Chapter 17. Learning and Memory
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Laura Sanders Using flashes of blue light, scientists have pulled forgotten memories out of the foggy brains of mice engineered to have signs of early Alzheimer’s disease. This memory rehab feat, described online March 16 in Nature, offers new clues about how the brain handles memories, and how that process can go awry. The result “provides a theoretical mechanism for reviving old, forgotten memories,” says Yale School of Medicine neurologist Arash Salardini. Memory manipulations, such as the retrieval of lost memories and the creation of false memories, were “once the realm of science fiction,” he says. But this experiment and other recent work have now accomplished these feats, at least in rodents (SN: 12/27/14, p. 19), he says. To recover a lost memory, scientists first had to mark it. Neuroscientist Susumu Tonegawa of MIT and colleagues devised a system that tagged the specific nerve cells that stored a memory — in this case, an association between a particular cage and a shock. A virus delivered a gene for a protein that allowed researchers to control this collection of memory-holding nerve cells. The genetic tweak caused these cells to fire off signals in response to blue laser light, letting Tonegawa and colleagues call up the memory with light delivered by an optic fiber implanted in the brain. A day after receiving a shock in a particular cage, mice carrying two genes associated with Alzheimer’s seemed to have forgotten their ordeal; when put back in that cage, these mice didn’t seem as frightened as mice without the Alzheimer’s-related genes. But when the researchers used light to restore this frightening memory, it caused the mice to freeze in place in a different cage. (Freezing in a new venue showed that laser activation of the memory cells, and not environmental cues, caused the fear reaction.) © Society for Science & the Public 2000 - 2016. All rights reserved.
THERE they are! Newborn neurons vital for memory have been viewed in a live brain for the first time. The work could aid treatments for anxiety and stress disorders. Attila Losonczy at Columbia University Medical Center in New York and his team implanted a tiny microscope into the brains of live mice, the brain cells of which had been modified to make newly made neurons glow. The mice then ran on a treadmill as the team tweaked the surrounding sights, smells and sounds. The researchers paired a small electric shock with some cues, so the mice learned to associate these with an unpleasant experience. They then deactivated the newborn neurons – present in areas of the brain responsible for learning and memory – using optogenetics, which switches off specific cells with light. After this, the mice were unable to tell the difference between the scary and safe cues, becoming fearful of them all (Neuron, doi.org/bc7v). “It suggests that newborn cells do something special that allows animals to tell apart and separate memories,” says Losonczy. An inability to discriminate between similar sensory information triggered by different events – such as the sound of a gunshot and a car backfiring – is often seen in panic and anxiety disorders, such as PTSD. This suggests that new neurons, or a lack of them, plays a part in such conditions and could guide novel treatments. © Copyright Reed Business Information Ltd.
Barbara Bradley Hagerty Faced with her own forgetfulness, former NPR correspondent and author Barbara Bradley Hagerty tried to do something about it. She's written about her efforts in her book on midlife, called Life Reimagined. To her surprise, she discovered that an older dog can learn new tricks. A confession: I loathe standardized tests, and one of the perks of reaching midlife is that I thought I'd never have to take another. But lately I've noticed that in my 50s, my memory isn't the same as it once was. And so I decided to take a radical leap into the world of brain training. At the memory laboratory at the University of Maryland, manager Ally Stegman slides a sheet of paper in front of me. It has a series of boxes containing different patterns and one blank space. My job is to figure out the missing pattern. The test measures a sort of raw intelligence, the ability to figure out novel problems. Time races by. It takes me two minutes to crack the first question. I am stumped by the second and third. Finally, I begin to guess. After 25 minutes, the test is over, and to my relief, Stegman walks in. This test was really, really hard. The reason I am here, voluntarily reliving my nightmare, is simple: I want to tune up my 50-something brain. So over the next month, I will do brain-training exercises, then come back, take the test again and see if I made myself smarter. © 2016 npr
By Julia Shaw Our brains play tricks on us all the time, and these tricks can mislead us into believing we can accurately reconstruct our personal past. In reality, false memories are everywhere. False memories are recollections of things that you never actually experienced. These can be small memory errors, such as thinking you saw a yield sign when you actually saw a stop sign, or big errors like thinking you took a hot air balloon ride that never actually happened. If you want to know more about how we can come to misremember complex autobiographical events, here is a recipe and here is a video with footage from my own research. A few weeks ago I reached out to see what you actually wanted to know about this phenomenon on Reddit, and here are the answers to my six favorite questions. 1. Is there any way a person can check if their own memories are real or false? The way that I have interpreted the academic literature, once they take hold false memories are no different from true memories in the brain. This means that they have the same properties as any other memories, and are indistinguishable from memories of events that actually happened. The only way to check, is to find corroborating evidence for any particular memory that you are interested in “validating”. © 2016 Scientific American
Keyword: Learning & Memory
Link ID: 21985 - Posted: 03.15.2016
By Emily Underwood Nestled deep within a brain region that processes memory is a sliver of tissue that continually sprouts brand-new neurons, at least into late adulthood. A study in mice now provides the first glimpse at how these newborn neurons behave in animals as they learn, and hints at the purpose of the new arrivals: to keep closely-related but separate memories distinct. A number of previous studies have suggested that the birth of new neurons is key to memory formation. In particular, scientists believe the new cell production—known as neurogenesis—plays a role in pattern separation, the ability to discriminate between similar experiences, events, or contexts based on sensory cues such as a certain smell or visual landmark. Pattern separation helps us use cues such as the presence of a particular tree or cars nearby, for example, to distinguish which parking space we chose today, as opposed to yesterday or the day before. This ability appears to be particularly diminished in people with anxiety and mood disorders. Scientists can produce deficits in pattern separation in animals by blocking neurogenesis, using x-ray radiation to kill targeted populations of cells in the dentate gyrus. Because such studies have not established the precise identity of which cells are being recorded from, however, no one has been able to address the “burning question” in the field: "how young, adult-born neurons and mature dentate granule neurons differ in their activity," says Amar Sahay, a neuroscientist at the Massachusetts General Hospital and Harvard Medical School. © 2016 American Association for the Advancement of Scienc
How is the brain able to use past experiences to guide decision-making? A few years ago, researchers supported by the National Institutes of Health discovered in rats that awake mental replay of past experiences is critical for learning and making informed choices. Now, the team has discovered key secrets of the underlying brain circuitry – including a unique system that encodes location during inactive periods. “Advances such as these in understanding cellular and circuit-level processes underlying such basic functions as executive function, social cognition, and memory fit into NIMH’s mission of discovering the roots of complex behaviors,” said NIMH acting director Bruce Cuthbert, Ph.D. While a rat is moving through a maze — or just mentally replaying the experience — an area in the brain’s memory hub, or hippocampus, specialized for locations, called CA1, communicates with a decision-making area in the executive hub or prefrontal cortex (PFC). A distinct subset of PFC neurons excited during mental replay of the experience are activated during movement, while another distinct subset, less engaged during movement in the maze – and therefore potentially distracting – are inhibited during replay. “Such strongly coordinated activity within this CA1-PFC circuit during awake replay is likely to optimize the brain’s ability to consolidate memories and use them to decide on future action” explained Shantanu Jadhav, Ph.D. (link is external), now an assistant professor at Brandeis University, Waltham, MA., the study’s co-first author. His contributions to this line of research were made possible, in part, by a Pathway to Independence award from the Office of Research Training and Career Development of the NIH’s National Institute of Mental Health (NIMH).
By Roberto A. Ferdman In the mid 1970s, psychologist Merrill Elias began tracking the cognitive abilities of more than a thousand people in the state of New York. The goal was fairly specific: to observe the relationship between people's blood pressure and brain performance. And for decades he did just that, eventually expanding the Maine-Syracuse Longitudinal Study (MSLS) to observe other cardiovascular risk factors, including diabetes, obesity, and smoking. There was never an inkling that his research would lead to any sort of discovery about chocolate. And yet, 40 years later, it seems to have done just that. Late in the study, Elias and his team had an idea. Why not ask the participants what they were eating too? It wasn't unreasonable to wonder if what someone ate might add to the discussion. Diets, after all, had been shown to affect the risk factors Elias was already monitoring. Plus, they had this large pool of participants at their disposal, a perfect chance to learn a bit more about the decisions people were making about food. The researchers incorporated a new questionnaire into the sixth wave of their data collection, which spanned the five years between 2001 and 2006 (there have been seven waves in all, each conducted in five year intervals). The questionnaire gathered all sorts of information about the dietary habits of the participants. And the dietary habits of the participants revealed an interesting pattern. "We found that people who eat chocolate at least once a week tend to perform better cognitively," said Elias. "It's significant—it touches a number of cognitive domains." © 1996-2016 The Washington Post
Mo Costandi Most of us are well aware of the health risks associated with obesity. Being overweight or obese is associated with an increased risk of numerous other conditions, from high blood pressure, heart disease and stroke, to diabetes, gout and some forms of cancer. Self-control saps memory resources Read more Research published over the past few years shows that obesity also has neurological consequences – it is associated with altered function in, and shrinkage of, certain parts of the brain, particularly the frontal lobes, which are the seat of intelligence, and the hippocampus, which is critical for memory formation. A new study now shows that this in turn is associated with impaired memory function. Lucy Cheke of the University of Cambridge and her colleagues recruited 50 volunteers aged between 18 and 35, with Body Mass Indexes (BMIs) ranging from 18 (underweight) to 51 (extremely obese), and asked them to perform a computerised memory test called the “Treasure Hunt Task”. This involved moving food items around around complex scenes, such as a desert with palm trees, hiding them in various locations, and indicating afterwards where they had hidden them. The participants were then shown various locations from the computerised scenes, and some of the food items, and asked if they had hidden something in each of the locations, or where they had hidden each of the items. Finally, they were shown pairs of the food items they had seen, and asked to indicate which of each pair they had hidden first. © 2016 Guardian News and Media Limited
By Gretchen Reynolds Learning in midlife to juggle, swim, ride a bicycle or, in my case, snowboard could change and strengthen the brain in ways that practicing other familiar pursuits such as crossword puzzles or marathon training will not, according to an accumulating body of research about the unique impacts of motor learning on the brain. When most of us consider learning and intelligence, we think of activities such as adding numbers, remembering names, writing poetry, learning a new language. Such complex thinking generally is classified as “higher-order” cognition and results in activity within certain portions of the brain and promotes plasticity, or physical changes, in those areas. There is strong evidence that learning a second language as an adult, for instance, results in increased white matter in the parts of the brain known to be involved in language processing. Regular exercise likewise changes the brain, as I frequently have written, with studies in animals showing that running and other types of physical activities increase the number of new brain cells created in parts of the brain that are integral to memory and thinking. But the impacts of learning on one of the most primal portions of the brain have been surprisingly underappreciated, both scientifically and outside the lab. Most of us pay little attention to our motor cortex, which controls how well we can move. “We have a tendency to admire motor skills,” said Dr. John Krakauer, a professor of neurology and director of the Center for the Study of Motor Learning and Brain Repair at Johns Hopkins University in Baltimore. We like watching athletes in action, he said. But most of us make little effort to hone our motor skills in adulthood, and very few of us try to expand them by, for instance, learning a new sport. We could be short-changing our brains. © 2016 The New York Times Company
By Jonathan Webb Science reporter, BBC News Three British researchers have won a prize worth one million euros, awarded each year for an "outstanding contribution to European neuroscience". Tim Bliss, Graham Collingridge and Richard Morris revealed how strengthened connections between brain cells can store our memories. Our present understanding of memory is built on their work, which unpicked the mechanisms and molecules involved. This is the first time the Brain Prize has been won by an entirely UK team. It is awarded by a Danish charitable foundation and the 2016 winners were announced in London on Tuesday. Speaking to journalists at a media conference, Prof Morris explained it was the "chemistry of memory" that he and his colleagues had managed to illuminate. Fire together, wire together "Before this team got going, we had some idea about particular areas of the brain that might be involved in memory… but what we didn't have was any real understanding of how it worked," explained the professor, who works at the University of Edinburgh. The "team" of three winners never worked together in the same laboratory, but they have collaborated over the years. "Memories change the brain - the brain is plastic," said Prof Bliss, who worked for many years at the National Institute of Medical Research in London and is now affiliated with the Francis Crick Institute. Those changes occur at the junctions between nerve cells - synapses - and were described in a pioneering study by Bliss and a Norwegian colleague, Terje Lømo, in the 1970s. © 2016 BBC.
Keyword: Learning & Memory
Link ID: 21947 - Posted: 03.03.2016
By James Gallagher Health editor, BBC News website People who are obese have a worse memory than their thinner friends, a small study shows. Tests on 50 people showed being overweight was linked to worse "episodic memory" or the ability to remember past experiences. The study in the Quarterly Journal of Experimental Psychology argues that a less vivid memory of recent meals may lead to overeating. However, other aspects of memory - such as general knowledge - were unaffected. Tests on rats have previously shown that with burgeoning waistlines come poorer performances in memory tests, but the evidence in humans has been mixed. The latest experiments looked at episodic memory - the video tape in your mind - that remembers the smell of a cup of coffee or the feel of holding someone's hand. Fifty people with a Body Mass Index (BMI) ranging from 18 (healthy) to 51 (very obese) took part in a memory test - a bit like doing a treasure hunt on your own. They had to "hide" objects at different times and on different scenes displayed on a computer screen. They were later asked to recall what they had hidden, when and where. The results showed obese people's scores were 15% lower than thinner people. Dr Lucy Cheke, from the University of Cambridge, told the BBC News website: "The suggestion we're making is that a higher BMI is having some reduction on the vividness of memory, but they're not drawing blanks and having amnesia. "But if they have a less strong memory of a recent meal, with a less strong impact in the mind, then they may have less ability to regulate how much they eat later on." Hunger hormones play a huge role in how much we eat, but it is already recognised that our minds have a key role too. © 2016 BBC
Keyword: Learning & Memory
Link ID: 21933 - Posted: 02.27.2016
The dodo is an extinct flightless bird whose name has become synonymous with stupidity. But it turns out that the dodo was no bird brain, but instead a reasonably brainy bird. Scientists said on Wednesday they figured out the dodo's brain size and structure based on an analysis of a well-preserved skull from a museum collection. They determined its brain was not unusually small but rather completely in proportion to its body size. They also found the dodo may have had a better sense of smell than most birds, with an enlarged olfactory region of the brain. This trait, unusual for birds, probably let it sniff out ripe fruit to eat. The research suggests the dodo, rather than being stupid, boasted at least the same intelligence as its fellow members of the pigeon and dove family. Mauritius Dodo bird A skeleton of a Mauritius Dodo bird stands at an exhibition in the Mauritius Institute Museum in Port Louis in this Dec. 27, 2005 file photo. (Reuters) "If we take brain size — or rather, volume, as we measured here — as a proxy for intelligence, then the dodo was as smart as a common pigeon," paleontologist Eugenia Gold of Stony Brook University in New York state said. "Common pigeons are actually smarter than they get credit for, as they were trained as message carriers during the world wars." ©2016 CBC/Radio-Canada.
by Giuseppe Gangarossa When we think about sex hormones, notably estrogens and androgens, we usually associate them with sex, gender and body development. Like all hormones, they are chemical messengers, substances produced in one part of the body that go on to tell other parts what to do. However, we often have the tendency to forget the enormous impact that these steroid hormones have on brain functions. From animal studies, it has become clear that during early development, exposure of the brain to testosterone and estradiol, hormones present in both males and females, leads to irreversible changes in the nervous system (McCarthy et al., 2012). A growing and very appealing body of science suggests that sex hormones play a neuromodulatory role in cognitive brain function (Janowsky, 2006). Moreover, testosterone dysfunctions (hypogonadism, chemical castration, etc.) have shown to be associated with memory defects. However, in spite of these advances, it still remains an enigma how sex hormones affect the brain. In an interesting paper published in PLOS ONE, Picot and colleagues tried to fill in one piece of the puzzle. They investigated the neurobiological effects of cerebral androgen receptor (AR) ablation on hippocampal plasticity and cognitive performance in male rodents (Picot et al., 2016). Although several reports have already highlighted a link between sex hormones and cognitive function (Galea et al., 2008; Janowsky, 2006), much more needs to be done to fully elucidate the “non-sexual” functions of androgens.
Meghan Rosen The people of Flint, Mich., are drinking bottled water now, if they can get it. Volunteers deliver it door-to-door and to local fire stations. The goal is to keep the city’s residents from ingesting so much lead. Success – or lack thereof – could have consequences not just now, but for generations to come. Late last year, scientists raised alarms over a link between the city’s lead-tainted water and the growing number of children with high lead levels in their blood. It’s a serious problem. Lead is toxic to the brain, something scientists have long known. “Lead is probably the most well-known neurotoxin to man,” says Mona Hanna-Attisha, the pediatrician who first connected lead in Flint’s water to lead exposure in kids. And as scientists are beginning to find out, the damage that lead inflicts on children may be long-lasting. In addition to harming kids during youth, lead could contribute to disorders that develop later in life, such as Alzheimer’s disease or schizophrenia. Lead’s reach could extend even further, too — beyond those who drank the contaminated water to their children and grandchildren. Flint’s kids “will have to be followed throughout their whole life, and maybe into the next generation or two,” says Douglas Ruden, a neural toxicologist at Wayne State University in Detroit. A few months of drinking clean water will help bring the kids’ lead levels back down, he says. “But the damage is done.” And it’s permanent. In the United States, lead is everywhere. Decades of burning leaded gasoline spewed lead into the air, and the element settled in the upper layer of soil, clinging to particles of dirt. © Society for Science & the Public 2000 - 2016.
By BENEDICT CAREY Over the past few decades, cognitive scientists have found that small alterations in how people study can accelerate and deepen learning, improving retention and comprehension in a range of subjects, including math, science and foreign languages. The findings come almost entirely from controlled laboratory experiments of individual students, but they are reliable enough that software developers, government-backed researchers and various other innovators are racing to bring them to classrooms, boardrooms, academies — every real-world constituency, it seems, except one that could benefit most: people with learning disabilities. Now, two new studies explore the effectiveness of one common cognitive science technique — the so-called testing effect — for people with attention-deficit problems, one of the most commonly diagnosed learning disabilities. The results were mixed. They hint at the promise of outfoxing learning deficits with cognitive science, experts said, but they also point to the difficulties involved. The learning techniques developed by cognitive psychologists seem, in some respects, an easy fit for people with attention deficits: breaking up study time into chunks, mixing related material in a session, varying study environments. Each can produce improvements in retention or comprehension, and taken together capture the more scattered spirit of those with attention deficit hyperactivity disorder, especially children. The testing effect has proved especially reliable for other students, and it is a natural first choice to measure the potential application to A.D.H.D. The principle is straightforward: Once a student is familiar with a topic, testing himself on it deepens the recall of the material more efficiently than restudying. © 2016 The New York Times Company
By SINDYA N. BHANOO The human brain is attracted to things that were once pleasing even if they no longer are, researchers report. Study participants were asked to find red and green objects on a computer screen filled with different colored objects. They received small rewards for finding the objects: $1.50 for the red ones and 25 cents for the green ones. The next day, while brain scans were conducted, participants were asked to find certain shapes on the screen. There was no reward, and color was irrelevant. Still, when a red object appeared, participants focused on it, and scans showed dopamine was released in their brains. “They are not getting a reward for that, yet part of the brain is saying, ‘Oh, there’s a reward — pay attention to it,’” said Susan M. Courtney, a cognitive neuroscientist at Johns Hopkins University and a co-author of the study in Current Biology. The findings may help researchers develop pharmaceutical treatments for problems like food or drug addiction. © 2016 The New York Times Company
Mo Costandi Tell me where dwell the thoughts, forgotten till thou call them forth? Tell me where dwell the joys of old, and where the ancient loves, And when will they renew again, and the night of oblivion past, That I might traverse times and spaces far remote, and bring Comforts into a present sorrow and a night of pain? Where goest thou, O thought? To what remote land is thy flight? If thou returnest to the present moment of affliction, Wilt thou bring comforts on thy wings, and dews and honey and balm, Or poison from the desert wilds, from the eyes of the envier? In his epic poem, Visions of the Daughters of Albion, William Blake wonders about the nature of memory, its ability to mentally transport us to distant times and places, and the powerful emotions, both positive and negative, that our recollections can evoke. The poem contains questions that remain highly pertinent today, such as what happens to our long-lost memories, and how do we retrieve them? More than two centuries later, the mechanisms of memory storage and retrieval are the most intensively studied phenomena in the brain sciences. It’s widely believed that memory formation involves the strengthening of connections between sparsely distributed networks of neurons in a brain structure called the hippocampus, and that subsequent retrieval involves reactivation of the same neuronal ensembles. And yet, neuroscientists still struggle to answer Blake’s questions definitely. Now, a team of researchers at the University of Geneva have made another important advance in our understanding of the neural mechanisms underlying memory formation. Using a state-of-the-art method called optogenetics, they show how the neuronal ensembles that encode memories emerge, revealing that ensembles containing too many neurons – or too few – impair memory retrieval. © 2016 Guardian News and Media Limited
Keyword: Learning & Memory
Link ID: 21893 - Posted: 02.13.2016
Sara Reardon Mice are sensitive to minor changes in food, bedding and light exposure. It’s no secret that therapies that look promising in mice rarely work in people. But too often, experimental treatments that succeed in one mouse population do not even work in other mice, suggesting that many rodent studies may be flawed from the start. “We say mice are simpler, but I think the problem is deeper than that,” says Caroline Zeiss, a veterinary neuropathologist at Yale University in New Haven, Connecticut. Researchers rarely report on subtle environmental factors such as their mice’s food, bedding or exposure to light; as a result, conditions vary widely across labs despite an enormous body of research showing that these factors can significantly affect the animals’ biology. “It’s sort of surprising how many people are surprised by the extent of the variation” between mice that receive different care, says Cory Brayton, a pathologist at Johns Hopkins University in Baltimore, Maryland. At a meeting on mouse models at the Wellcome Genome Campus in Hinxton, UK, on 9–11 February, she and others explored the many biological factors that prevent mouse studies from being reproduced. Christopher Colwell, a neuroscientist at the University of California, Los Angeles, has first-hand experience with these issues. He and a colleague studied autism in the same genetically modified mouse line, but obtained different results on the same behaviour tests. Eventually they worked out why: Colwell, who studies circadian rhythms, keeps his mice dark in the daytime to trick their body clocks into thinking day is night, so that the nocturnal animals are more alert when tested during the day. His colleague does not. © 2016 Nature Publishing Group
By Uri Bram Early-life exposure to pathogenic bacteria can induce a lifelong imprinted olfactory memory in C. elegans through two distinct neural circuits, according to a study published today (February 11) in Cell. Researchers from Rockefeller University in New York City have shown that early-life pathogen exposure leads the nematode to have a lifelong aversion to the specific associated bacterial odors, whereas later-in-life exposure spurs only transient aversion. “This study is very exciting,” said Yun Zhang of Harvard who studies learning in C. elegans but was not involved in the present work. “Imprinting is a form of learning widely observed in many animals [but] finding this in C. elegans is very meaningful because this nematode is genetically tractable, and its small nervous system is well described.” A classic example of imprinting is how geese form attachments to the first moving object they see after birth; Nobel laureate Konrad Lorenz famously showed that the “moving object” could be himself instead of a mother goose. During the critical period at the start of life, animals often have unusual abilities to create and maintain long-term memories. For the present study, Rockefeller’s Xin Jin and colleagues described a form of aversive imprinting in their C. elegans: newly hatched nematodes exposed to Pseudomonas aeruginosa PA14 or toxin-emitting Escherichia coli BL21 established a long-term olfactory aversion to it. Animals that experienced the pathogen immediately after hatching were able to synthesize and maintain the aversive memory for the whole of their four-day lifespans, while animals trained in adulthood only retained the aversive memory for up to 24 hours. © 1986-2016 The Scientist