Posts tagged memory

Posts tagged memory
Why do some memories last a lifetime while others disappear quickly?

(Image: Tim Vernon, LTH NHS TRUST/SCIENCE PHOTO LIBRARY)
A new study suggests that memories rehearsed, during either sleep or waking, can have an impact on memory consolidation and on what is remembered later.
The new Northwestern University study shows that when the information that makes up a memory has a high value (associated with, for example, making more money), the memory is more likely to be rehearsed and consolidated during sleep and, thus, be remembered later.
Also, through the use of a direct manipulation of sleep, the research demonstrated a way to encourage the reactivation of low-value memories so they too were remembered later.
Delphine Oudiette, a postdoctoral fellow in the department of psychology at Northwestern and lead author of the study, designed the experiment to study how participants remembered locations of objects on a computer screen. A value assigned to each object informed participants how much money they could make if they remembered it later on the test.
"The pay-off was much higher for some of the objects than for others," explained Ken Paller, professor of psychology at Northwestern and co-author of the study. "In other words, we manipulated the value of the memories — some were valuable memories and others not so much, just as the things we experience each day vary in the extent to which we’d like to be able to remember them later."
When each object was shown, it was accompanied by a characteristic sound. For example, a tea kettle would appear with a whistling sound. During both states of wakefulness and sleep, some of the sounds were played alone, quite softly, essentially reminding participants of the low-value items.
Participants remembered the low-value associations better when the sound presentations occurred during sleep.
"We think that what’s happening during sleep is basically the reactivation of that information," Oudiette said. "We can provoke the reactivation by presenting those sounds, therefore energizing the low-value memories so they get stored better."
The research poses provocative implications about the role memory reactivation during sleep could play in improving memory storage,” said Paller, director of the Cognitive Neuroscience Program at Northwestern. “Whatever makes you rehearse during sleep is going to determine what you remember later, and conversely, what you’re going to forget.”
Many memories that are stored during the day are not remembered.
"We think one of the reasons for that is that we have to rehearse memories in order to keep them. When you practice and rehearse, you increase the likelihood of later remembering," Oudiette said. "And a lot of our rehearsal happens when we don’t even realize it — while we’re asleep."
Paller said selectivity of memory consolidation is not well understood. Most efforts in memory research have focused on what happens when you first form a memory and on what happens when you retrieve a memory.
"The in-between time is what we want to learn more about, because a fascinating aspect of memory storage is that it is not static," Paller said. "Memories in our brain are changing all of the time. Sometimes you improve memory storage by rehearsing all the details, so maybe later you remember better — or maybe worse if you’ve embellished too much.
"The fact that this critical memory reactivation transpires during sleep has mostly been hidden from us, from humanity, because we don’t realize so much of what’s happening while we’re asleep," he said.
(Source: eurekalert.org)
New learning and memory neurons uncovered
A University of Queensland study has identified precisely when new neurons become important for learning.
Lead researcher Dr Jana Vukovic from UQ’s Queensland Brain Institute (QBI) said the study highlighted the importance of new neuron development.
“New neurons are continually produced in the brain, passing through a number of developmental stages before becoming fully mature,” Dr Vukovic said.
“Using a genetic technique to delete immature neurons in animal models, we found they had great difficulty learning a new spatial task.
“There are ways to encourage the production of new neurons – including physical exercise – to improve learning.
“The new neurons appear particularly important for the brain to detect subtle but critical differences in the environment that can impact on the individual.”
The study, performed in QBI Director Professor Perry Bartlett’s laboratory, also demonstrates that immature neurons, born in a region of the brain known as the hippocampus, are required for learning but not for the retrieval of past memories.
“On the other hand, if the animals needed to remember a task they had already mastered in the past, before these immature neurons were deleted, their ability to perform the task was the same – so, they’ve remembered the task they learned earlier,” Dr Vukovic said.
This research allows for better understanding of the processes underlying learning and memory formation.
(Image Caption: Newly generated neurons doublecortin positive in the dentate gyrus of a degenerating hippocampus in mutant mice lacking the transcription factor TIF-IA. Credit: Rosanna Parlato (AG Schütz, DKFZ-ZMBH Alliance)
Sound stimulation during sleep can enhance memory
Slow oscillations in brain activity, which occur during so-called slow-wave sleep, are critical for retaining memories. Researchers reporting online April 11 in the Cell Press journal Neuron have found that playing sounds synchronized to the rhythm of the slow brain oscillations of people who are sleeping enhances these oscillations and boosts their memory. This demonstrates an easy and noninvasive way to influence human brain activity to improve sleep and enhance memory.
"The beauty lies in the simplicity to apply auditory stimulation at low intensities—an approach that is both practical and ethical, if compared for example with electrical stimulation—and therefore portrays a straightforward tool for clinical settings to enhance sleep rhythms," says coauthor Dr. Jan Born, of the University of Tübingen, in Germany.
Dr. Born and his colleagues conducted their tests on 11 individuals on different nights, during which they were exposed to sound stimulations or to sham stimulations. When the volunteers were exposed to stimulating sounds that were in sync with the brain’s slow oscillation rhythm, they were better able to remember word associations they had learned the evening before. Stimulation out of phase with the brain’s slow oscillation rhythm was ineffective.
"Importantly, the sound stimulation is effective only when the sounds occur in synchrony with the ongoing slow oscillation rhythm during deep sleep. We presented the acoustic stimuli whenever a slow oscillation "up state" was upcoming, and in this way we were able to strengthen the slow oscillation, showing higher amplitude and occurring for longer periods," explains Dr. Born.
The researchers suspect that this approach might also be used more generally to improve sleep. “Moreover, it might be even used to enhance other brain rhythms with obvious functional significance—like rhythms that occur during wakefulness and are involved in the regulation of attention,” says Dr. Born.
Brain Games are Bogus
A decade ago, a young Swedish researcher named Torkel Klingberg made a spectacular discovery. He gave a group of children computer games designed to boost their memory, and, after weeks of play, the kids showed improvements not only in memory but in overall intellectual ability. Spending hours memorizing strings of digits and patterns of circles on a four-by-four grid had made the children smarter. The finding countered decades of psychological research that suggested training in one area (e.g., recalling numbers) could not bring benefits in other, unrelated areas (e.g., reasoning). The Klingberg experiment also hinted that intelligence, which psychologists considered essentially fixed, might be more mutable: that it was less like eye color and more like a muscle.
It seemed like a breakthrough, offering new approaches to education and help for people with A.D.H.D., traumatic brain injuries, and other ailments. In the years since, other, similar experiments yielded positive results, and Klingberg helped found a company, Cogmed, to commercialize the software globally. (Pearson, the British publishing juggernaut, purchased it in 2010.) Brain training has become a multi-million-dollar business, with companies like Lumosity, Jungle Memory, and CogniFit offering their own versions of neuroscience-you-can-use, and providing ambitious parents with new assignments for overworked but otherwise healthy children. The brain-training concept has made Klingberg a star, and he now enjoys a seat on an assembly that helps select the winners of the Nobel Prize in Physiology or Medicine. The field has become a staple of popular writing. Last year, the New York Times Magazine published a glowing profile of the young guns of brain training called “CAN YOU MAKE YOURSELF SMARTER?”
The answer, however, now appears to be a pretty firm no—at least, not through brain training. A pair of scientists in Europe recently gathered all of the best research—twenty-three investigations of memory training by teams around the world—and employed a standard statistical technique (called meta-analysis) to settle this controversial issue. The conclusion: the games may yield improvements in the narrow task being trained, but this does not transfer to broader skills like the ability to read or do arithmetic, or to other measures of intelligence. Playing the games makes you better at the games, in other words, but not at anything anyone might care about in real life.
A “light switch” in the brain illuminates neural networks
Researchers from NTNU’s Kavli Institute of Systems Neuroscience are able to see which cells communicate with each other in the brain by flipping a neural light switch. The results of their efforts are presented in an article in the 5 April issue of Science magazine.
There are cells in your brain that recognize very specific places, and have that and nothing else as their job. These cells, called place cells, are found in an area behind your temple called the hippocampus. While these cells must be sent information from nearby cells to do their job, so far no one has been able to determine exactly what kind of cells work with place cells to craft the code they create for each location. Neurons come in many different types with specialized functions. Some respond to edges and borders, others to specific locations, others act like a compass and react to which way you turn your head.
Now, researchers at the Kavli Institute for Systems Neuroscience have developed a range of advanced techniques that enable them to identify which neurons communicate with each other at different times in the rat brain, and in doing so, create the animal’s sense of direction.
"A rat’s brain is the size of a grape. Inside there are about fifty million neurons that are connected together at a staggering 450 billion places (roughly)," explains Professor Edvard Moser, director of the Kavli Institute. "Inside this grape-sized brain are areas on each side that are smaller than a grape seed, where we know that memory and the sense of location reside. This is also where we find the neurons that respond to specific places, the place cells. But from which cells do these place cells get information?"
From spaghetti to light switches
The problem is, of course, that researchers cannot simply cut open the rat brain to see which cells have had contact. That would be the equivalent of taking a giant pile of cooked spaghetti, chopping it into little pieces, and then trying to figure out how the various spaghetti strands were tangled together before the pile was cut up.
A job like this requires the use of a completely different set of neural tools, which is where the “light switches” come into play.
Neurons share many similarities with electric cables when they send signals to each other. They send an electric current in one direction – from the “body” of the neuron and down a long arm, called the axon, which goes to another nerve cell next in line. Place cells thus get their small electric signals from a whole series of such arms.
So how do light switches play into all of this?
Viruses do the work
“What we did first was to give these nerve arms a harmless viral infection,” Moser says. “We designed a unique virus that does not cause disease, but that acts as a pathway for delivering genes to specific cells. The virus creeps into the neurons, crawls up against the electric current, and uses the nerve cell’s own factory to make the genetic recipe that we gave to the virus to carry.”
The genetic recipe enabled the cell to make the equivalent of a light switch. Our eyes actually contain the same kind of biological light switch, which allows us to see. The virus infection converts neurons that have previously existed only in darkness, deep inside the brain, to now be sensitive to light.
Then the researchers inserted optical fibres in the rat’s brain to transmit light to the place cells that had light switches in them. They also implanted thin microelectrodes down between the cells so they could detect the signals sent through the axons every time the light from the optical fibre was turned on.
"Now we had everything set up, with light switches installed in cells around the place cells, a lamp, and a way to record the activity," Moser said.
10,000 times
The researchers then turned the lights on and off more than ten thousand times in their rat lab partners, while they monitored and recorded the activity of hundreds of individual cells in the rats’ grape-sized brains. The researchers did this research while the rats ran around in a metre-square box, gathering treats. As the rats explored their box and found the treats, the researchers were able to use the light-sensitive cells to reveal how the rat’s brain created the map of where the rat had been.
When the researchers put together all the information afterwards they concluded that there is a whole range of different specialized cells that together provide place cells their information. The brain’s GPS – its sense of place – is created by signals from head direction cells, border cells, cells that have no known function in creating location points and grid cells. Place cells receive both information about the rat’s surroundings and landmarks, but also continuously update their own movement, which is actually independent on sensory input.
"The biggest mystery is the role that the cells that are not part of the sense of direction play. They send signals to place cells, but what do they actually do?" wonders Moser.
"We also wonder how the cells in the hippocampus are able to sort out the various signals they receive. Do they ‘listen’ to all of the cells equally effectively all the time, or are there some cells that get more time than others to ‘talk’ to place cells?"
Risk prediction tools that estimate future risk of heart disease and stroke may be more useful predictors of future decline in cognitive abilities, or memory and thinking, than a dementia risk test, according to a new study published in the April 2, 2013, print issue of Neurology®, the medical journal of the American Academy of Neurology.
“This is the first study that compares these risk scores with a dementia risk score to study decline in cognitive abilities 10 years later,” said Sara Kaffashian, PhD, with the French National Institute of Health and Medical Research (INSERM) in Paris, France.
The study involved 7,830 men and women with an average age of 55. Risk of heart disease and stroke (cardiovascular disease) and risk of dementia were calculated for each participant at the beginning of the study. The heart disease risk score included the following risk factors: age, blood pressure, treatment for high blood pressure, high density lipoprotein (HDL) cholesterol, total cholesterol, smoking, and diabetes. The stroke risk score included age, blood pressure, treatment for high blood pressure, diabetes, smoking, history of heart disease, and presence of cardiac arrhythmia (irregular heart beat).
The dementia risk score included age, education, blood pressure, body mass index (BMI), total cholesterol, exercise, and whether a person had the APOE ?4 gene, a gene associated with dementia.
Memory and thinking abilities were measured three times over 10 years.
The study found that all three risk scores predicted 10-year decline in multiple cognitive tests. However, heart disease risk scores showed stronger links with cognitive decline than a dementia risk score. Both heart and stroke risk were associated with decline in all cognitive tests except memory; dementia risk was not linked with decline in memory and verbal fluency.
“Although the dementia and cardiovascular risk scores all predict cognitive decline starting in late middle age, cardiovascular risk scores may have an advantage over the dementia risk score for use in prevention and for targeting changeable risk factors since they are already used by many physicians. The findings also emphasize the importance of risk factors for cardiovascular disease such as high cholesterol and high blood pressure in not only increasing risk of heart disease and stroke but also having a negative impact on cognitive abilities,” said Kaffashian.
Scientists have identified a key molecule responsible for triggering the chemical processes in our brain linked to our formation of memories. The findings, published in the journal Frontiers in Neural Circuits, reveal a new target for therapeutic interventions to reverse the devastating effects of memory loss.

The BBSRC-funded research, led by scientists at the University of Bristol, aimed to better understand the mechanisms that enable us to form memories by studying the molecular changes in the hippocampus — the part of the brain involved in learning.
Previous studies have shown that our ability to learn and form memories is due to an increase in synaptic communication called Long Term Potentiation [LTP]. This communication is initiated through a chemical process triggered by calcium entering brain cells and activating a key enzyme called ‘Ca2+ responsive kinase’ [CaMKII]. Once this protein is activated by calcium it triggers a switch in its own activity enabling it to remain active even after the calcium has gone. This special ability of CaMKII to maintain its own activity has been termed ‘the molecular memory switch’.
Until now, the question still remained as to what triggers this chemical process in our brain that allows us to learn and form long-term memories. The research team, comprising scientists from the University’s School of Physiology and Pharmacology, conducted experiments using the common fruit fly [Drosophila] to analyse and identify the molecular mechanisms behind this switch. Using advanced molecular genetic techniques that allowed them to temporarily inhibit the flies’ memory the team were able to identify a gene called CASK as the synaptic molecule regulating this ‘memory switch’.
Dr James Hodge, the study’s lead author, said: “Fruit flies are remarkably compatible for this type of study as they possess similar neuronal function and neural responses to humans. Although small they are very smart, for instance, they can land on the ceiling and detect that the fruit in your fruit bowl has gone off before you can.”
“In experiments whereby we tested the flies’ learning and memory ability, involving two odours presented to the flies with one associated with a mild shock, we found that around 90 per cent were able to learn the correct choice remembering to avoid the odour associated with the shock. Five lessons of the odour with punishment made the fly remember to avoid that odour for between 24 hours and a week, which is a long time for an insect that only lives a couple of months.“
By localising the function of the key molecules CASK and CaMKII to the flies’ equivalent brain area to the human hippocampus, the team found that the flies lacking these genes showed disrupted memory formation. In repeat memory tests those lacking these key genes were shown to have no ability to remember at three hours (mid-term memory) and 24 hours (long-term memory) although their initial learning or short-term memory wasn’t affected.
Finally, the team introduced a copy of the human CASK gene — it is 80 per cent identical to the fly CASK gene — into the genome of a fly that completely lacked its own CASK gene and was therefore not usually able to remember. The researchers found that flies which had a copy of the human CASK gene could remember like a normal wildtype fly.
Dr Hodge, from the University’s School of Physiology and Pharmacology, said: “Research into memory is particularly important as it gives us our sense of identity, and deficits in learning and memory occur in many diseases, injuries and during aging”.
“CASK’s control of CaMKII ‘molecular memory switch’ is clearly a critical step in how memories are written into neurons in the brain. These findings not only pave the way for to developing new therapies which reverse the effects of memory loss but also prove the compatibility of Drosophila to model these diseases in the lab and screen for new drugs to treat these diseases. Furthermore, this work provides an important insight into how brains have evolved their huge capacity to acquire and store information.”
These findings clearly demonstrate that neuronal function of CASK is conserved between flies and human, validating the use of Drosophila to understand CASK function in both the healthy and diseased brain. Mutations in human CASK gene have been associated with neurological and cognitive defects including severe learning difficulties.
(Source: bristol.ac.uk)

Pesticide combination affects bees’ ability to learn
Two new studies have highlighted a negative impact on bees’ ability to learn following exposure to a combination of pesticides commonly used in agriculture. The researchers found that the pesticides, used in the research at levels shown to occur in the wild, could interfere with the learning circuits in the bee’s brain. They also found that bees exposed to combined pesticides were slower to learn or completely forgot important associations between floral scent and food rewards.
In the study published today (27 March 2013) in Nature Communications, the University of Dundee’s Dr Christopher Connolly and his team investigated the impact on bees’ brains of two common pesticides: pesticides used on crops called neonicotinoid pesticides, and another type of pesticide, coumaphos, that is used in honeybee hives to kill the Varroa mite, a parasitic mite that attacks the honey bee.
The intact bees’ brains were exposed to pesticides in the lab at levels predicted to occur following exposure in the wild and brain activity was recorded. They found that both types of pesticide target the same area of the bee brain involved in learning, causing a loss of function. If both pesticides were used in combination, the effect was greater.
The study is the first to show that these pesticides have a direct impact on pollinator brain physiology. It was prompted by the work of collaborators Dr Geraldine Wright and Dr Sally Williamson at Newcastle University who found that combinations of these same pesticides affected learning and memory in bees. Their studies established that when bees had been exposed to combinations of these pesticides for 4 days, as many as 30% of honeybees failed to learn or performed poorly in memory tests. Again, the experiments mimicked levels that could be seen in the wild, this time by feeding a sugar solution mixed with appropriate levels of pesticides.
Dr Geraldine Wright said: “Pollinators perform sophisticated behaviours while foraging that require them to learn and remember floral traits associated with food. Disruption in this important function has profound implications for honeybee colony survival, because bees that cannot learn will not be able to find food.”
Together the researchers expressed concerns about the use of pesticides that target the same area of the brain of insects and the potential risk of toxicity to non-target insects. Moreover, they said that exposure to different combinations of pesticides that act at this site may increase this risk.
Dr Christopher Connolly said: “Much discussion of the risks posed by the neonicotinoid insecticides has raised important questions of their suitability for use in our environment. However, little consideration has been given to the miticidal pesticides introduced directly into honeybee hives to protect the bees from the Varroa mite. We find that both have negative impact on honeybee brain function.
"Together, these studies highlight potential dangers to pollinators of continued exposure to pesticides that target the insect nervous system and the importance of identifying combinations of pesticides that could profoundly impact pollinator survival."

The memories of near death experiences (NDE): more real than reality?
University of Liège researchers have demonstrated that the physiological mechanisms triggered during NDE lead to a more vivid perception not only of imagined events in the history of an individual but also of real events which have taken place in their lives! These surprising results – obtained using an original method which now requires further investigation – are published in PLOS ONE.
Seeing a bright light, going through a tunnel, having the feeling of ending up in another ‘reality’ or leaving one’s own body are very well known features of the complex phenomena known as ‘Near-Death Experiences ‘ (NDE), which people who are close to death can experience in particular. Products of the mind? Psychological defence mechanisms? Hallucinations? These phenomena have been widely documented in the media and have generated numerous beliefs and theories of every kind. From a scientific point of view, these experiences are all the more difficult to understand in that they come into being in chaotic conditions, which make studying them in real time almost impossible. The University of Liège’s researchers have thus tried a different approach.
Working together, researchers at the Coma Science Group (Directed by Steven Laureys) and the University of Liège’s Cognitive Psychology Research (Professor Serge Brédart and Hedwige Dehon), have looked into the memories of NDE with the hypothesis that if the memories of NDE were pure products of the imagination, their phenomenological characteristics (e.g., sensorial, self referential, emotional, etc. details) should be closer to those of imagined memories. Conversely, if the NDE are experienced in a way similar to that of reality, their characteristics would be closer to the memories of real events.
The researchers compared the responses provided by three groups of patients, each of which had survived (in a different manner) a coma, and a group of healthy volunteers. They studied the memories of NDE and the memories of real events and imagined events with the help of a questionnaire which evaluated the phenomenological characteristics of the memories. The results were surprising. From the perspective being studied, not only were the NDEs not similar to the memories of imagined events, but the phenomenological characteristics inherent to the memories of real events (e.g. memories of sensorial details) are even more numerous in the memories of NDE than in the memories of real events.
The brain, in conditions conducive to such phenomena occurring, is prey to chaos. Physiological and pharmacological mechanisms are completely disturbed, exacerbated or, conversely, diminished. Certain studies have put forward a physiological explanation for certain components of NDE, such as Out-of-Body Experiences, which could be explained by dysfunctions of the temporo-parietal lobe. In this context the study published in PLOS ONE suggests that these same mechanisms could also ‘create’ a perception – which would thus be processed by the individual as coming from the exterior – of reality. In a kind of way their brain is lying to them, like in a hallucination. These events being particularly surprising and especially important from an emotional and personal perspective, the conditions are ripe for the memory of this event being extremely detailed, precise and durable.
Numerous studies have looked into the physiological mechanisms of NDE, the production of these phenomena by the brain, but, taken separately, these two theories are incapable of explaining these experiences in their entirety. The study published in PLOS ONE does not claim to offer a unique explanation for NDE, but it contributes to study pathways which take into account psychological phenomena as factors associated with, and not contradictory to, physiological phenomena.