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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: Biological Basis 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

By David Robson William’s internal clock is eternally jammed at 13:40 on 14 March 2005 – right in the middle of a dentist appointment. A member of the British Armed Forces, he had returned to his post in Germany the night before after attending his grandfather’s funeral. He had gym in the morning, where he played volleyball for 45 minutes. He then entered his office to clear a backlog of emails, before heading to the dentist’s for root-canal surgery. “I remember getting into the chair and the dentist inserting the local anaesthetic,” he tells me. After that? A complete blank. It is as if all new memories are being written in invisible ink that slowly disappears. Since then, he has been unable to remember almost anything for longer than 90 minutes. So while he can still tell me about the first time he met the Duke of York for a briefing at the Ministry of Defence, he can’t even remember where he’s living now; he wakes up every morning believing he is still in Germany in 2005, waiting to visit the dentist. Without a record of new experiences, the passing of time means nothing to him. Today, he only knows that there is a problem because he and his wife have written detailed notes on his smartphone, in a file labelled “First thing – read this”. It is as if all new memories are being written in invisible ink that slowly disappears. How could minor dental work have affected his brain in such a profound way? This real-life medical mystery offers a rare glimpse at the hidden depths of the brain’s workings. © 2015 BBC.

Related chapters from BP7e: Chapter 17: Learning and Memory; Chapter 14: Biological Rhythms, Sleep, and Dreaming
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 10: Biological Rhythms and Sleep
Link ID: 21137 - Posted: 07.06.2015

By SINDYA N. BHANOO Learning can be traced back to individual neurons in the brain, according to a new study. “What we wanted to do was see if we could actually create a new association — a memory — and see if we would be able to see actual change in the neurons,” said Matias Ison, a neuroscientist at the University of Leicester in England and one of the study’s authors. He and his colleagues were able to monitor the brain activity of neurosurgical patients at UCLA Medical Center. The patients already had electrodes implanted in their medial temporal lobes for clinical reasons. The patients were first presented with images of notable people — like Jennifer Aniston, Clint Eastwood and Halle Berry. Then, they were shown images of the same people against different backdrops — like the Eiffel Tower, the Leaning Tower of Pisa and the Sydney Opera House. The same neurons that fired for the images of each of the actors also fired when patients were shown the associated landmark images. In other words, the researchers were able to watch as the patients’ neurons recorded a new memory — not just of a particular person, but of the person at a particular place. © 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: 21126 - Posted: 07.02.2015

Jon Hamilton If you run into an old friend at the train station, your brain will probably form a memory of the experience. And that memory will forever link the person you saw with the place where you saw them. For the first time, researchers have been able to see that sort of link being created in people's brains, according to a study published Wednesday in the journal Neuron. The process involves neurons in one area of the brain that change their behavior as soon as someone associates a particular person with a specific place. "This type of study helps us understand the neural code that serves memory," says Itzhak Fried, an author of the paper and head of the Cognitive Neurophysiology Laboratory at UCLA. It also could help explain how diseases like Alzheimer's make it harder for people to form new memories, Fried says. The research is an extension of work that began more than a decade ago. That's when scientists discovered special neurons in the medial temporal lobe that respond only to a specific place, or a particular person, like the actress Jennifer Aniston. The experiment used a fake photo of actor Clint Eastwood and Pisa's leaning tower to test how the brain links person and place. More recently, researchers realized that some of these special neurons would respond to two people, but only if the people were connected somehow. For example, "a neuron that was responding to Jennifer Aniston was also responding to pictures of Lisa Kudrow," [another actress on the TV series Friends], says Matias Ison of the University of Leicester in the U.K. © 2015 NPR

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: 21125 - Posted: 07.02.2015

By Sunnie Huang, CBC News The story of a Newfoundland man who was struck by a moose but doesn't remember it is not just a curious tale of luck. It also highlights the complex underpinnings of human memory, a neuroscience expert says. Stephen Bromley, from Conche, N.L., struck a moose with his car on Monday, but said he had no recollection it, even days after the collision. It's not the first time that something was amiss about human memory after a moose encounter. hi-moose-car-2012 Michelle Higgins said the roof of her car was peeled back "like a sardine can" after she struck a moose. Another Newfoundlander drove about 40 kilometres with her car's roof peeled back "like a sardine can" after crashing into a moose in 2012. Three years later, she said she still can't recall the incident. The blackout doesn't surprise Scott Watter, a McMaster University professor who specializes in neuroscience, psychology and behaviour. "They are lucky in that sense, but it doesn't seem like a thing that breaks the rules of everything we know about how brains work," he told CBC News. People who sustain head trauma often have poor memory of the event, especially when tested on specific details, Watter said. Also, the more severe the injury gets, the further back the memory loss extends, Watter said. The system at the heart of our memory is a seahorse-shaped section of the brain called the hippocampus, Watter explained. It's responsible for linking different parts of human experience to form a coherent memory. In the most severe — but rare — cases of hippocampus damage, the person can no longer create or retain new memory, as seen in Christopher Nolan's 2000 box office hit Memento. ©2015 CBC/Radio-Canada.

Related chapters from BP7e: Chapter 17: Learning and Memory
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 21106 - Posted: 06.29.2015

Children who have a good memory are better at telling lies, say child psychology researchers. They tested six and seven-year-olds who were given an opportunity to cheat in a trivia game and then lie about their actions. Children who were good liars performed better in tests of verbal memory - the number of words they could remember. This means they are good at juggling lots of information, even if they do tell the odd fib. Writing in the Journal of Experimental Child Psychology, researchers from the Universities of North Florida, Sheffield and Stirling, recruited 114 children from four British schools for their experiment. Using hidden cameras during a question-and-answer game, they were able to identify the children who peeked at the answer to a fictitious question, even though they were told not to. A potentially surprising finding (for parents) is that only a quarter of the children cheated by looking at the answer. Further questioning allowed the researchers to work out who was a good liar or a bad liar. They were particularly interested in children's ability to maintain a good cover story for their lie. In separate memory tests, the good liars showed they had a better working memory for words - but they didn't show any evidence of being better at remembering pictures (visuo-spatial memory). The researchers said this was because lying involves keeping track of lots of verbal information, whereas keeping track of images is less important. © 2015 BBC

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: 21079 - Posted: 06.22.2015

Helen Shen Boosting activity in neurons that have stored happy memories might help to treat depression — at least according to results in mice. In a study published today (17 June) in Nature, neuroscientist Susumu Tonegawa and his colleagues at the Massachusetts Institute of Technology in Cambridge report how they reversed a depression-like state in rodents by using light to stimulate clusters of brain cells believed to have stored memories of a positive experience1. The findings are preliminary, but they hint that areas of the brain involved in storing memories could one day be a target to treat mental disorders in humans, says Tonegawa. “I want to be very careful not to give false expectations to patients. We are doing very basic science,” he adds. “This is exactly the type of work that psychiatry needs right now,” says Robert Malenka, a behavioural scientist at Stanford University in California. “This is an elegant paper.” The work has grown out of studies by Tonegawa’s lab and others that aimed to locate the memory ‘engram’ — the physical trace of a memory, thought to be encoded in an ensemble of neurons2–6. In 2012, Tonegawa and his team provided one of the clearest demonstrations of an engram. They engineered mice with light-sensitive proteins that were expressed when neurons fired. As a result, they could track any neurons that activated while the mice were given a fearful memory by being trained with repeated electric shocks to be scared of a cage3. The researchers later used blue flashes of light to make the same neurons fire again — a technique known as optogenetics — and found that they could make the animals freeze up, presumably because the fearful memory had been reawoken. © 2015 Nature Publishing Group

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: 21073 - Posted: 06.18.2015

You remember your first kiss. You remember your childhood phone number, where you parked your car, and the last time you got really drunk. You probably remember the digits of pi, or at least the first three of them (slacker). Each day you accumulate fresh memories—kissing new people, acquiring different phone numbers and (possibly) competing in pi-memorizing championships (we would root for you). With all those new adventures stacking up, you might start worrying that your brain is growing full. But, wait—is that how it works? Can your brain run out of space, like a hard drive? It depends on what kind of memory you’re talking about. “It’s not like each memory takes a cell and then that cell is used up,” says Nelson Cowan, cognitive psychologist at the University of Missouri. Over the long term, memories are encoded in neural patterns—circuits of connected neurons. And your brain’s ability to knit together new patterns is limitless, so theoretically the number of memories stored in those patterns is limitless as well. Memories don’t always keep to themselves, though. They can crossbreed, like similar but distinct species, creating the recollection equivalent of a mule. If you can’t remember it, a memory is pretty much worthless—and similar memories can interfere with each other, getting in the way of surfacing the right one. Though memory interference is well documented, researchers like Cowan are still guessing at the phenomenon’s neural mechanics.

Related chapters from BP7e: Chapter 17: Learning and Memory
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 21061 - Posted: 06.17.2015

By Nicholas Bakalar Statins, the widely used cholesterol-lowering drugs, have been blamed for memory loss, but a new study suggests that the association is an illusion. The report, in JAMA Internal Medicine, found that the apparent association was likely a result of detection bias — visiting the doctor and starting a new medicine makes people more acutely aware of health issues they might otherwise not notice. Researchers compared 482,543 statin users with the same number of people using no lipid-lowering drugs and with 26,484 people using non-statin lipid lowering drugs. Use of statin drugs was associated with an increase in memory loss during the first 30 days of starting the drugs compared with people who did not take cholesterol-lowering drugs. But so was use of non-statin lipid-lowering drugs. After accounting for many health and behavioral variables, the scientists concluded that either all lipid lowering drugs, statins or not, cause memory loss or, more likely, that previous findings were based on the expectations of the patients rather than any physiological effect of the medicine. “As you think about whether you should be taking statins, there are questions about uncommon side effects worth raising,” said the lead author, Dr. Brian L. Strom, chancellor of Rutgers Biomedical and Health Sciences. “But the question of impairing memory is a nonissue.” © 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: 21047 - Posted: 06.15.2015

James Gorman When researchers found a group of brain cells in the fruit fly that function like a compass, they were very satisfied. They had found what they were looking for. But, said Vivek Jayaraman, when he and Johannes D. Seelig realized that the cells were actually arranged in a physical circle in the brain, so they looked just like a compass, they were taken aback. “It’s kind of like a cosmic joke that they are arranged like that,” he said. Dr. Jayaraman was investigating a kind of navigation called dead reckoning, or, in technical terms, angular path integration. It is the most basic way a moving creature knows where it is and where it is going. In dead reckoning, animals use visual cues, like landmarks, and also a sense of where their bodies are pointed. It is very different from other ways animals navigate, such as the use of polarized light from the sun or sensitivity to the earth’s magnetic field. The researchers published their findings in Nature last month. Dr. Jayaraman had narrowed down the likely location of directional tracking based on other research. So he expected to find activity in the ellipsoid body, a very small region of a very small brain. Dr. Jayaraman and Mr. Seelig, at the Janelia Research Campus of the Howard Hughes Medical Institute in Virginia, engineered neurons there to light up when they were active, and they recorded the activity with a microscopic technique called two-photon calcium imaging that gives a real-time visual picture of the brain in action in a living animal. © 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: 21027 - Posted: 06.08.2015

By Fiona Kumfor, Sicong Tu and The Conversation The brain is truly a marvel. A seemingly endless library, whose shelves house our most precious memories as well as our lifetime’s knowledge. But is there a point where it reaches capacity? In other words, can the brain be “full”? The answer is a resounding no, because, well, brains are more sophisticated than that. A study published in Nature Neuroscience earlier this year shows that instead of just crowding in, old information is sometimes pushed out of the brain for new memories to form. Previous behavioural studies have shown that learning new information can lead to forgetting. But in this study, researchers used new neuroimaging techniques to demonstrate for the first time how this effect occurs in the brain. The experiment The paper’s authors set out to investigate what happens in the brain when we try to remember information that’s very similar to what we already know. This is important because similar information is more likely to interfere with existing knowledge, and it’s the stuff that crowds without being useful. To do this, they examined how brain activity changes when we try to remember a “target” memory, that is, when we try to recall something very specific, at the same time as trying to remember something similar (a “competing” memory). Participants were taught to associate a single word (say, the word sand) with two different images—such as one of Marilyn Monroe and the other of a hat. © 2015 Scientific American

Related chapters from BP7e: Chapter 17: Learning and Memory
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 21013 - Posted: 06.03.2015

by Jessica Hamzelou Memories that seem to be lost forever may be lurking in the brain after all, ready to be reawakened. The finding, based on experiments in mice, could eventually give us a way to revive memories in people with Alzheimer's or amnesia. When we learn something, sets of neurons in the brain strengthen their mutual connections to lay down lasting memories. Or at least that's the theory. Susumu Tonegawa and his colleagues at the Massachusetts Institute of Technology decided to put it to the test. The team first developed a clever technique to selectively label the neurons representing what is known as a memory engram – in other words, the brain cells involved in forming a specific memory. They did this by genetically engineering mice so they had extra genes in all their neurons. As a result, when neurons fire as a memory is formed, they produce red proteins visible under a microscope, allowing the researchers to tell which cells were part of the engram. They also inserted a gene that made the neurons fire when illuminated by blue light. To mimic memory loss, some of the mice were given a drug that blocks the strengthening of connections between neurons. This made the animals forget their fear of the cage. But the telltale red proteins allowed Tonegawa's team to work out which neurons had been involved in storing the fear memory. They then attempted to reactivate just these neurons using blue light. Sure enough, after the engram had been reactivated, the mice again acted as if they were afraid of the cage. © 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: 21001 - Posted: 05.30.2015