Posts tagged learning
Articles and news from the latest research reports.
Scientists learn more about how inhibitory brain cells get excited
Scientists have found an early step in how the brain’s inhibitory cells get excited. A natural balance of excitement and inhibition keeps the brain from firing electrical impulses randomly and excessively, resulting in problems such as schizophrenia and seizures. However excitement is required to put on the brakes.
“When the inhibitory neuron is excited, its job is to suppress whatever activity it touches,” said Dr. Lin Mei, Director of the Institute of Molecular Medicine and Genetics at the Medical College of Georgia at Georgia Regents University and corresponding author of the study in Nature Neuroscience.
Mei and his colleagues found that the protein erbin, crucial to brain development, is critical to the excitement.
Research Institute Study Shows How Brain Cells Shape Temperature Preferences
While the wooly musk ox may like it cold, fruit flies definitely do not. They like it hot, or at least warm. In fact, their preferred optimum temperature is very similar to that of humans—76 degrees F.
Scientists have known that a type of brain cell circuit helps regulate a variety of innate and learned behavior in animals, including their temperature preferences. What has been a mystery is whether or not this behavior stems from a specific set of neurons (brain cells) or overlapping sets.
Now, a new study from The Scripps Research Institute (TSRI) shows that a complex set of overlapping neuronal circuits work in concert to drive temperature preferences in the fruit fly Drosophila by affecting a single target, a heavy bundle of neurons within the fly brain known as the mushroom body. These nerve bundles, which get their name from their bulbous shape, play critical roles in learning and memory.
The study, published in the January 30, 2013 edition of the Journal of Neuroscience, shows that dopaminergic circuits—brain cells that synthesize dopamine, a common neurotransmitter—within the mushroom body do not encode a single signal, but rather perform a more complex computation of environmental conditions.
“We found that dopamine neurons process multiple inputs to generate multiple outputs—the same set of nerves process sensory information and reward-avoidance learning,” said TSRI Assistant Professor Seth Tomchik. “This discovery helps lay the groundwork to better understand how information is processed in the brain. A similar set of neurons is involved in behavior preferences in humans—from basic rewards to more complex learning and memory.”
Using imaging techniques that allow scientists to visualize neuron activity in real time, the study illuminated the response of dopaminergic neurons to changes in temperature. The behavioral roles were then examined by silencing various subsets of these neurons. Flies were tested using a temperature gradient plate; the flies moved from one place to another to express their temperature preferences.
As it turns out, genetic silencing of dopaminergic neurons innervating the mushroom body substantially reduces cold avoidance behavior. “If you give the fly a choice, it will pick San Diego weather every time,” Tomchik said, “but if you shut down those nerves, they suddenly don’t mind being in Minnesota.”
The study also showed dopaminergic neurons respond to cooling with sudden a burst of activity at the onset of a drop in temperature, before settling down to a lower steady-state level. This initial burst of dopamine could function to increase neuronal plasticity—the ability to adapt—during periods of environmental change when the organism needs to acquire new associative memories or update previous associations with temperature changes.
(Image: ALAMY)
Learning and Memory May Play a Central Role in Synesthesia
People with color-grapheme synesthesia experience color when viewing written letters or numerals, usually with a particular color evoked by each grapheme (i.e., the letter ‘A’ evokes the color red). In a new study, researchers Nathan Witthoft and Jonathan Winawer of Stanford University present data from 11 color grapheme synesthetes who had startlingly similar color-letter pairings that were traceable to childhood toys containing magnetic colored letters.
Their findings are published in Psychological Science, a journal of the Association for Psychological Science.
Matching data from the 11 participants showed reliably consistent letter-color matches, both within and between testing sessions (data collected online at http://www.synesthete.org/). Participants’ matches were consistent even after a delay of up to seven years since their first session.
Participants also performed a timed task, in which they were presented with colored letters for 1 second each and required to indicate whether the color was consistent with their synesthetic association. Their data show that they were able to perform the task rapidly and accurately.
Together, these data suggest that the participants’ color-letter associations are specific, automatic, and relatively constant over time, thereby meeting the criteria for true synesthesia.
The degree of similarity in the letter-color pairings across participants, along with the regular repeating pattern in the colors found in each individual’s letter-color pairings, indicates that the pairings were learned from the magnetic colored letters that the participants had been exposed to in childhood.
According to the researchers, these are the first and only data to show learned synesthesia of this kind in more than a single individual.
They point out that this does not mean that exposure to the colored letter magnets was sufficient to induce synesthesia in the participants, though it may have increased the chances. After all, many people who do not have synesthesia played with the same colored letter magnets as kids.
Based on their findings, Witthoft and Winawer conclude that a complete explanation of synesthesia must incorporate a central role for learning and memory.
(Image: Shutterstock)
The Connection Between Memory and Sleep
Researchers found information can be better retained with reinforcing stimuli delivered during sleep
When you’re studying for an exam, is there something you can do while you sleep to retain the information better?
"The question is, ‘What determines which information is going to be kept and which information is lost?’" says neuroscientist Ken Paller.
With support from the National Science Foundation (NSF), Paller and his team at Northwestern University are studying the connection between memory and sleep, and the possibilities of boosting memory storage while you snooze.
"We think many stages of sleep are important for memory. However, a lot of the evidence has shown that slow-wave sleep is particularly important for some types of memory," explains Paller.
Slow-wave sleep is often referred to as “deep sleep,” and consists of stages 3 and 4 of non-rapid-eye-movement sleep.
Paller’s lab group members demonstrated for Science Nation two of the tests they run on study participants. In the first experiment, the subjects learned two pieces of music in a format similar to the game Guitar Hero. During a short nap following learning, just one of the learned tunes was played softly several times, to selectively reinforce the memory for playing that tune without any reinforcement but not for the other tune. Paller wanted to know whether the test subjects could more accurately produce the tune played during sleep.
In the second exercise, the subjects were asked to memorize the location of 50 objects on a computer screen. The presentation of each object was coupled with a unique sound. During the post-learning nap, memory for the location of 25 objects was reinforced by the play-back of only 25 of the sounds. In this case, Paller wanted to know whether the subjects could remember object locations better if the associated sounds were played during sleep.
Researchers recorded electrical activity generated in the brain using EEG electrodes attached to the scalp. They thus determined whether the subjects entered “deep sleep,” and only those who did participated in the reinforcement experiments. In both experiments, participants did a better job remembering what was reinforced while they slept, compared to what was not reinforced.
"We think that memory processing happens during sleep every night," says Paller. "We’re at the beginning of finding out what types of memory can be reinforced, how large reinforcement effects can be, and what sorts of stimuli can be used to reactivate memories so that they can be better consolidated."
Paller’s goal is to better understand the fundamental brain mechanisms responsible for memory. And that, in turn, may help people with memory problems, including those who find themselves more forgetful as they age.
"We experience progressively less slow-wave sleep as we age. Of course, many brain mechanisms come into play to allow us to remember, including some processing that transpires during sleep. So, there’s a lot to figure out about how memory works, but I think it’s fair to say that the person you are when you’re awake is partly a function of what your brain does when you’re asleep," explains Paller. He says these reactivation techniques could turn out to be valuable for enhancing what people have learned.
"What is beautiful about this set of experiments is that Dr. Paller identified ‘deep sleep’ as a critical time window during which memory for specific experiences can be selectively enhanced by the method of reactivation without conscious effort," says Akaysha Tang, director of the cognitive neuroscience program in the NSF Directorate for Social, Behavioral and Economic Sciences.
"Normally, conscious rehearsal of memorized material is needed if one wants to remember something better or retain it for longer, and one has to find time to review or rehearse," continues Tang. "Dr. Paller and the members of his lab group showed that such selective enhancement could be achieved without conscious effort and without demanding more of one’s waking hours. So, instead of pulling that all-nighter to memorize the material, in the future, it may be possible to consolidate the memory by sleeping with a scientifically programmed lullaby!"
(Source: nsf.gov)
How The Memory Works In Learning
Teachers are the caretakers of the development of students’ highest brain during the years of its most extensive changes. As such, they have the privilege and opportunity to influence the quality and quantity of neuronal and connective pathways so all children leave school with their brains optimized for future success.
This introduction to the basics of the neuroscience of learning includes information that should be included in all teacher education programs. It is intentionally brief such that it can be taught in a single day of instruction. Ideally there would be additional opportunities for future teachers to pursue further inquiry into the science of how the brain learns, retrieves, and applies information.
Eliminating useless information important to learning, making new memories
As we age, it just may be the ability to filter and eliminate old information – rather than take in the new stuff – that makes it harder to learn, scientists report.
“When you are young, your brain is able to strengthen certain connections and weaken certain connections to make new memories,” said Dr. Joe Z. Tsien, neuroscientist at the Medical College of Georgia at Georgia Regents University and Co-Director of the GRU Brain & Behavior Discovery Institute.
It’s that critical weakening that appears hampered in the older brain, according to a study in the journal Scientific Reports.
The NMDA receptor in the brain’s hippocampus is like a switch for regulating learning and memory, working through subunits called NR2A and NR2B. NR2B is expressed in higher percentages in children, enabling neurons to talk a fraction of a second longer; make stronger bonds, called synapses; and optimize learning and memory. This formation of strong bonds is called long-term potentiation. The ratio shifts after puberty, so there is more NR2A and slightly reduced communication time between neurons.
When Tsien and his colleagues genetically modified mice that mimic the adult ratio – more NR2A, less NR2B – they were surprised to find the rodents were still good at making strong connections and short-term memories but had an impaired ability to weaken existing connections, called long-term depression, and to make new long-term memories as a result. It’s called information sculpting and adult ratios of NMDA receptor subunits don’t appear to be very good at it.
“If you only make synapses stronger and never get rid of the noise or less useful information then it’s a problem,” said Tsien, the study’s corresponding author. While each neuron averages 3,000 synapses, the relentless onslaught of information and experiences necessitates some selective whittling. Insufficient sculpting, at least in their mouse, meant a reduced ability to remember things short-term – like the ticket number at a fast-food restaurant – and long-term – like remembering a favorite menu item at that restaurant. Both are impacted in Alzheimer’s and age-related dementia.
All long-term depression was not lost in the mice, rather just response to the specific electrical stimulation levels that should induce weakening of the synapse. Tsien expected to find the opposite: that long-term potentiation was weak and so was the ability to learn and make new memories. “What is abnormal is the ability to weaken existing connectivity.”
Acknowledging the leap, this impaired ability could also help explain why adults can’t learn a new language without their old accent and why older people tend to be more stuck in their ways, the memory researcher said.
“We know we lose the ability to perfectly speak a foreign language if we learn than language after the onset of sexual maturity. I can learn English but my Chinese accent is very difficult to get rid of. The question is why,” Tsien said.
Tsien and his colleagues already have learned what happens when NR2B is overexpressed. He and East China Normal University researchers announced in 2009 the development of Hobbie-J, a smarter than average rat. A decade earlier, Tsien reported in the journal Nature the development of a smart mouse dubbed Doogie using the same techniques to over-express the NR2B gene in the hippocampus.
Doogie, Hobbie-J and their descendants have maintained superior memory as they age. Now Tsien is interested in following the NR2A over-expressing mouse to see what happens.
(Source: news.georgiahealth.edu)
Newly found ‘volume control’ in the brain promotes learning, memory
Scientists have long wondered how nerve cell activity in the brain’s hippocampus, the epicenter for learning and memory, is controlled — too much synaptic communication between neurons can trigger a seizure, and too little impairs information processing, promoting neurodegeneration. Researchers at Georgetown University Medical Center say they now have an answer. In the January 10 issue of Neuron, they report that synapses that link two different groups of nerve cells in the hippocampus serve as a kind of “volume control,” keeping neuronal activity throughout that region at a steady, optimal level.
"Think of these special synapses like the fingers of God and man touching in Michelangelo’s famous fresco in the Sistine Chapel," says the study’s senior investigator, Daniel Pak, PhD, an associate professor of pharmacology. "Now substitute the figures for two different groups of neurons that need to perform smoothly. The touching of the fingers, or synapses, controls activity levels of neurons within the hippocampus."
The hippocampus is a processing unit that receives input from the cortex and consolidates that information in terms of learning and memory. Neurons known as granule cells, located in the hippocampus’ dentate gyrus, receive transmissions from the cortex. Those granule cells then pass that information to the other set of neurons (those in the CA3 region of the hippocampus, in this study) via the synaptic fingers.
Those fingers dial up, or dial down, the volume of neurotransmission from the granule cells to the CA3 region to keep neurotransmission in the learning and memory areas of the hippocampus at an optimal flow — a concept known as homeostatic plasticity. “If granule cells try to transmit too much activity, we found, the synaptic junction tamps down the volume of transmission by weakening their connections, allowing the proper amount of information to travel to CA3 neurons,” says Pak. “If there is not enough activity being transmitted by the granule cells, the synapses become stronger, pumping up the volume to CA3 so that information flow remains constant.”
There are many such touching fingers in the hippocampus, connecting the so-called “mossy fibers” of the granule cells to neurons in the CA3 region. But importantly, not every one of the billions of neurons in the hippocampus needs to set its own level of transmission from one nerve cell to the other, says Pak.
To explain, he uses another analogy. “It had previously been thought that neurons act separately like cars, each working to keep their speed at a constant level even though signal traffic may be fast or slow. But we wondered how these neurons could process learning and memory information efficiently, while also regulating the speed by which they process and communicate that information.
"We believe, based on our study, that only the mossy fiber synapses on the CA3 neurons control the level of activity for the hippocampus — they are like the engine on a train that sets the speed for all the other cars, or neurons, attached to it," Pak says. "That frees up the other neurons to do the job they are tasked with doing — processing and encoding information in the forms of learning and memory."
Not only does the study offer a new model for how homeostatic plasticity in the hippocampus can co-exist with learning and memory, it also suggests a new therapeutic avenue to help patients with uncontrollable seizures, he says.
"The CA3 region is highly susceptible to seizures, so if we understand how homeostasis is maintained in these neurons, we could potentially manipulate the system. When there is an excessive level of CA3 neuronal activity in a patient, we could learn how to therapeutically turn it down."
(Source: eurekalert.org)
Newborn memories of the “oohs” and “ahs” heard in the womb
Newborns are much more attuned to the sounds of their native language than first thought. In fact, these linguistic whizzes can up pick on distinctive sounds of their mother tongue while in utero, a new study has concluded.
Research led by Christine Moon, a professor of psychology at Pacific Lutheran University, shows that infants, only hours old showed marked interest for the vowels of a language that was not their mother tongue.
"We have known for over 30 years that we begin learning prenatally about voices by listening to the sound of our mother talking," Moon said. "This is the first study that shows we learn about the particular speech sounds of our mother’s language before we are born."
Before the study, the general consensus was that infants learned about the small parts of speech, the vowels and the consonants, postnatally. Moon added. “This study moves the measurable result of experience with individual speech sounds from six months of age to before birth,” she said. The findings were published in Acta Paediatrica.
The Role of Medial Prefrontal Cortex in Memory and Decision Making
Some have claimed that the medial prefrontal cortex (mPFC) mediates decision making. Others suggest mPFC is selectively involved in the retrieval of remote long-term memory. Yet others suggests mPFC supports memory and consolidation on time scales ranging from seconds to days. How can all these roles be reconciled? We propose that the function of the mPFC is to learn associations between context, locations, events, and corresponding adaptive responses, particularly emotional responses. Thus, the ubiquitous involvement of mPFC in both memory and decision making may be due to the fact that almost all such tasks entail the ability to recall the best action or emotional response to specific events in a particular place and time. An interaction between multiple memory systems may explain the changing importance of mPFC to different types of memories over time. In particular, mPFC likely relies on the hippocampus to support rapid learning and memory consolidation.
Many causes for learning lags in tumor disorder
The causes of learning problems associated with an inherited brain tumor disorder are much more complex than scientists had anticipated, researchers at Washington University School of Medicine in St. Louis report.
The disorder, neurofibromatosis 1 (NF1), is among the most common inherited pediatric brain cancer syndromes. Children born with NF1 can develop low-grade brain tumors, but their most common problems are learning and attention difficulties.
“While one of our top priorities is halting tumor growth, it’s also important to ensure that these children don’t have the added challenges of living with learning and behavioral problems,” says senior author David H. Gutmann, MD, PhD, the Donald O. Schnuck Family Professor of Neurology. “Our results suggest that learning problems in these patients can be caused by more than one factor. Successful treatment depends on identifying the biological reasons underlying the problems seen in individual patients with NF1.”
The study appears online in Annals of Neurology.
According to Gutmann, who is director of the Washington University Neurofibromatosis Center, scientists are divided when considering the basis for NF1-associated learning abnormalities and attention deficits.
Mutations in the Nf1 gene can disrupt normal regulation of an important protein called RAS in the hippocampus, a brain region critical for learning. Initial work from other investigators had shown that increased RAS activity due to defective Nf1 gene function impairs memory and attention in some Nf1 mouse models.
However, earlier studies by Gutmann and collaborator David F. Wozniak, PhD, research professor in psychiatry, showed that a mutation in the Nf1 gene lowers levels of dopamine, a neurotransmitter involved in attention. In this Nf1 mouse model, Gutmann and his colleagues found that the branches of dopamine-producing nerve cells were unusually short, limiting their ability to make and distribute dopamine and leading to reduced attention in those mice.
The new research suggests that both sides may be right.
In the latest study, postdoctoral fellow Kelly Diggs-Andrews, PhD, found that the branches of dopamine-producing nerve cells that normally extend into the hippocampus are shorter in Nf1 mice. As a result, dopamine levels are lower in that part of the brain.
Charles F. Zorumski, MD, the Samuel B. Guze Professor and head of the Department of Psychiatry, showed that the low dopamine levels disrupts the ability of nerve cells in the hippocampus to modulate the way they communicate with each other. These communication adjustments are a primary way the brain creates memories.
Researchers then found that giving Nf1 mice L-DOPA, which increases dopamine levels, restored their nerve cell branch lengths to normal and corrected the hippocampal communication defect. L-DOPA also eliminated the memory and learning deficits in these mice.
“These results and the earlier findings suggest that there are a variety of ways that NF1 may cause cognitive dysfunction in people,” Gutmann says. “Some may have problems caused only by increased RAS function, others may be having problems attributable to reduced dopamine, and a third group may be having difficulties caused by both RAS and dopamine abnormalities.”
To customize patient therapy, Gutmann and his colleagues are now working to develop ways to quantify the contributions of dopamine and RAS to NF1-related learning disorders.
(Source: news.wustl.edu)