Chapter 13. Memory, Learning, and Development

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By Kimberly G. Noble What if we could draw a line from key areas of a low-income child’s brain to a policy intervention that would dramatically reduce his or her chances of staying in poverty, dropping out of school and entering the criminal justice or social welfare system? Wouldn’t we want to make that policy prescription as widely available as any vaccination against childhood disease? Thanks to remarkable advances in neuroscience and the social sciences, we are closing in on this possibility. In a study published this year in Nature Neuroscience, several co-authors and I found that family income is significantly correlated with children’s brain size — specifically, the surface area of the cerebral cortex, which is the outer layer of the brain that does most of the cognitive heavy lifting. Further, we found that increases in income were associated with the greatest increases in brain surface area among the poorest children. Not surprisingly, our findings made many people uncomfortable. Some feared the study would be used to reinforce the notion that people remain in poverty because they are less capable than those with higher incomes. As neuroscientists, we interpret the results very differently. We know that the brain is most malleable in the early years of life and that experiences during that time have lifelong effects on the mind. Work by social scientists such as Sendhil Mullainathan at Harvard University and Eldar Shafir at Princeton University has shown that poverty depletes parents’ cognitive resources, leaving less capacity for making everyday decisions about parenting. These parents are also at far greater risk for depression and anxiety — poverty’s “mental tax.” All of this has important implications for children.

Keyword: Development of the Brain; Learning & Memory
Link ID: 21477 - Posted: 10.05.2015

Gareth Cook talks to Douwe Draaisma Much has been written on the wonders of human memory: its astounding feats of recall, the way memories shape our identities and are shaped by them, memory as a literary theme and a historical one. But what of forgetting? This is the topic of a new book by Douwe Draaisma, author of The Nostalgia Factory: Memory, Time and Ageing (Yale University Press, 2013; 176 pages) and a professor of the history of psychology at the University of Groningen in the Netherlands. In Forgetting: Myths, Perils and Compensations (Yale University Press, 2015; 288 pages), Draaisma considers dreaming, amnesia, dementia and all the ways in which our minds—and lives—are shaped by memory’s opposite. He answered questions from contributing editor Gareth Cook. What is your earliest memory, and why, do you suppose, have you not forgotten it? Quite a few early memories in the Netherlands involve bicycles; mine is no exception. I was two and a half years old when my aunts walked my mother to the train station. They had taken a bike to transport her bags. I was sitting on the back of the bike. Suddenly the whole procession came to a halt when my foot got caught between the spokes of a wheel. I am pretty sure this memory is accurate because I had to see a doctor, and there is a dated medical record. It is a brief, snapshotlike memory, black-and-white. I do not remember any pain, but I do remember the consternation among my mom and her sisters. Looking back on this memory from a professional perspective, I would say that it has the flashlike character typical for first memories from before age three; “later” first memories are usually a bit longer and more elaborate. © 2015 Scientific American

Keyword: Learning & Memory
Link ID: 21474 - Posted: 10.05.2015

By Steve Mirsky Harvard neuroscientist Beth Stevens, talking about glia cells, which make up more than half the human brain. This week Stevens got a MacArthur Fellowship, the so-called genius grant, for her studies of glia. “These cells are incredibly responsive to damage or injury. They can protect our brain by, for example, clearing bacteria or debris in the brain in the case of injury and disease… “Until about 10 years ago, almost all of the research devoted to these cells was in these contexts. We discovered that there was another role for these cells in the normal healthy brain, in particular during development… “So a synapse is the junction of communication between two neurons, it’s how neurons talk to each other…we’re actually born with an excess of synaptic connections…and through this normal developmental process called pruning, a large number of these extra synapses get permanently removed or eliminated while others get strengthened and maintained. These microglial cells were in fact engulfing or eating these extra synapses. So these cells are necessary to do this and now of course we’re trying to better understand how it is that they know which synapse to prune and which synapse to leave alone. “A hallmark of many neurodegenerative diseases, including Alzheimer’s disease, is the early loss of synaptic connections or synapses…And what’s most striking about this is, it’s thought that the synapse loss happens years before you see signs of cognitive impairment or pathology. © 2015 Scientific American

Keyword: Development of the Brain; Glia
Link ID: 21470 - Posted: 10.03.2015

By Lisa Sanders, M.d. On Thursday we challenged Well readers to solve the case of a 27-year-old woman who had vomiting, weakness and confusion months after having weight loss surgery. More than 200 readers offered their perspective on the case. Most of you recognized it as a nutritional deficiency, and nearly half of you totally nailed it. The diagnosis is: Wernicke’s encephalopathy due to thiamine (vitamin B1) deficiency. The very first reader to post a comment, Dr. Adrian Budhram, figured it out. His answer landed on our doorstep just five minutes after the case went up. Dr. Budhram is a second year neurology resident at Western University in London, Ontario. He says that Wernicke’s is on the list of diseases he thinks about every time someone is brought to the hospital because they are confused. Thiamine, or vitamin B1, is a nutrient essential for the body to break down and use sugars and proteins. It is found in many foods, including beans, brown rice, pork and cereals. Although the body only stores enough of the vitamin to last three to four weeks, deficiencies are rare when a full and varied diet is available. Diseases caused by a thiamine deficiency were described in Chinese medicine as early as 2600 B.C. – well before the vitamin was identified chemically. Western medicine came to know the disease as beriberi – a Sinhalese term meaning weak (apparently from the phrase “I can’t, I can’t”) characterized by either numbness and weakness in the legs (dry beriberi) or a weakened heart leading to hugely swollen legs (wet beriberi). © 2015 The New York Times Company

Keyword: Learning & Memory
Link ID: 21469 - Posted: 10.03.2015

James Hamblin Mental exercises to build (or rebuild) attention span have shown promise recently as adjuncts or alternatives to amphetamines in addressing symptoms common to Attention Deficit Hyperactivity Disorder (ADHD). Building cognitive control, to be better able to focus on just one thing, or single-task, might involve regular practice with a specialized video game that reinforces "top-down" cognitive modulation, as was the case in a popular paper in Nature last year. Cool but still notional. More insipid but also more clearly critical to addressing what's being called the ADHD epidemic is plain old physical activity. This morning the medical journal Pediatrics published research that found kids who took part in a regular physical activity program showed important enhancement of cognitive performance and brain function. The findings, according to University of Illinois professor Charles Hillman and colleagues, "demonstrate a causal effect of a physical program on executive control, and provide support for physical activity for improving childhood cognition and brain health." If it seems odd that this is something that still needs support, that's because it is odd, yes. Physical activity is clearly a high, high-yield investment for all kids, but especially those attentive or hyperactive. This brand of research is still published and written about as though it were a novel finding, in part because exercise programs for kids remain underfunded and underprioritized in many school curricula, even though exercise is clearly integral to maximizing the utility of time spent in class.

Keyword: ADHD; Attention
Link ID: 21463 - Posted: 10.01.2015

By Nicholas Bakalar Breast-feeding has many benefits, but a new study suggests that it has no effect on a child’s IQ from toddlerhood through adolescence. The idea that breast-feeding might have an effect on cognition is plausible, since long-chain polyunsaturated fatty acids, which are important in neurological development, are more plentiful in breast-fed babies. British researchers studied 11,582 children born between 1994 and 1996. About two-thirds were breast-fed, for an average of four months. They followed them through age 16 and administered nine intelligence tests at regular intervals over the years. The study is in PLOS One. After controlling for parental education, maternal age, socioeconomic status and other variables, they found that girls who had been breast-fed had a weak but statistically insignificant advantage in early life over those who had not been, but the effect was not apparent in boys. Breast-feeding was not associated with gains in IQ through adolescence for either girls or boys. The lead author, Sophie von Stumm, a senior lecturer in psychology at Goldsmiths University of London, said that mothers who do not breast-feed are sometimes criticized. “It’s almost an accusation these days,” she said, “that you’re purposely harming your child. That’s not the case, and it’s not helpful for new mothers. Kids do lots of things that have an influence on IQ. Breast-feeding has no effect that can be distinguished from family background or socioeconomic status.” © 2015 The New York Times Company

Keyword: Development of the Brain; Intelligence
Link ID: 21462 - Posted: 10.01.2015

Allison Aubrey We might not be able to remember every stressful episode of our childhood. But the emotional upheaval we experience as kids — whether it's the loss of a loved one, the chronic stress of economic insecurity, or social interactions that leave us tearful or anxious — may have a lifelong impact on our health. In fact, a study published this week in the Journal of the American College of Cardiology indicates that emotional distress during childhood — even in the absence of high stress during adult years — can increase the risk of developing heart disease and metabolic disorders such as diabetes in adulthood. Robert Wood Johnson Foundation Shots - Health News Take The ACE Quiz — And Learn What It Does And Doesn't Mean "We know that the childhood period is really important for setting up trajectories of health and well-being," explains Ashley Winning, an author of the study and postdoctoral research fellow in social and behavioral sciences at the Harvard T.H. Chan School of Public Health. To assess the connection between childhood stress and the risk of disease, Winning and her colleagues analyzed data from the 1958 British Birth Cohort Study, a long-running study that documented the diets, habits and emotional health of thousands of British children born during the same week that year. As the children entered school, the classroom became the laboratory for observation. © 2015 NPR

Keyword: Stress; Development of the Brain
Link ID: 21460 - Posted: 09.30.2015

By Nicholas Bakalar Agitation and aggression are common in Alzheimer’s patients, and there is no known safe and effective treatment. Now researchers report that a combination drug already in use for treating certain neurological problems may be a better remedy. Dextromethorphan is a cough suppressant commonly found in over-the-counter cough medicines, and quinidine is a drug used to control heart rhythm disorders. In combination, they are used to treat certain neurological disorders involving involuntary movement of the facial muscles. The scientists randomized 152 Alzheimer’s patients to a 10-week course of dextromethorphan-quinidine and 127 to placebo. Researchers then rated them using a well-validated scale that measures aggression and agitation. The study is in the Sept. 22 issue of JAMA. Aggression scores declined to 3.8 from 7.1 in the dextromethorphan-quinidine group and to 5.3 from 7.0 in those who took a placebo. Then the researchers re-randomized those who did not respond to placebo to receive either drugs or placebo, and found similar encouraging results for the drug combination. “Fifty-five percent of the people who were on drugs had a 50 percent reduction in their agitation,” said the lead author, Dr. Jeffrey L. Cummings, director of the Cleveland Clinic Lou Ruvo Center for Brain Health. “That’s a lot when a patient is striking and hitting and cussing. There are no currently approved treatments for agitation, and we’re very enthusiastic about this finding.” © 2015 The New York Times Company

Keyword: Alzheimers; Aggression
Link ID: 21459 - Posted: 09.30.2015

By Kelly Servick Children born to obese mothers arrive already predisposed to obesity and other health problems themselves. Exactly what happens in the uterus to transmit this risk still isn’t clear, but a new study on mice points to the placenta as a key actor. The study shows that a hormone acting on the placenta can protect the offspring of obese mice from being born overweight. It suggests ways to break the cycle of obesity in humans—although other researchers caution there's a long way to go. Researchers discovered decades ago that conditions in the uterus can “program” a fetus to be more susceptible to certain health problems. People conceived during the 1944 famine in the Netherlands, for example, suffered higher rates of cardiovascular disease, diabetes, cancer, and other problems later in life. Recent animal studies suggest that malnourishment in the womb changes the expression of DNA in ways that can be passed down for generations. But researchers are now increasingly concerned with the opposite problem. Obese women tend to give birth to larger babies with more body fat, and these children are more likely to develop metabolic syndrome—the cluster of conditions including obesity and high blood sugar that can lead to diabetes and heart disease. To probe the roots of fetal “overgrowth,” developmental biologists at the University of Colorado, Denver, looked to the placenta—the whoopee cushion–shaped organ wedged between the fetus and the wall of the uterus, where branching arteries from the umbilical cord take up oxygen and nutrients from the mother’s blood vessels. The placenta “has always been viewed as a passive organ—whatever happens to the mother is translated toward the fetus,” says lead author Irving Aye, now at the University of Cambridge in the United Kingdom. However, recent research has shown that the placenta is less an indiscriminate drainpipe than a subtle gatekeeper. © 2015 American Association for the Advancement of Science.

Keyword: Obesity; Development of the Brain
Link ID: 21456 - Posted: 09.29.2015

By Judith Berck The 73-year-old widow came to see Dr. David Goodman, an assistant professor in the psychiatry and behavioral sciences department at Johns Hopkins School of Medicine, after her daughter had urged her to “see somebody” for her increasing forgetfulness. She was often losing her pocketbook and keys and had trouble following conversations, and 15 minutes later couldn’t remember much of what was said. But he did not think she had early Alzheimer’s disease. The woman’s daughter and granddaughter had both been given a diagnosis of A.D.H.D. a few years earlier, and Dr. Goodman, who is also the director of a private adult A.D.H.D. clinical and research center outside of Baltimore, asked about her school days as a teenager. “She told me: ‘I would doodle because I couldn’t pay attention to the teacher, and I wouldn’t know what was going on. The teacher would move me to the front of the class,’ ” Dr. Goodman said, After interviewing her extensively, noting the presence of patterns of impairment that spanned the decades, Dr. Goodman diagnosed A.D.H.D. He prescribed Vyvanse, a short-acting stimulant of the central nervous system. A few weeks later, the difference was remarkable. “She said: ‘I’m surprised, because I’m not misplacing my keys now, and I can remember things better. My mind isn’t wandering off, and I can stay in a conversation. I can do something until I finish it,’ ” Dr. Goodman said. Once seen as a disorder affecting mainly children and young adults, attention deficit hyperactivity disorder is increasingly understood to last throughout one’s lifetime. © 2015 The New York Times Company

Keyword: ADHD; Alzheimers
Link ID: 21455 - Posted: 09.29.2015

Linda Geddes Jack struggled in regular school. Diagnosed with dyslexia and the mathematical equivalent, dyscalculia, as well as the movement disorder dyspraxia, Jack (not his real name) often misbehaved and played the class clown. So the boy’s parents were relieved when he was offered a place at Fairley House in London, which specializes in helping children with learning difficulties. Fairley is also possibly the first school in the world to have offered pupils the chance to undergo electrical brain stimulation. The stimulation was done as part of an experiment in which twelve eight- to ten-year-olds, including Jack, wore an electrode-equipped cap while they played a video game. Neuroscientist Roi Cohen Kadosh of the University of Oxford, UK, who led the pilot study in 2013, is one of a handful of researchers across the world who are investigating whether small, specific areas of a child’s brain can be safely stimulated to overcome learning difficulties. “It would be great to be able to understand how to deliver effective doses of brain stimulation to kids’ brains, so that we can get ahead of developmental conditions before they really start to hold children back in their learning,” says psychologist Nick Davis of Swansea University, UK. The idea of using magnets or electric currents to treat psychiatric or learning disorders — or just to enhance cognition — has generated a flurry of excitement over the past ten years. The technique is thought to work by activating neural circuits or by making it easier for neurons to fire. The research is still in its infancy, but at least 10,000 adults have undergone such stimulation, and it seems to be safe — at least in the short term. One version of the technology, called transcranial magnetic stimulation (TMS), has been approved by the US Food and Drug Administration to treat migraine and depression in adults. © 2015 Nature Publishing Group,

Keyword: Dyslexia; Attention
Link ID: 21441 - Posted: 09.24.2015

Erin Wayman Priya Rajasethupathy’s research has been called groundbreaking, compelling and beautifully executed. It’s also memorable. Rajasethupathy, a neuroscientist at Stanford University, investigates how the brain remembers. Her work probes the molecular machinery that governs memories. Her most startling — and controversial — finding: Enduring memories may leave lasting marks on DNA. Being a scientist wasn’t her first career choice. Although Rajasethupathy inherited a love of computation from her computer scientist dad, she enrolled in Cornell University as a pre-med student. After graduating in three years, she took a year off to volunteer in India, helping people with mental illness. During that year she also did neuroscience research at the National Centre for Biological Sciences in Bangalore. While there, she began to wonder whether microRNAs, tiny molecules that put protein production on pause, could play a role in regulating memory. She pursued that question as an M.D. and Ph.D. student at Columbia University (while intending, at least initially, to become a physician). She found some answers in the California sea slug (Aplysia californica). In 2009, she and colleagues discovered a microRNA in the slug’s nerve cells that helps orchestrate the formation of memories that linger for at least 24 hours. © Society for Science & the Public 2000 - 2015.

Keyword: Learning & Memory
Link ID: 21434 - Posted: 09.23.2015

Rachel Ehrenberg If not for a broken piece of lab equipment and a college crush, Steve Ramirez might never have gone into neuroscience. As an undergraduate at Boston University his interests were all over the place: He was taking a humanities course and classes in philosophy and biochemistry while working several hours a week in a biology lab. When the lab’s centrifuge, a device that spins liquids, broke, Ramirez had to use one in another lab. “I was trying to make small talk with this girl who was using the centrifuge, ‘What’s your major?’ kind of thing,” Ramirez recalls. Hearing of his myriad interests, the student suggested that Ramirez talk with neuroscientist Paul Lipton. That led to a conversation with Howard Eichenbaum, a leading memory researcher. Eichenbaum told him that everything Ramirez was interested in was about the brain. “Everything from the pyramids to putting a man on the moon, it’s all the product of the human brain, which is kind of crazy when you think about it,” Ramirez says. Studying “the most interdisciplinary organ in existence,” as Ramirez calls it, was a natural fit. While working in Eichenbaum’s lab, Ramirez got turned on to how the brain forms memories. Those explorations led to a Ph.D. program at MIT in the lab of Nobel laureate Susumu Tonegawa, where Ramirez focused on the individual brain cells that hold specific memories. © Society for Science & the Public 2000 - 2015.

Keyword: Emotions; Learning & Memory
Link ID: 21433 - Posted: 09.23.2015

Claudia Dreifus Cornelia Bargmann, a neurobiologist at Rockefeller University in New York, studies how genes interact with neurons to create behavior. Two years ago, President Obama named Dr. Bargmann, who is known as Cori, a co-chairwoman of the advisory commission for the Brain Initiative, which he has described as “giving scientists the tools they need to get a dynamic picture of the brain in action.” I spoke with Dr. Bargmann, 53, for two hours at the Manhattan apartment she shares with her husband, Dr. Richard Axel, a neuroscientist at Columbia University. Our interview has been edited and condensed. Q. As an M.I.T. graduate student, you made a discovery that ultimately led to the breast cancer drug Herceptin. How did it happen? A. What I did was discover a mutated gene that triggered an obscure cancer in rats. Afterwards, it was discovered — by others — that this same gene is also altered in human breast cancers. Since our work in the rat cancer showed that the immune system could attack the product of this gene, Genentech developed a way to deploy the immune system. That’s Herceptin. It is an antibody against the gene that sits on the surface of a cancer cell. It can attack the cancer cell growing because of that gene. Currently, you spend your time trying to understand the nervous system of a tiny worm, C. elegans. Why do you study this worm? Well, the reason is this: Understanding the human brain is a great and complex problem. To solve the brain’s mysteries, you often have to break a problem down to a simpler form. Your brain has 86 billion nerve cells, and in any mental process, millions of them are engaged. Information is sweeping across these millions of neurons. With present technology, it’s impossible to study that process at the level of detail and speed you would want. © 2015 The New York Times Company

Keyword: Brain imaging; Development of the Brain
Link ID: 21430 - Posted: 09.22.2015

by Laura Sanders Like every other person who carries around a smartphone, I take a lot of pictures, mostly of my kids. I thought I was bad with a few thousand snaps filling my phone’s memory. But then I talked to MIT researcher Deb Roy. For three years, Roy and a small group of researchers recorded every waking moment of Roy’s son’s life at home, amassing over 200,000 hours of video and audio recordings. Roy’s intention wasn’t to prove he was the proudest parent of all time. Instead, he wanted to study how babies learn to say words. As a communication and machine learning expert, Roy and his wife Rupal Patel, also a speech researcher, recognized that having a child would be a golden research opportunity. The idea to amass this gigantic dataset “was kicking around and something we thought about for years,” Roy says. So after a pregnancy announcement and lots of talking and planning and “fascinating conversations” with the university administration in charge of approving human experiments, the researchers decided to go for it. To the delight of his parents, a baby boy arrived in 2005. When Roy and Patel brought their newborn home, the happy family was greeted by 11 cameras and 14 microphones, tucked up into the ceiling. From that point on, cameras rolled whenever the baby was awake. © Society for Science & the Public 2000 - 2015

Keyword: Language; Development of the Brain
Link ID: 21429 - Posted: 09.22.2015

Steve Connor A painkiller widely used to treat rheumatoid arthritis has been shown to reverse the symptoms of dementia in the brains of laboratory mice, raising hope that there may soon be an effective treatment for Alzheimer’s disease, scientists have said. The drug, salsalate, is a licensed pain killer but in mice with a form of dementia similar to Alzheimer’s it reversed the changes to a key protein in the brain that builds up in patients with the debilitating neurological disease, they found. The researchers said it is the first time any drug has been shown to have an effect on the “tau” protein that accumulates in the brain of people with Alzheimer’s and a range of similar dementias known as “tauopathies”. It could lead to an effective therapy even for patients in the later stages of disease, the researchers said. “We identified for the first time a pharmacological approach that reverses all aspects of tau toxicity," said Li Gan, PhD of the Gladstone Institutes, a non-profit research organisation affiliated with the University of California, San Francisco. “Remarkably, the profound protective effects of salsalate were achieved even though it was administered after disease onset, indicating that it may be an effective treatment option,” said Dr Gan a senior co-author of the study published in the journal Nature Medicine. As many as 800,000 people in Britain are already affected by Alzheimer’s disease and a new study has suggested that as many as one in three babies born this year will get dementia in their lifetime, largely as a result of people living longer. Age is the biggest risk factor for the disease. ©

Keyword: Alzheimers
Link ID: 21428 - Posted: 09.22.2015

By John Pavlus The “brain in a vat” has long been a staple of philosophical thought experiments and science fiction. Now scientists are one step closer to creating the real thing, which could enable groundbreaking experiments of a much more empirical kind. Research teams at Stanford University and the RIKEN Center for Developmental Biology in Japan have each discovered methods for coaxing human stem cells to form three-dimensional neural structures that display activity associated with that of an adult brain. By applying a variety of chemical growth factors, the RIKEN researchers transformed human embryonic stem cells into neurons that self-organized in patterns unique to the cerebellum, a region of the brain that coordinates movement. The Stanford team worked with induced pluripotent stem cells derived from skin cells and chemically nudged them to become neurons that spontaneously wired up into networks of 3-D circuits, much like the ones found in the cerebral cortex—the wrinkled gray matter of the brain that supports attention, memory and self-awareness in humans. “For years people have used mouse embryonic stem cells to generate teratomas—things that look like they could be organs,” says David Panchision, a neuroscientist at the National Institutes of Health, which supported the Stanford research. “But it's not organized and systematic, the way a developing brain needs to be to function.” In contrast, the Stanford team's neural structures not only self-assembled as cortexlike tissue, the neurons also sent signals to one another in coordinated patterns—just as they would in a brain. The cerebellar tissue generated by the Japanese scientists did, too. © 2015 Scientific American

Keyword: Development of the Brain
Link ID: 21427 - Posted: 09.21.2015

By Michael Balter Are some animals smarter than others? It’s hard to say, because you can’t sit a chimpanzee or a mouse down at a table for an IQ test. But a new study, in which scientists tested wild robins on a variety of skills, concludes that they do differ in the kind of “general intelligence” that IQ tests are supposed to measure. General intelligence is usually defined as the ability to do well on multiple cognitive tasks, from math skills to problem solving. For years, researchers have questioned whether measurable differences exist in humans and nonhumans alike. In humans, factors like education and socioeconomic status can affect performance. When it comes to animals, the problem is compounded for two main reasons: First, it is very difficult to design and administer tests that pick up on overall smarts instead of specific skills, such as the keen memories of food-hoarding birds or the fine motor skills of chimpanzees that make tools for finding insects in trees. Second, differences in animal test scores can depend on how motivated they are to perform. Because most experiments award would-be test-takers with food, an empty (or a full) stomach might be all it takes to skew the results. Thus, even studies that suggest variations in intelligence among mice, birds, and apes all carry the caveat that alternative explanations could be at play. To get around some of these limitations, a team led by Rachael Shaw, an animal behavior researcher at Victoria University of Wellington, turned to a population of New Zealand North Island robins for a new round of experiments. The robins live at the Zealandia wildlife sanctuary, a 225-hectare nature paradise in Wellington where more than 700 of the birds live wild and protected from predators in the middle of the city. © 2015 American Association for the Advancement of Science.

Keyword: Intelligence; Evolution
Link ID: 21424 - Posted: 09.20.2015

Mo Costandi The human brain is often said to be the most complex object in the known universe, and there’s good reason to believe that this old cliché is true. Even the apparently simple task of compiling a census of the different types of cells it contains has proven to be extremely difficult. Researchers still can’t agree on the best way to classify the numerous sub-types of neurons, and different methods produce different results, so estimates range from several hundred to over a thousand. Basket cells illustrate this neuronal identity crisis perfectly. They are currently sub-divided into multiple different types, according to their shape, electrical properties, and molecular profiles. After nearly ten years of detective work, researchers at King’s College London now reveal them to be masters of disguise. In a surprising new study, they show that these cells can dynamically switch from one identity to another in response to neuronal network activity. Basket cells are a type of interneuron, which are found scattered throughout the cerebral cortex, hippocampus, and cerebellum, and make up about 5% of the total number of cells in these brain regions. They form local circuits with each other and with pyramidal neurons, the much larger and more numerous cells that transmit information to distant parts of the brain, and synthesize the inhibitory neurotransmitter GABA, which dampens pyramidal cell activity when released. These enigmatic cells are thought to exist in more than twenty different types, the best known being the fast-spiking ones, which respond rapidly to incoming signals, and slower ones, which respond after a delay. During brain development, immature forms of all types of basket cells are created in a structure called the medial ganglionic eminence, along with various other types of brain cells. They then migrate into the developing cerebral cortex, before going on to form synaptic connections with other cells. © 2015 Guardian News and Media Limited

Keyword: Development of the Brain
Link ID: 21423 - Posted: 09.20.2015

By BENEDICT CAREY Fourteen years ago, a leading drug maker published a study showing that the antidepressant Paxil was safe and effective for teenagers. On Wednesday, a major medical journal posted a new analysis of the same data concluding that the opposite is true. That study — featured prominently by the journal BMJ — is a clear break from scientific custom and reflects a new era in scientific publishing, some experts said, opening the way for journals to post multiple interpretations of the same experiment. It comes at a time of self-examination across science — retractions are at an all-time high; recent cases of fraud have shaken fields as diverse as anesthesia and political science; and earlier this month researchers reported that less than half of a sample of psychology papers held up. “This paper is alarming, but its existence is a good thing,” said Brian Nosek, a professor of psychology at the University of Virginia, who was not involved in either the original study or the reanalysis. “It signals that the community is waking up, checking its work and doing what science is supposed to do — self-correct.” The authors of the reanalysis said that many clinical studies had some of the same issues as the original Paxil study, and that data should be made freely available across clinical medicine, so that multiple parties could analyze them. The dispute itself is a long-running one: Questions surrounding the 2001 study played a central role in the so-called antidepressant wars of the early 2000s, which led to strong warnings on the labels of Paxil and similar drugs citing the potential suicide risk for children, adolescents and young adults. The drugs are considered beneficial and less risky for many adults over 25 with depression. © 2015 The New York Times Company

Keyword: Depression; Development of the Brain
Link ID: 21422 - Posted: 09.20.2015