Links for Keyword: Learning & Memory

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Richard A. Friedman YOU can increase the size of your muscles by pumping iron and improve your stamina with aerobic training. Can you get smarter by exercising — or altering — your brain? Stories from Our Advertisers This is hardly an idle question considering that cognitive decline is a nearly universal feature of aging. Starting at age 55, our hippocampus, a brain region critical to memory, shrinks 1 to 2 percent every year, to say nothing of the fact that one in nine people age 65 and older has Alzheimer’s disease. The number afflicted is expected to grow rapidly as the baby boom generation ages. Given these grim statistics, it’s no wonder that Americans are a captive market for anything, from supposed smart drugs and supplements to brain training, that promises to boost normal mental functioning or to stem its all-too-common decline. The very notion of cognitive enhancement is seductive and plausible. After all, the brain is capable of change and learning at all ages. Our brain has remarkable neuroplasticity; that is, it can remodel and change itself in response to various experiences and injuries. So can it be trained to enhance its own cognitive prowess? The multibillion-dollar brain training industry certainly thinks so and claims that you can increase your memory, attention and reasoning just by playing various mental games. In other words, use your brain in the right way and you’ll get smarter. A few years back, a joint study by BBC and Cambridge University neuroscientists put brain training to the test. Their question was this: Do brain gymnastics actually make you smarter, or do they just make you better at doing a specific task? For example, playing the math puzzle KenKen will obviously make you better at KenKen. But does the effect transfer to another task you haven’t practiced, like a crossword puzzle? © 2015 The New York Times Company

Related chapters from BP7e: Chapter 17: Learning and Memory; Chapter 1: Biological Psychology: Scope and Outlook
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 1: An Introduction to Brain and Behavior
Link ID: 21567 - Posted: 10.26.2015

Keikantse Matlhagela Susumu Tonegawa unlocked the genetic secrets behind antibodies' diverse structures, which earned him the Nobel Prize in Physiology or Medicine in 1987. Having since moved fields, he tells Keikantse Matlhagela about his latest work on the neuroscience of happy and sad memories. You started as a chemist, then you moved into molecular biology and now you are a neuroscientist. Why change fields? Strangely, the only people to ask me about this are journalists — my students never ask. I see myself as a scientist who is interested in what's going on inside of us. It doesn't matter whether it is chemistry or immunology or neuroscience, I just do research on what I find interesting. The switch from chemistry to immunology did not seem like a big shift when I was young, but immunology to neuroscience was. After about 15 years spent researching immunology I wanted to explore an area of science where there are still big, unresolved questions. The brain is probably the most mysterious subject there is. Do you keep up to date with the field in which you won your Nobel prize? I am sorry to say that I haven't been paying a lot of attention to immunology in recent years because I am preoccupied with my work on memory. I have friends, of course, from that time — very close friends. But my friends are not young. Even though they are experts, they are also retired. We tend not to talk about immunology a whole lot. © 2015 Macmillan Publishers Limited

Related chapters from BP7e: Chapter 17: Learning and Memory
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 21542 - Posted: 10.22.2015

By Emily Underwood CHICAGO—In 1898, Italian biologist Camillo Golgi found something odd as he examined slices of brain tissue under his microscope. Weblike lattices, now known as "perineuronal nets," surrounded many neurons, but he could not discern their purpose. Many dismissed the nets as an artifact of Golgi's staining technique; for the next century, they remained largely obscure. Today, here at the annual meeting of the Society for Neuroscience, researchers offered tantalizing new evidence that holes in these nets could be where long-term memories are stored. Scientists now know that perineuronal nets (PNNS) are scaffolds of linked proteins and sugars that resemble cartilage, says neuroscientist Sakina Palida, a graduate student in Roger Tsien's lab at the University of California,San Diego, and co-investigator on the study. Although it's still unclear precisely what the nets do, a growing body of research suggests that PNNs may control the formation and function of synapses, the microscopic junctions between neurons that allow cells to communicate, and that may play a role in learning and memory, Palida says. One of the most pressing questions in neuroscience is how memories—particularly long-term ones—are stored in the brain, given that most of the proteins inside neurons are constantly being replaced, refreshing themselves anywhere from every few days to every few hours. To last a lifetime, Palida says, some scientists believe that memories must somehow be encoded in a persistent, stable molecular structure. Inspired in part by evidence that destroying the nets in some brain regions can reverse deeply ingrained behaviors, Palida’s adviser Tsien, a Nobel-prize-winning chemist, recently began to explore whether PNNs could be that structure. Adding to the evidence were a number of recent studies linking abnormal PNNs to brain disorders including schizophrenia and Costello syndrome, a form of intellectual disability. © 2015 American Association for the Advancement of Science.

Related chapters from BP7e: Chapter 17: Learning and Memory; Chapter 2: Functional Neuroanatomy: The Nervous System and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 2: Cells and Structures: The Anatomy of the Nervous System
Link ID: 21540 - Posted: 10.21.2015

By LISA SANDERS, M.D. The middle-aged couple knocked at the door of the townhouse. When no one answered, the woman took her key and let them in. She called her daughter’s name as she hurried through the rooms. They had been trying to reach their 27-year-old daughter by phone all day, and she hadn’t answered. They found her upstairs, lying in bed and mumbling incoherently. The mother rushed over, but her daughter showed no signs of recognition. She and her husband quickly carried her to the car. Four months before, the mother told the emergency-room doctor at SSM Health St. Mary’s Hospital in St. Louis, her daughter had a procedure called gastric-sleeve surgery to help her lose weight. She came home after just a couple of days and felt great. She looked bright and eager. Once she started to eat, though, nausea and vomiting set in. After almost every meal, she would throw up. It’s an unusual but well-known complication of this kind of surgery. The cause is not clearly understood, but the phenomenon is sometimes linked to reflux. The surgeon tried different medications to stop the nausea and vomiting and to reduce the acid in her stomach, but they didn’t help. She had the surgery in order to lose weight, but now she was losing weight too quickly. After a month of vomiting, her doctors thought maybe she had developed gallstones — a common problem after rapid weight loss. But even after her gallbladder was removed, the young woman continued to vomit after eating. © 2015 The New York Times Company

Related chapters from BP7e: Chapter 17: Learning and Memory; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 21534 - Posted: 10.21.2015

By Hanae Armitage Schools of fish clump together for a very simple reason: safety in numbers. But for some, banding together offers more than just protection. It’s a way of getting to the head of the class. Schooling fish learn from each other, and new research shows that when they’re taken out of their normal social group, individuals struggle to learn on their own. Scientists have long known that schooling fish observe and learn from each other’s failures and successes, behaviors that stimulate neural development, especially in the part of the brain responsible for memory and learning. But this is the first time they have found evidence of that link in spatial learning. To test their theory, scientists divided a school of social cichlid fish into two categories: 14 social fish and 15 loners. Researchers kept the social fish grouped together while they partitioned the loners into single-fish isolation tanks. They ran both groups through a simple T-shaped maze, color coding the side that harbored food—a yellow mark for food, a green mark for no food. Seven of the 14 socialized fish learned to associate yellow with food (high marks for the cichlids, which are not the brightest fish in the animal kingdom), whereas only three of the 15 isolated fish successfully made the same association. Writing in this month’s issue of Applied Animal Behaviour Science, the researchers say this suggests fish in group settings are able to learn better and faster than their singled out counterparts. The moral? Simple: Fish should stay in school. © 2015 American Association for the Advancement of Science

Related chapters from BP7e: Chapter 17: Learning and Memory; Chapter 6: Evolution of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 21495 - Posted: 10.10.2015

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

Related chapters from BP7e: Chapter 17: Learning and Memory
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 21474 - Posted: 10.05.2015

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

Related chapters from BP7e: Chapter 17: Learning and Memory
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 21469 - Posted: 10.03.2015

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.

Related chapters from BP7e: Chapter 17: Learning and Memory
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 21434 - Posted: 09.23.2015

We all have our favourite movie moments, ones we love to watch again from time to time. Now it seems chimpanzees and bonobos, too, have the nous to recall thrilling scenes in movies they have previously seen and anticipate when they are about to come up. The results suggest apes can readily recall and anticipate significant recent events, just by watching those events once. Rather than use hidden food as a memory test, Japanese researchers made short movies and showed them to apes on two consecutive days. “We showed a movie instead, and asked whether they remember it when they only watch an event once, and an event totally new to them,” says Fumihiro Kano of Kyoto University in Japan. “Their anticipatory glances told us that they did.” Plot moment Kano and his colleague Satoshi Hirata made and starred in two short films. Another of the characters was a human dressed up as an ape in a King Kong costume who carried out attacks on people, providing the key plot moment in the first movie (see video). Both films were designed to contain memorable dramatic events, and the researchers deployed laser eye-tracking technology to see if the animals preferentially noticed and remembered these moments. © Copyright Reed Business Information Ltd.

Related chapters from BP7e: Chapter 17: Learning and Memory
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 21421 - Posted: 09.20.2015

By AMY HARMON Some neuroscientists believe it may be possible, within a century or so, for our minds to continue to function after death — in a computer or some other kind of simulation. Others say it’s theoretically impossible, or impossibly far off in the future. A lot of pieces have to fall into place before we can even begin to start thinking about testing the idea. But new high-tech efforts to understand the brain are also generating methods that make those pieces seem, if not exactly imminent, then at least a bit more plausible. Here’s a look at how close, and far, we are to some requirements for this version of “mind uploading.” The hope of mind uploading rests on the premise that much of the key information about who we are is stored in the unique pattern of connections between our neurons, the cells that carry electrical and chemical signals through living brains. You wouldn't know it from the outside, but there are more of those connections — individually called synapses, collectively known as the connectome — in a cubic centimeter of the human brain than there are stars in the Milky Way galaxy. The basic blueprint is dictated by our genes, but everything we do and experience alters it, creating a physical record of all the things that make us US — our habits, tastes, memories, and so on. It is exceedingly tricky to transition that pattern of connections, known as the connectome, into a state where it is both safe from decay and can be verified as intact. But in recent months, two sets of scientists said they had devised separate ways to do that for the brains of smaller mammals. If either is scaled up to work for human brains — still a big if — then theoretically your brain could sit on a shelf or in a freezer for centuries while scientists work on the rest of these steps. © 2015 The New York Times Company

Related chapters from BP7e: Chapter 17: Learning and Memory; Chapter 18: Attention and Higher Cognition
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 14: Attention and Consciousness
Link ID: 21407 - Posted: 09.14.2015

By Gretchen Reynolds At the age of 93, Olga Kotelko — one of the most successful and acclaimed nonagenarian track-and-field athletes in history — traveled to the University of Illinois to let scientists study her brain. Ms. Kotelko held a number of world records and had won hundreds of gold medals in masters events. But she was of particular interest to the scientific community because she hadn’t begun serious athletic training until age 77. So scanning her brain could potentially show scientists what late-life exercise might do for brains. Ms. Kotelko died last year at the age of 95, but the results of that summer brain scan were published last month in Neurocase. And indeed, Ms. Kotelko’s brain looked quite different from those of other volunteers aged 90-plus who participated in the study, the scans showed. The white matter of her brain — the cells that connect neurons and help to transmit messages from one part of the brain to another — showed fewer abnormalities than the brains of other people her age. And her hippocampus, a portion of the brain involved in memory, was larger than that of similarly aged volunteers (although it was somewhat shrunken in comparison to the brains of volunteers decades younger than her). Over all, her brain seemed younger than her age. But because the scientists didn’t have a scan showing Ms. Kotelko’s brain before she began training, it’s impossible to know whether becoming an athlete late in life improved her brain’s health or whether her naturally healthy brain allowed her to become a stellar masters athlete. © 2015 The New York Times Company

Related chapters from BP7e: Chapter 17: Learning and Memory; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 13: Memory, Learning, and Development
Link ID: 21372 - Posted: 09.02.2015

By Laura Sanders By tweaking a single gene, scientists have turned average mice into supersmart daredevils. The findings are preliminary but hint at therapies that may one day ease the symptoms of such disorders as Alzheimer’s disease and schizophrenia, scientists report August 14 in Neuropsychopharmacology. The altered gene provides instructions for a protein called phosphodiesterase-4B, or PDE4B, which has been implicated in schizophrenia. It’s too early to say whether PDE4B will turn out to be a useful target for drugs that treat these disorders, cautions pharmacologist Ernesto Fedele of the University of Genoa in Italy. Nonetheless, the protein certainly deserves further investigation, he says. The genetic change interfered with PDE4B’s ability to do its job breaking down a molecular messenger called cAMP. Mice designed to have this disabled form of PDE4B showed a suite of curious behaviors, including signs of smarts, says study coauthor Alexander McGirr of the University of British Columbia. Compared with normal mice, these mice more quickly learned which objects in a cage had been moved to a new location, for instance, and could better recognize a familiar mouse after 24 hours. “The system is primed and ready to learn, and it doesn’t require the same kind of input as a normal mouse,” McGirr says. These mice also spent more time than usual exploring brightly lit spaces, spots that normal mice avoid. But this devil-may-care attitude sometimes made the “smart” mice blind to risky situations. The mice were happy to spend time poking around an area that had been sprinkled with bobcat urine. “Not being afraid of cat urine is not a good thing for a mouse,” McGirr says. © Society for Science & the Public 2000 - 2015

Related chapters from BP7e: Chapter 17: Learning and Memory; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 21338 - Posted: 08.26.2015

By Kate Kelland LONDON (Reuters) - Scientists have genetically modified mice to be super-intelligent and found they are also less anxious, a discovery that may help the search for treatments for disorders such as Alzheimer's, schizophrenia and post traumatic stress disorder (PTSD). Researchers from Britain and Canada found that altering a single gene to block the phosphodiesterase-4B (PDE4B) enzyme, which is found in many organs including the brain, made mice cleverer and at the same time less fearful. "Our work using mice has identified phosphodiesterase-4B as a promising target for potential new treatments," said Steve Clapcote, a lecturer in pharmacology at Britain's Leeds University, who led the study. He said his team is now working on developing drugs that will specifically inhibit PDE4B. The drugs will be tested first in animals to see whether any of them might be suitable to go forward into clinical trials in humans. In the experiments, published on Friday in the journal Neuropsychopharmacology, the scientists ran a series of behavioral tests on the PDE4B-inhibited mice and found they tended to learn faster, remember events longer and solve complex problems better than normal mice. The "brainy" mice were better at recognizing a mouse they had seen the previous day, the researchers said, and were also quicker at learning the location of a hidden escape platform.

Related chapters from BP7e: Chapter 17: Learning and Memory
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 21306 - Posted: 08.18.2015

Ashley Yeager A mouse scurries across a round table rimmed with Dixie cup–sized holes. Without much hesitation, the rodent heads straight for the hole that drops it into a box lined with cage litter. Any other hole would have led to a quick fall to the floor. But this mouse was more than lucky. It had an advantage — human glial cells were growing in its brain. Glia are thought of as the support staff for the brain’s nerve cells, or neurons, which transmit and receive the brain’s electrical and chemical signals. Named for the Greek term for “glue,” glia have been known for nearly 170 years as the cells that hold the brain’s bits together. Some glial cells help feed neurons. Other glia insulate nerve cell branches with myelin. Still others attack brain invaders responsible for infection or injury. Glial cells perform many of the brain’s most important maintenance jobs. But recent studies suggest they do a lot more. Glia can shape the conversation between neurons, speeding or slowing the electrical signals and strengthening neuron-to-neuron connections. When scientists coaxed human glia to grow in the brains of baby mice, the mice grew up to be supersmart, navigating tabletops full of holes and mastering other tasks much faster than normal mice. This experiment and others suggest that glia may actually orchestrate learning and memory, says neuroscientist R. Douglas Fields. “Glia aren’t doing vibrato. That’s for the neurons,” says Fields, of the National Institute of Child Health and Human Development in Bethesda, Md. “Glia are the conductors.” © Society for Science & the Public 2000 - 2015

Related chapters from BP7e: Chapter 17: Learning and Memory; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 21289 - Posted: 08.12.2015

Tina Hesman Saey Memory Transfer Seen — Experiments with rats, showing how chemicals from one rat brain influence the memory of an untrained animal, indicate that tinkering with the brain of humans is also possible. In the rat tests, brain material from an animal trained to go for food either at a light flash or at a sound signal was injected into an untrained rat. The injected animals then "remembered" whether light or sound meant food. — Science News Letter, August 21, 1965 Update: After this report, scientists from eight labs attempted to repeat the memory transplants. They failed, as they reported in Science in 1966. Science fiction authors and futurists often predict that a person’s memories might be transferred to another person or a computer, but the idea is likely to remain speculation, says neuroscientist Eric Kandel, who won a Nobel Prize in 2000 for his work on memory. Brain wiring is too intricate and complicated to be exactly replicated, and scientists are still learning about how memories are made, stored and retrieved. W. L. Byrne et al. Technical Comments: Memory Transfer. Science Vol. 153, August 5, 1966, p. 658. doi:10.1126/science.153.3736.658 © Society for Science & the Public 2000 - 2015

Related chapters from BP7e: Chapter 17: Learning and Memory
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 21271 - Posted: 08.08.2015

By Robert Gebelhoff Just in case sea snails aren't slow enough, new research has found that they get more sluggish when they grow old — and the discovery is helping us to understand how memory loss happens in humans. It turns out that the sea snail, which has a one-year lifespan, is actually a good model to study nerve cells and how the nervous system works in people. How neurons work is fundamentally identical in almost all animals, and the simplicity of the snail's body gives researchers the chance to view how different the system works more directly. "You can count the number of nerve cells that are relevant to a reflex," said Lynne Fieber, a professor at the University of Miami who leads research with the snails at the school. She and a team of researchers have been using the slimy little critters to learn how nerve cells respond to electric shock. They "taught" the snails to quickly contract their muscle tails by administering electric shocks and then poking the tails, a process called "sensitization." They then studied the responses at various ages. The scientists, whose work was published this week in the journal PlOS One, found that as the senior citizen specimens do not learn to contract from the shock very well. As the snails grow older, their tail startle reflex lessened, and then disappeared. So I guess you could say the frail snails' tails fail to avail (okay, I'll stop).

Related chapters from BP7e: Chapter 17: Learning and Memory; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 13: Memory, Learning, and Development
Link ID: 21245 - Posted: 08.01.2015

By Bret Stetka The brain is extraordinarily good at alerting us to threats. Loud noises, noxious smells, approaching predators: they all send electrical impulses buzzing down our sensory neurons, pinging our brain’s fear circuitry and, in some cases, causing us to fight or flee. The brain is also adept at knowing when an initially threatening or startling stimulus turns out to be harmless or resolved. But sometimes this system fails and unpleasant associations stick around, a malfunction thought to be at the root of post-traumatic stress disorder (PTSD). New research has identified a neuronal circuit responsible for the brain’s ability to purge bad memories, findings that could have implications for treating PTSD and other anxiety disorders. Like most emotions, fear is neurologically complicated. But previous work has consistently implicated two specific areas of the brain as contributing to and regulating fear responses. The amygdala, two small arcs of brain tissue deep beneath our temples, is involved in emotional reactions, and it flares with activity when we are scared. If a particular threat turns out to be harmless, a brain region behind the forehead called the prefrontal cortex steps in and the fright subsides. Our ability to extinguish painful memories is known to involve some sort of coordinated effort between the amygdala and the prefrontal cortex. The new study, led by Andrew Holmes at the National Institutes of Health, however, confirms that a working connection between the two brain regions is necessary to do away with fear. Normally mice that repeatedly listen to a sound previously associated with a mild foot shock will learn that on its own the tone is harmless, and they will stop being afraid. Using optogenetic stimulation technology, or controlling specific neurons and animal behavior using light, the authors found that disrupting the amygdala–prefrontal cortex connection prevents mice from overcoming the negative association with the benign tone. In neurobiology speak, memory “extinction” fails to occur. They also found that the opposite is true—that stimulating the circuit results in increased extinction of fearful memories. © 2015 Scientific American

Related chapters from BP7e: Chapter 17: Learning and Memory; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 11: Emotions, Aggression, and Stress
Link ID: 21243 - Posted: 08.01.2015

By Emily Underwood Glance at a runner's wrist or smartphone, and you'll likely find a GPS-enabled app or gadget ticking off miles and minutes as she tries to break her personal record. Long before FitBit or MapMyRun, however, the brain evolved its own system for tracking where we go. Now, scientists have discovered a key component of this ancient navigational system in rats: a group of neurons called "speed cells" that alter their firing rates with the pace at which the rodents run. The findings may help explain how the brain maintains a constantly updated map of our surroundings. In the 1970s, neuroscientist John O'Keefe, now at University College London, discovered neurons called place cells, which fire whenever a rat enters a specific location. Thirty-five years later, neuroscientists May-Britt and Edvard Moser, now at the Norwegian University of Science and Technology in Trondheim, Norway, discovered a separate group of neurons, called grid cells, which fire at regular intervals as rats traverse an open area, creating a hexagonal grid with coordinates similar to those in GPS. The Mosers and O'Keefe shared last year's Nobel Prize in Physiology and Medicine for their findings, which hint at how the brain constructs a mental map of an animal's environment. Still mysterious, however, is how grid and place cells obtain the information that every GPS system requires: the angle and speed of an object's movement relative to a known starting point, says Edvard Moser, co-author of the new study along with May-Britt Moser, his spouse and collaborator. If the brain does indeed contain a dynamic, internal map of the world, "there has to be a speed signal" that tells the network how far an animal has moved in a given period of time, he says. © 2015 American Association for the Advancement of Science.

Related chapters from BP7e: Chapter 17: Learning and Memory
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 21178 - Posted: 07.16.2015

By Sarah C. P. Williams The next time you forget where you left your car keys, you might be able blame an immune protein that builds up in your blood as you age. The protein impairs the formation of new brain cells and contributes to age-related memory loss—at least in mice, according to a new study. Blocking it could help prevent run-of-the-mill memory decline or treat cognitive disorders, the researchers say. “The findings are really exciting,” says neurologist Dena Dubal of the University of California, San Francisco (UCSF), who was not involved in the study. “The importance of this work cannot be underestimated as the world’s population is aging rapidly.” Multiple groups of scientists have shown that adding the blood of older mice to younger animals’ bodies makes them sluggish, weaker, and more forgetful. Likewise, young blood can restore the memory and energy of older mice. Neuroscientist Saul Villeda of UCSF homed in on one actor he thought might be responsible for some of that effect: β2 microglobulin (B2M), an immune protein normally involved in distinguishing one’s own cells from invading pathogens. B2M has also been found at increased levels in patients with Alzheimer’s disease and other cognitive disorders. Villeda and his colleagues first measured B2M levels in the blood of both people and mice of different ages; they found that those levels increased with age. When the researchers injected B2M into 3-month-old mice, the young animals suddenly had trouble remembering how to complete a water maze, making more than twice as many errors after they’d already been trained to navigate the maze. Moreover, their brains had fewer new neurons than other mice. Thirty days later, however, when the protein had been cleared from their bodies, the animals' memory troubles were gone as well, and the number of newly formed brain cells was back to normal. © 2015 American Association for the Advancement of Science

Related chapters from BP7e: Chapter 17: Learning and Memory; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 13: Memory, Learning, and Development
Link ID: 21144 - Posted: 07.07.2015

By Michael T. Ullman and Mariel Y. Pullman The human brain possesses an incredible capacity to adapt to new conditions. This plasticity enables us not only to constantly learn but also to overcome brain injury and loss of function. Take away one capability, and little by little we often compensate for these deficits. Our brain may be especially well suited to overcome limitations in the case of psychiatric or neurological conditions that originate early in life, what clinicians call neurodevelopmental disorders. Given the brain's considerable plasticity during early years, children with these disorders may have particular advantages in learning compensatory strategies. It now appears that a single brain system—declarative memory—can pick up slack for many kinds of problems across multiple neurodevelopmental disorders. This system, rooted in the brain's hippocampus, is what we typically refer to when we think of learning and memory. It allows us to memorize facts and names or recall a first grade teacher or a shopping list. Whereas other memory systems are more specialized—helping us learn movements or recall emotional events, for instance—declarative memory absorbs and retains a much broader range of knowledge. In fact, it may allow us to learn just about anything. Given declarative memory's powerful role in learning, one might expect it to help individuals acquire all kinds of compensatory strategies—as long as it remains functional. Indeed, research suggests that it not only remains largely intact but also compensates for diverse impairments in five common conditions that are rarely studied in conjunction: autism spectrum disorder, obsessive-compulsive disorder (OCD), Tourette's syndrome, dyslexia and developmental language disorder (which is often referred to as specific language impairment, or SLI). © 2015 Scientific American

Related chapters from BP7e: Chapter 17: Learning and Memory
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 21143 - Posted: 07.07.2015