Chapter 17. Learning and Memory

Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.


Links 21 - 40 of 1145

OLIVER SACHGAU Marc Lewis spends a lot of his time thinking about addiction. He has good reason to: In his 20s he struggled with his own addiction to opiates. He was eventually able to quit, and began researching addiction and neuroscience. Mr. Lewis became a professor of developmental psychology at the University of Toronto in 1989, and moved to Radboud University in the Netherlands in 2010. His new book, The Biology of Desire: Why Addiction is Not a Disease, looks at the neuroscience of addiction, mixing personal narratives with scientific data. The book will be released in Canada on Aug. 4. You argue addiction is not a disease, but an example of very normal brain activity. What do you mean? [It’s] an exaggerated form of learning. Let’s put it that way. People in neuroscience agree that addiction corresponds with brain changes, and that’s the basis of the disease argument: That addiction changes the brain, or hijacks the brain, as they say. As though it were a pathology or disease process. Whereas I argue that all learning changes – the brain is designed to change – but when you have highly motivated learning, especially something that gets repeated over and over, then the learning curve rises extremely rapidly, and you have a kind of exaggerated learning phenomenon, where the learning is deep and specialized, and blots out other available habits or other available perceptions. You chose to mix hard scientific data with these anecdotal stories. How come? I love that way of writing. It seems to me so amazing that brain changes are going on at the same time as lived experiences: The moment-to-moment changes of thoughts and feelings are completely yoked to changes and activity in your brain, but it’s almost impossible to tell both stories at the same time, because one is under the skin, in terms of cell firings and electrochemical impulses and stuff, and the other one is in terms of behavior and human values and norms and so forth. © Copyright 2015 The Globe and Mail Inc

Keyword: Drug Abuse; Learning & Memory
Link ID: 21163 - Posted: 07.13.2015

Zoë Corbyn Jesper Noehr, 30, reels off the ingredients in the chemical cocktail he’s been taking every day before work for the past six months. It’s a mixture of exotic dietary supplements and research chemicals that he says gives him an edge in his job without ill effects: better memory, more clarity and focus and enhanced problem-solving abilities. “I can keep a lot of things on my mind at once,” says Noehr, who is chief technology officer for a San Francisco startup. The chemicals he takes, dubbed nootropics from the Greek “noos” for “mind”, are intended to safely improve cognitive functioning. They must not be harmful, have significant side-effects or be addictive. That means well-known “smart drugs” such as the prescription-only stimulants Adderall and Ritalin, popular with swotting university students, are out. What’s left under the nootropic umbrella is a dizzying array of over-the-counter supplements, prescription drugs and unclassified research chemicals, some of which are being trialled in older people with fading cognition. There is no official data on their usage, but nootropics as well as other smart drugs appear popular in the Silicon Valley. “I would say that most tech companies will have at least one person on something,” says Noehr. It is a hotbed of interest because it is a mentally competitive environment, says Jesse Lawler, a LA based software developer and nootropics enthusiast who produces the podcast Smart Drug Smarts. “They really see this as translating into dollars.” But Silicon Valley types also do care about safely enhancing their most prized asset – their brains – which can give nootropics an added appeal, he says. © 2015 Guardian News and Media Limited

Keyword: Drug Abuse; Learning & Memory
Link ID: 21158 - Posted: 07.11.2015

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

Keyword: Learning & Memory; Alzheimers
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

Keyword: Learning & Memory
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.

Keyword: Learning & Memory
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

Keyword: Learning & Memory
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

Keyword: Learning & Memory; Attention
Link ID: 21125 - Posted: 07.02.2015

By Erika Beras Marijuana is the drug of choice for people who drink alcohol. And people who use both are twice as likely to do so at the same time than to indulge in just one or the other. That’s according to a study in the journal Alcoholism: Clinical and Experimental Research. [Meenakshi S. Subbaraman and William C. Kerr, Simultaneous Versus Concurrent Use of Alcohol and Cannabis in the National Alcohol Survey The data came from self-reported answers that more than 8,600 people provided to what’s called the National Alcohol Surveys, done by phone in 2005 and 2010. People who used pot and alcohol were about twice as likely to drive drunk than those who just drank. And they doubled their chances of what are referred to as negative social consequences, such as arrests, fights and job problems. Meanwhile, another new study finds that if you’re chronically stoned, you’re more likely to remember things differently from how they happened, or not at all. Researchers showed a series of words to people who do not use marijuana and to regular pot users who had not partaken in a month. A few minutes later, all participants were shown the same list of words along with other words. The volunteers were then asked to identify only the original words. The pot smokers thought more of the new words were in the original list than did the nonusers. And brain scans revealed that the regular pot users showed less activity in brain regions associated with memory and cognitive resources than did the nonusers. The study is in the journal Molecular Psychiatry. [J. Riba et al, Telling true from false: cannabis users show increased susceptibility to false memories] © 2015 Scientific American

Keyword: Drug Abuse; Learning & Memory
Link ID: 21118 - Posted: 07.02.2015

By Ariana Eunjung Cha One of the most heartbreaking things about Alzheimer's is that it has been impossible for doctors to predict who will get it before symptoms begin. And without early detection, researchers say, a treatment or cure may be impossible. Governments, drug companies and private foundations have poured huge amounts of money into trying to come up with novel ways to detect risk through cutting-edge technologies ranging from brain imaging, protein analysis of cerebrospinal fluid and DNA profiling. Now a new study, published in the journal Neurology, shows that perhaps something more old-fashioned could be the answer: a memory test. The researchers tracked 2,125 participants in four Chicago neighborhoods for 18 years, giving them tests of memory and thinking every three years. They found that those who scored lowest on the tests during the first year were 10 times more likely to be diagnosed with Alzheimer's down the road -- indicating that cognitive impairment may be affecting the brain "substantially earlier than previously established," the researchers wrote.

Keyword: Alzheimers; Learning & Memory
Link ID: 21109 - Posted: 06.30.2015

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.

Keyword: Learning & Memory
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

Keyword: Learning & Memory; Development of the Brain
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

Keyword: Learning & Memory; Depression
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.

Keyword: Learning & Memory
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

Keyword: Learning & Memory
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

Keyword: Learning & Memory
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

Keyword: Learning & Memory
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.

Keyword: Learning & Memory
Link ID: 21001 - Posted: 05.30.2015

By Esther Hsieh Imagine you are enjoying your golden years, driving to your daily appointment for some painless brain zapping that is helping to stave off memory loss. That's the hope of a new study, in which people who learned associations (such as a random word and an image) after transcranial magnetic stimulation (TMS) were better able to learn more pairings days and weeks later—with no further stimulation needed. TMS uses a magnetic coil placed on the head to increase electrical signaling a few centimeters into the brain. Past studies have found that TMS can boost cognition and memory during stimulation, but this is the first to show that such gains can last even after the TMS regimen is completed. In the new study, which was published in Science, neuroscientists first used brain imaging to identify the associative memory network of 16 young, healthy participants. This network, based around the hippocampus, glues together things such as sights, places, sounds and time to form a memory, explains neuroscientist Joel Voss of Northwestern University, a senior author of the paper. Next, the researchers applied TMS behind the left ear of each participant for 20 minutes for five consecutive days to stimulate this memory network. To see if participants' associative memory improved, one day after the stimulation regimen finished they were tested for their ability to learn random words paired with faces. Subjects who had had TMS performed 33 percent better, compared with those who received placebo treatments, such as sham stimulation. © 2015 Scientific American

Keyword: Learning & Memory; Brain imaging
Link ID: 20977 - Posted: 05.25.2015

Athletes who lose consciousness after concussions may be at greater risk for memory loss later in life, a small study of retired National Football League players suggests. Researchers compared memory tests and brain scans for former NFL players and a control group of people who didn't play college or pro football. After concussions that resulted in lost consciousness, the football players were more likely to have mild cognitive impairment and brain atrophy years later. "Our results do suggest that players with a history of concussion with a loss of consciousness may be at greater risk for cognitive problems later in life," senior study author Munro Cullum, chief of neuropsychology at the University of Texas Southwestern Medical Center in Dallas, said by email. "We are at the early stages of understanding who is actually at risk at the individual level." Cullum and colleagues recruited 28 retired NFL players living in Texas: eight who were diagnosed with mild cognitive impairment and 20 who didn't appear to have any memory problems. They ranged in age from 36 to 79, and were an average of about 58 years old. All but three former athletes experienced at least one concussion, and they typically had more than three. Researchers compared these men to 27 people who didn't play football but were similar in age, education, and mental capacity to the retired athletes, including six with cognitive impairment. These men were 41 to 77 years old, and about 59 on average. ©2015 CBC/Radio-Canada

Keyword: Brain Injury/Concussion; Learning & Memory
Link ID: 20965 - Posted: 05.21.2015

By Susan Cosier Once a memory is lost, is it gone forever? Most research points to yes. Yet a study published in the online journal eLife now suggests that traces of a lost memory might remain in a cell's nucleus, perhaps enabling future recall or at least the easy formation of a new, related memory. The current theory accepted by neurobiologists is that long-term memories live at synapses, which are the spaces where impulses pass from one nerve cell to another. Lasting memories are dependent on a strong network of such neural connections; memories weaken or fade if the synapses degrade. In the new study, researchers at the University of California, Los Angeles, studied sea slugs' neurons in a cell culture dish. Over several days the neurons spontaneously formed a number of synapses. The scientists then administered the neurotransmitter serotonin to the neurons, causing them to create many more synapses—the same process by which a living creature would form a long-term memory. When they inhibited a memory-forming enzyme and checked the neurons after 48 hours, the number of synapses had returned to the initial number—but they were not the same individual synapses as before. Some of the original and some of the new synapses retracted to create the exact number the cells started with. The finding is surprising because it suggests that a nerve cell body “knows” how many synapses it is supposed to form, meaning it is encoding a crucial part of memory. The researchers also ran a similar experiment on live sea slugs, in which they found that a long-term memory could be totally erased (as gauged by its synapses being destroyed) and then re-formed with only a small reminder stimulus—again suggesting that some information was being stored in a neuron's body. © 2015 Scientific American

Keyword: Learning & Memory
Link ID: 20958 - Posted: 05.20.2015