Chapter 13. Memory, Learning, and Development
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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
By Jessica Schmerler Approximately one in 68 children is identified with some form of autism, from extremely mild to severe, according to the U.S. Centers for Disease Control. On average, diagnosis does not occur until after age four, yet all evidence indicates that early intervention is the best way to maximize the treatment impact. Various tests that look for signs of autism in infants have not been conclusive but a new exercise could improve early diagnosis, and also help reduce worry among parents that they did not intervene as soon as possible. The two most widely used tests to measure symptoms, the Autism Observation Scale for Infants (AOSI) and the Autism Diagnostic Observation Schedule (ADOS), cannot be used before the ages of 12 or 16 months respectively. The AOSI measures precursors to symptoms, such as a baby’s response to name, eye contact, social reciprocity, and imitation. The ADOS measures the characteristics and severity of autism symptoms such as social affectation and repetitive and restrictive behaviors. Now a group of scientists at the Babylab at Birkbeck, University of London think they have identified a marker that can predict symptom development more accurately and at an earlier age: enhanced visual attention. Experts have long recognized that certain individuals with autism have superior visual skills, such as increased visual memory or artistic talent. Perhaps the most well known example is Temple Grandin, a high-functioning woman with autism who wrote, “I used to become very frustrated when a verbal thinker could not understand something I was trying to express because he or she couldn’t see the picture that was crystal clear to me.” © 2015 Scientific American
Owning a cat as a kid could put you at risk for schizophrenia and bipolar disorder later on because of parasites found in feline feces, new research says. Previous studies have linked the parasite toxoplasma gondii (T. gondii) to the development of mental disorders, and two more research papers published recently provide further evidence. Researchers from the Academic Medical Centre in Amsterdam looked at more than 50 studies and found that a person infected with the parasite is nearly twice as likely to develop schizophrenia. The other study, led by Dr. Robert H. Yolken of Johns Hopkins University School of Medicine in Baltimore, confirmed the results of a 1982 questionnaire that found half of people who had a cat as a kid were diagnosed with mental illnesses later in life compared to 42% of those who didn't grow up with a cat. "Cat ownership in childhood has now been reported in three studies to be significantly more common in families in which the child is later diagnosed with schizophrenia or another serious mental illness," the authors said in a press release. The findings were published in Schizophrenia Research and Acta Psychiatrica Scandinavica. T. gondii, which causes the disease toxoplasma, is especially risky for pregnant women and people with weak immune symptoms. The parasite can also be found in undercooked meat and unwashed fruits and vegetables.
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 Sue Bailey, The Canadian Press Scientific studies increasingly suggest marijuana may not be the risk-free high that teens — and sometimes their parents — think it is, researchers say. Yet pot is still widely perceived by young smokers as relatively harmless, said Dr. Romina Mizrahi, director of the Focus on Youth Psychosis Prevention clinic and research program at the Centre for Addiction and Mental Health. She cites a growing body of research that warns of significantly higher incidence of hallucinations, paranoia and the triggering of psychotic illness in adolescent users who are most predisposed. "When you look at the studies in general, you can safely say that in those that are vulnerable, it doubles the risk." Such fallout is increasingly evident in the 19-bed crisis monitoring unit at the Children's Hospital of Eastern Ontario in Ottawa. "I see more and more cases of substance-induced psychosis," said Dr. Sinthu Suntharalingam, a child and adolescent psychiatrist. "The most common substance that's abused is cannabis." One or two cases a week are now arriving on average. "They will present with active hallucinations," Suntharalingam said. "Parents will be very scared. They don't know what's going on. "They'll be seeing things, hearing things, sometimes they will try to self-harm or go after other people." Potential effects need to be better understood She and Mizrahi, an associate professor in psychiatry at University of Toronto, are among other front-line professionals who say more must be done to help kids understand potential effects. "They know the hard drugs, what they can do," Suntharalingam said. "Acid, they'll tell us it can cause all these things so they stay away from it. But marijuana? They'll be: 'Oh, everybody does it."' Mizrahi said the message isn't getting through. ©2015 CBC/Radio-Canada.
by Helen Thomson For the first time, scientists have discovered a mechanism in humans that could explain how your lifestyle choices may impact your children and grandchildren's genes. Mounting evidence suggests that environmental factors such as smoking, diet and stress, can leave their mark on the genes of your children and grandchildren. For example, girls born to Dutch women who were pregnant during a long famine at the end of the second world war had twice the usual risk of developing schizophrenia. Likewise, male mice that experience early life stress give rise to two generations of offspring that have increased depression and anxiety, despite being raised in a caring environment. This has puzzled many geneticists, as genetic information contained in sperm and eggs is not supposed to be affected by the environment, a principle called the August Weismann barrier. But we also know the activity of our own genes can be changed by our environment, through epigenetic mechanisms . These normally work by turning a gene on or off by adding or subtracting a methyl group to or from its DNA. These methyl groups can inactivate genes by making their DNA curl up, so that enzymes can no longer access the gene and read its instructions. Such epigenetic mechanisms are high on the list of suspects when it comes to explaining how environmental factors that affect parents can later influence their children, such as in the Dutch second world war study, but just how these epigenetic changes might be passed on to future generations is a mystery. © Copyright Reed Business Information Ltd.
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
Rebecca Hersher Greg O'Brien sees things that he knows aren't there, and these visual disturbances are becoming more frequent. That's not uncommon; up to 50 percent of people who have Alzheimer's disease experience hallucinations, delusions or psychotic symptoms, recent research suggests. At first, he just saw spider-like forms floating in his peripheral vision, O'Brien says. "They move in platoons." But in the last year or so, the hallucinations have been more varied, and often more disturbing. A lion. A bird. Sprays of blood among the spiders. Over the past five months, O'Brien has turned on an audio recorder when the hallucinations start, in hopes of giving NPR listeners insight into what Alzheimer's feels like. For now, he says, "I'm able to function. But I fear the day, which I know will come, when I can't." Interview Highlights [It's] St. Patrick's Day, about 9 o'clock in the morning in my office, and they're coming again. Those hallucinations. Those things that just come into the mind when the mind plays games. And then I see the bird flying in tighter and tighter and tighter circles. And all of a sudden, the bird — beak first — it darted almost in a suicide mission, exploding into my heart. Today I'm just seeing this thing in front of me. It looks like a lion, almost looks like something you'd see in The Lion King, and there are birds above it. It's floating, and it disintegrates ... it disintegrates ... it disintegrates.
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
Boer Deng The ability of the bizarre prion protein to cause an array of degenerative brain conditions may help solve a puzzle in Alzheimer's research — why the disease sometimes kills within a few years, but usually causes a slow decline that can take decades. By adopting tools used to study the prion protein, PrP, researchers have found variations in the shape of a protein involved in Alzheimer’s that may influence how much damage it causes in the brain. At the Prion 2015 meeting, held on 26–29 May in Fort Collins, Colorado, neuroscientist Lary Walker described how he has borrowed a technique from prion research to study different ‘strains’ of the amyloid-β protein, which accumulates in clumps in the brains of people with Alzheimer’s. It may be that differences between the strains account for variations in the disease’s symptoms and rate of progression. “The Alzheimer’s field has not been paying enough attention to what’s happening in the prion field,” says Walker, who is based at Emory University in Atlanta, Georgia. Similarities between rare prion diseases and common neurodegenerative diseases such as Alzheimer’s have been noted for decades: both are thought to involve proteins in the nervous system that change shape and clump together. In prion diseases, a misfolded, often foreign, protein induces cascading malformation of the native prion protein in a patient’s brain. In Alzheimer’s, proteins called tau and amyloid-β accumulate within and around nerve cells, though what triggers that process — and the role of the deposits in the disease — is unclear. © 2015 Nature Publishing Group,
A patient tormented by suicidal thoughts gives his psychiatrist a few strands of his hair. She derives stem cells from them to grow budding brain tissue harboring the secrets of his unique illness in a petri dish. She uses the information to genetically engineer a personalized treatment to correct his brain circuit functioning. Just Sci-fi? Yes, but... An evolving “disease-in-a-dish” technology, funded by the National Institutes of Health (NIH), is bringing closer the day when such a seemingly futuristic personalized medicine scenario might not seem so far-fetched. Scientists have perfected mini cultured 3-D structures that grow and function much like the outer mantle – the key working tissue, or cortex — of the brain of the person from whom they were derived. Strikingly, these “organoids” buzz with neuronal network activity. Cells talk with each other in circuits, much as they do in our brains. Sergiu Pasca, M.D. External Web Site Policy, of Stanford University, Palo Alto, CA, and colleagues, debut what they call “human cortical spheroids,” May 25, 2015 online in the journal Nature Methods. Prior to the new study, scientists had developed a way to study neurons differentiated from stem cells derived from patients’ skin cells — using a technology called induced pluripotent stem cells (iPSCs). They had even produced primitive organoids by coaxing neurons and support cells to organize themselves, mimicking the brain’s own architecture. But these lacked the complex circuitry required to even begin to mimic the workings of our brains.
Keyword: Development of the Brain
Link ID: 20998 - Posted: 05.30.2015
by Andy Coghlan A man in his mid-50s with Parkinson's disease had fetal brain cells injected into his brain last week. He is the first person in nearly 20 years to be treated this way – and could recover full control of his movements in roughly five years. "It seemed to go fine," says Roger Barker of the University of Cambridge, who is leading the international team that is reviving the procedure. The treatment was pioneered 28 years ago in Sweden, but two trials in the US reported no significant benefit within the first two years following the injections, and the procedure was abandoned in favour of deep brain stimulation treatments. What these trials overlooked is that it takes several years for fetal cells to "bed in" and connect properly to the recipient's brain. Many Swedish and North American recipients improved dramatically, around three years or more after the implants – long after the trials had finished. "In the best cases, patients who had the treatment pretty much went back to normal," says Barker. After the fetal cells were wired up properly in their brains, they started producing the brain signalling chemical dopamine – low levels of this cause the classic Parkinson's symptom of uncontrolled movements. In fact, the cells produced so much dopamine that many patients could stop taking their Parkinson's drugs. "The prospect of not having to take medications for Parkinson's is fantastic," says James Beck of the Parkinson's Disease Foundation in the US. © Copyright Reed Business Information Ltd
Children developed better fine-motor skills when the clamping of their umbilical cord at birth was delayed several minutes compared with just seconds, according to a new randomized trial. Delaying clamping allows fetal blood circulating in the placenta to be transfused to the infant, which has been shown to reduce iron deficiency at four to six months of age. Now the longer term benefits of a delay are becoming clearer. Researchers in Sweden randomly assigned 382 full-term infants born after low-risk pregnancies to be clamped at least three minutes after delivery or within 10 seconds of birth. When the children were four, a psychologist assessed them on standard tests of IQ, motor skills and behaviour. The parents also filled in questionnaires about their child's communication and social skills. "Delayed cord clamping compared with early cord clamping improved scores and reduced the number of children having low scores in fine-motor skills and social domains," the study's lead author, Dr. Ola Andersson of Uppsala University in Sweden, and his co-authors said in Tuesday's issue of JAMA Pediatrics. The fine-motor skill tests showed those in the delayed clamping group had a more mature pencil grip. There was also a difference in boys, who researchers said are generally more prone to iron deficiency than girls. Boys showed more improvements in fine-motor skills with delayed clamping. Andersson said delayed cord clamping can have quite an effect on the amount of iron in the blood, which is important for brain development just after birth. ©2015 CBC/Radio-Canada.
Keyword: Development of the Brain
Link ID: 20988 - Posted: 05.27.2015
By Tina Hesman Saey Combatants in the age-old battle of nature versus nurture may finally be able to lay down their arms. On average, both nature and nurture contribute roughly equally to determining human traits. Researchers compiled data from half a century’s worth of studies on more than 14 million pairs of twins. The researchers measured heritability — the amount of variation in a characteristic that can be attributed to genes — for a wide variety of human traits including blood pressure, the structure of the eyeball and mental or behavioral disorders. All traits are heritable to some degree, the researchers report May 18 in Nature Genetics. Traits overall had an average heritability of 49 percent, meaning it’s a draw between genes and environment. Individual traits can be more strongly influenced by one or the other. 100% Fraction of human traits with a genetic component 49% Fraction of variability in human traits determined by genes T.J.C. Polderman et al. Meta-analysis of the heritability of human traits based on fifty years of twin studies. Nature Genetics. Published online May 18, 2015. doi:10.1038/ng.3285. © Society for Science & the Public 2000 - 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
By Tara Haelle Thousands of infants each year die in their cribs from sudden infant death syndrome (SIDS) for reasons that have remained largely a mystery. A study published May 25 provides strong evidence that oxygen deprivation plays a big role. One reason the cause of SIDS has been so difficult to study is the sheer number of variables researchers have had to account for: whether the infant sleeps face down, breathes secondhand smoke or has an illness as well as whether the child has an unidentified underlying susceptibility. To isolate the effects of oxygen concentration, researchers from the University of Colorado compared the rate of SIDS in infants living at high altitudes, where the air is thin, to those living closer to sea level. Infants at high altitudes, they found, were more than twice as likely to die from SIDS. It was “very clever of the authors,” says Michael Goodstein, a pediatrician and member of the 2010–2011 Task Force on Sudden Infant Death Syndrome who was not involved in the study. “The authors did a good job controlling for other variables,” he adds. Beyond the risk of living at high altitudes, the study suggests a common link among different risk factors about the causes of SIDS. For example, the authors note that sleeping on the stomach and exposure to tobacco smoke can also contribute to hypoxia—insufficient oxygen reaching the tissues. Similarly, past research has suggested that sleeping on soft surfaces may shift the chin down, partly obstructing the airway, which might cause an infant to breathe in less oxygen. It’s unclear how hypoxia might contribute to SIDS but it could have to do with a buildup of carbon dioxide in the tissues when a child does not wake up. © 2015 Scientific American
Nala Rogers Alzheimer’s disease may have evolved alongside human intelligence, researchers report in a paper posted this month on BioRxiv1. The study finds evidence that 50,000 to 200,000 years ago, natural selection drove changes in six genes involved in brain development. This may have helped to increase the connectivity of neurons, making modern humans smarter as they evolved from their hominin ancestors. But that new intellectual capacity was not without cost: the same genes are implicated in Alzheimer's disease. Kun Tang, a population geneticist at the Shanghai Institutes for Biological Sciences in China who led the research, speculates that the memory disorder developed as ageing brains struggled with new metabolic demands imposed by increasing intelligence. Humans are the only species known to develop Alzheimer's; the disease is absent even in closely related primate species such as chimpanzees. Tang and his colleagues searched modern human DNA for evidence of this ancient evolution. They examined the genomes of 90 people with African, Asian or European ancestry, looking for patterns of variation driven by changes in population size and natural selection. Marked by selection The analysis was tricky, because the two effects can mimic each other. To control for the effects of population changes ― thereby isolating the signatures of natural selection — the researchers estimated how population sizes changed over time. Then they identified genome segments that did not match up with the population history, revealing the DNA stretches that were most likely shaped by selection. © 2015 Nature Publishing Group
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
Scientists at Mayo Clinic, Jacksonville, Florida created a novel mouse that exhibits the symptoms and neurodegeneration associated with the most common genetic forms of frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS, Lou Gehrig’s disease), both of which are caused by a mutation in the a gene called C9ORF72. The study was partially funded by the National Institutes of Health and published in the journal Science. More than 30,000 Americans live with ALS, which destroys nerves that control essential movements, including speaking, walking, breathing and swallowing. After Alzheimer’s disease, FTD is the most common form of early onset dementia. It is characterized by changes in personality, behavior and language due to loss of neurons in the brain’s frontal and temporal lobes. Patients with mutations in the chromosome 9 open reading frame 72 (C9ORF72) gene have all or some symptoms associated with both disorders. “Our mouse model exhibits the pathologies and symptoms of ALS and FTD seen in patients with theC9ORF72 mutation,” said the study’s lead author, Leonard Petrucelli, Ph.D., chair and Ralph and Ruth Abrams Professor of the Department of Neuroscience at Mayo Clinic, and a senior author of the study. “These mice could greatly improve our understanding of ALS and FTD and hasten the development of effective treatments.” To create the model, Ms. Jeannie Chew, a Mayo Graduate School student and member of Dr. Petrucelli’s team, injected the brains of newborn mice with a disease-causing version of the C9ORF72 gene. As the mice aged, they became hyperactive, anxious, and antisocial, in addition to having problems with movement that mirrored patient symptoms.
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