their bodies become longer, heavier and stronger, so do their brains. Between birth and a child’s first birthday, her brain nearly triples in size as torrents of newborn nerve cells create neural pathways. This incredible growth can be influenced by a baby’s early life environment, scientists have found. Tragic cases of severe neglect or abuse can throw brain development off course, resulting in lifelong impairments. But in happier circumstances, warm caregivers influence a baby’s brain, too. A new study in rats provides a glimpse of how motherly actions influence a pup’s brain. Scientists recorded electrical activity in the brains of rat pups as their mamas nursed, licked and cared for their offspring. The results, published in the July 21 Current Biology, offer a fascinating minute-to-minute look at the effects of parenting. Researchers led by Emma Sarro of New York University’s medical school implanted electrodes near six pups’ brains to record neural activity. Video cameras captured mother-pup interactions, allowing the scientists to link specific maternal behaviors to certain sorts of brain activity. Two types of brain patterns emerged: a highly alert state and a sleepier, zoned-out state, Sarro and colleagues found. Pups’ brains were alert while they were drinking milk and getting groomed by mom. Pups’ brains’ were similarly aroused when the pups were separated from their mom and siblings. Some scientists think that these bursts of brain activity help young brains form the right connections between regions. © Society for Science & the Public 2000 - 2013.
By Sandhya Somashekhar The first time Jeremy Clark met his 18-year-old client, the teenager was sitting in his vice principal’s office, the drawstrings of his black hoodie pulled tight. Jacob had recently disclosed to his friends on Facebook that he was hearing voices, and their reaction had been less than sympathetic. So Clark was relieved when a beaming Jacob showed up on time for their next meeting, at a comic book shop. As the pair bantered about “Star Wars” and a recent Captain America movie, however, Clark picked up troubling signs: Jacob said he was “detaching” from his family, often huddling alone in his room. As the visit ended, Clark gave the teen a bear hug and made a plan. “Let’s get together again next week,” he said. The visit was part of a new approach being used nationwide to find and treat teenagers and young adults with early signs of schizophrenia. The goal is to bombard them with help even before they have had a psychotic episode — a dramatic and often devastating break with reality that is a telltale sign of the disease. The program involves an intensive two-year course of socialization, family therapy, job and school assistance, and, in some cases, antipsychotic medication. What makes the treatment unique is that it focuses deeply on family relationships, and occurs early in the disease, often before a diagnosis. So far, the results have been striking: In Portland, Maine, where the treatment was pioneered, the rate of hospitalizations for first psychotic episodes fell by 34 percent over a six-year period, according to a March study. And just last month, a peer-reviewed study published in the journal Schizophrenia Bulletin found that young people undergoing the treatment at six sites around the country were more likely to be in school or working than adolescents who were not in the program. The research was funded by a $17 million grant from the Robert Wood Johnson Foundation.
Older people who have a severe vitamin D deficiency have an increased risk of developing dementia, a study has suggested. UK researchers, writing in Neurology, looked at about 1,650 people aged over 65. This is not the first study to suggest a link - but its authors say it is the largest and most robust. However, experts say it is still too early to say elderly people should take vitamin D as a preventative treatment. There are 800,000 people with dementia in the UK with numbers set to rise to more than one million by 2021. Vitamin D comes from foods - such as oily fish, supplements and exposing skin to sunlight. However older people's skin can be less efficient at converting sunlight into Vitamin D, making them more likely to be deficient and reliant on other sources. The international team of researchers, led by Dr David Llewellyn at the University of Exeter Medical School, followed people for six years. All were free from dementia, cardiovascular disease and stroke at the start of the study. At the end of the study they found the 1,169 with good levels of vitamin D had a one in 10 chance of developing dementia. Seventy were severely deficient - and they had around a one in five risk of dementia. 'Delay or even prevent' Dr Llewellyn said: "We expected to find an association between low vitamin D levels and the risk of dementia and Alzheimer's disease, but the results were surprising - we actually found that the association was twice as strong as we anticipated." He said further research was needed to establish if eating vitamin D rich foods such as oily fish - or taking vitamin D supplements - could "delay or even prevent" the onset of Alzheimer's disease and dementia. But Dr Llewellyn added: "We need to be cautious at this early stage and our latest results do not demonstrate that low vitamin D levels cause dementia. BBC © 2014
by Bethany Brookshire Every day sees a new research article on addiction, be it cocaine, heroin, food or porn. Each one takes a specific angle on how addiction works in the brain. Perhaps it’s a disorder of reward, with drugs hijacking a natural system that is meant to respond to food, sex and friendship. Possibly addiction is a disorder of learning, where our brains learn bad habits and responses. Maybe we should think of addiction as a combination of an environmental stimulus and vulnerable genes. Or perhaps it’s an inappropriate response to stress, where bad days trigger a relapse to the cigarette, syringe or bottle. None of these views are wrong. But none of them are complete, either. Addiction is a disorder of reward, a disorder of learning. It has genetic, epigenetic and environmental influences. It is all of that and more. Addiction is a display of the brain’s astounding ability to change — a feature called plasticity — and it showcases what we know and don’t yet know about how brains adapt to all that we throw at them. “A lot of people think addiction is what happens when someone finds a drug to be the most rewarding thing they’ve ever experienced,” says neuroscientist George Koob, director of the National Institute on Alcohol Abuse and Alcoholism in Bethesda, Md. “But drug abuse is not just feeling good about drugs. Your brain is changed when you misuse drugs. It is changed in ways that perpetuate the problem.” The changes associated with drug use affect how addicts respond to drug cues, like the smell of a cigarette or the sight of a shot of vodka. Drug abuse also changes how other rewards, such as money or food are processed, decreasing their relative value. © Society for Science & the Public 2000 - 2013
By DOUGLAS QUENQUA A tiny part of the brain keeps track of painful experiences and helps determine how we will react to them in the future, scientists say. The findings could be a boon to depression treatments. The habenula (pronounced ha-BEN-you-la), a part of the brain less than half the size of a pea, has been shown in animal studies to activate during painful or unpleasant episodes. Using M.R.I.s to produce powerful brain scans, researchers at University College London tracked the habenulas in subjects who were hooked up to electric shock machines. The subjects were presented with a series of photographs, some of which were followed by increasingly strong shocks. Soon, when the subjects were shown pictures associated with shocks, their habenulas would light up. “The habenula seems to track the associations with electric shocks becoming stronger and stronger,” said Jonathan Roiser, a neuroscientist at the college and an author of the study, published in The Proceedings of the National Academy of Sciences. The habenula appeared to have an effect on motivation, too. The subjects had been asked to occasionally press a button, just to show they were awake. They were much slower to do so when their habenula was active. In fact, the more slowly they responded, the more reliably their habenulas tracked associations with shocks. In animals, the habenula has been shown to suppress production of dopamine, a chemical that drives motivation. Perhaps, the researchers say, an overactive habenula can cause the feelings of impending doom and low motivation common in people with depression. © 2014 The New York Times Company