Posts tagged neuroscience
Articles and news from the latest research reports.
Chimpanzees successfully play the Ultimatum Game
Researchers at the Yerkes National Primate Research Center, Emory University, are the first to show chimpanzees possess a sense of fairness that has previously been attributed as uniquely human. Working with colleagues from Georgia State University, the researchers played the Ultimatum Game with the chimpanzees to determine how sensitive the animals are to the reward distribution between two individuals if both need to agree on the outcome.
The researchers say the findings, available in an early online edition of the Proceedings of the National Academy of Sciences (PNAS) available this week, suggest a long evolutionary history of the human aversion to inequity as well as a shared preference for fair outcomes by the common ancestor of humans and apes.
According to first author Darby Proctor, PhD, “We used the Ultimatum Game because it is the gold standard to determine the human sense of fairness. In the game, one individual needs to propose a reward division to another individual and then have that individual accept the proposition before both can obtain the rewards. Humans typically offer generous portions, such as 50 percent of the reward, to their partners, and that’s exactly what we recorded in our study with chimpanzees.”
Co-author Frans de Waal, PhD, adds, “Until our study, the behavioral economics community assumed the Ultimatum Game could not be played with animals or that animals would choose only the most selfish option while playing. We’ve concluded that chimpanzees not only get very close to the human sense of fairness, but the animals may actually have exactly the same preferences as our own species.” For purposes of direct comparison, the study was also conducted separately with human children.
In the study, researchers tested six adult chimpanzees (Pan troglodytes) and 20 human children (ages 2 – 7 years) on a modified Ultimatum Game. One individual chose between two differently colored tokens that, with his or her partner’s cooperation, could be exchanged for rewards (small food rewards for chimpanzees and stickers for children). One token offered equal rewards to both players, whereas the other token favored the individual making the choice at the expense of his or her partner. The chooser then needed to hand the token to the partner, who needed to exchange it with the experimenter for food. This way, both individuals needed to be in agreement.
Both the chimpanzees and the children responded like adult humans typically do. If the partner’s cooperation was required, the chimpanzees and children split the rewards equally. However, with a passive partner, who had no chance to reject the offer, chimpanzees and children chose the selfish option.
Chimpanzees, who are highly cooperative in the wild, likely need to be sensitive to reward distributions in order to reap the benefits of cooperation. Thus, this study opens the door for further explorations into the mechanisms behind this human-like behavior.
Parkinson’s Treatment Can Trigger Creativity
Parkinson’s experts across the world have been reporting a remarkable phenomenon — many patients treated with drugs to increase the activity of dopamine in the brain as a therapy for motor symptoms such as tremors and muscle rigidity are developing new creative talents, including painting, sculpting, writing, and more.
Prof. Rivka Inzelberg of Tel Aviv University’s Sackler Faculty of Medicinefirst noticed the trend in her own Sheba Medical Center clinic when the usual holiday presents from patients — typically chocolates or similar gifts — took a surprising turn. “Instead, patients starting bringing us art they had made themselves,” she says.
Inspired by the discovery, Prof. Inzelberg sought out evidence of this rise in creativity in current medical literature. Bringing together case studies from around the world, she examined the details of each patient to uncover a common underlying factor — all were being treated with either synthetic precursors of dopamine or dopamine receptor agonists, which increase the amount of dopamine activity in the brain by stimulating receptors. Her report published in the journal Behavioral Neuroscience.
Giving in to artistic impulse
Dopamine is involved in several neurological systems, explains Prof. Inzelberg. Its main purpose is to aid in the transmission of motor commands, which is why a lack of dopamine in Parkinson’s patients is associated with tremors and a difficulty in coordinating their movements.
But it’s also involved in the brain’s “reward system” — the satisfaction or happiness we experience from an accomplishment. This is the system which Prof. Inzelberg predicts is associated with increasing creativity. Dopamine and artistry have long been connected, she points out, citing the example of the Vincent Van Gogh, who suffered from psychosis. It’s possible that his creativity was the result of this psychosis, thought to be caused by a spontaneous spiking of dopamine levels in the brain.
There are seemingly no limits to the types of artistic work for which patients develop talents, observes Prof. Inzelberg. Cases include an architect who began to draw and paint human figures after treatment, and a patient who, after treatment, became a prize-winning poet though he had never been involved in the arts before.
It’s possible that these patients are expressing latent talents they never had the courage to demonstrate before, she suggests. Dopamine-inducing therapies are also connected to a loss of impulse control, and sometimes result in behaviors like excessive gambling or obsessional hobbies. An increase in artistic drive could be linked to this lowering of inhibitions, allowing patients to embrace their creativity. Some patients have even reported a connection between their artistic sensibilities and medication dose, noting that they feel they can create more freely when the dose is higher.
Therapeutic value
Prof. Inzelberg believes that such artistic expressions have promising therapeutic potential, both psychologically and physiologically. Her patients report being happier when they are busy with their art, and have noted that motor handicaps can lessen significantly. One such patient is usually wheelchair-bound or dependent on a walker, but creates intricate wooden sculptures that have been displayed in galleries. External stimuli can sometimes bypass motor issues and foster normal movement, she explains. Similar types of art therapy are already used for dementia and stroke patients to help mitigate the loss of verbal communication skills, for example.
The next step is to try to characterize those patients who become more creative through treatment through comparing them to patients who do not experience a growth in artistic output. “We want to screen patients under treatment for creativity and impulsivity to see if we can identify what is unique in those who do become more creative,” says Prof. Inzelberg. She also believes that such research could provide valuable insights into creativity in healthy populations, too.
Protein identified that can disrupt embryonic brain development and neuron migration
Interneurons – nerve cells that function as ‘dimmers’ – play an important role in the brain. Their formation and migration to the cerebral cortex during the embryonic stage of development is crucial to normal brain functioning. Abnormal interneuron development and migration can eventually lead to a range of disorders and diseases, from epilepsy to Alzheimer’s. New research by Dr. Eve Seuntjens and Dr. Veronique van den Berghe of the Department of Development and Regeneration (Danny Huylebroeck laboratory, Faculty of Medicine) has identified two proteins, Sip1 and Unc5b, that play an important role in the development and migration of interneurons to the cerebral cortex – a breakthrough in our understanding of early brain development.
Two types of nerve cells are crucial to healthy brain functioning. Projection neurons, the more widely known of the two, make connections between different areas of the brain. Interneurons, a second type, work as dimmers that regulate the signalling processes of projection neurons. A shortage or irregular functioning of interneurons can cause short circuits in the nervous system. This can lead to seizures, a common symptom of many brain disorders. Interneuron dysfunction even appears to play a role in schizophrenia, autism and neurodegenerative diseases such as Alzheimer’s, Parkinson’s and ALS.
Trailblazers
Researchers have only recently understood how different kinds of neuron are formed during embryonic development. During early brain development, stem cells form projection neurons in the cerebral cortex. Interneurons are made elsewhere in the brain. These interneurons then migrate to the cortex to mix with the projection neurons. Dr. Eve Seuntjens of the Celgen laboratory led by Professor Danny Huylebroeck explains: “The journey of interneurons is very complex: their environment changes constantly during growth and there are no existing structures — such as nerve pathways — available for them to follow.”
The question is how young interneurons receive their ‘directions’ to the cerebral cortex. Several proteins play a role, says Dr. Seuntjens. “We changed the gene containing the production code for the protein Sip1 in mice so that this protein was no longer produced during brain development. In those mice, the interneurons never made it to the cerebral cortex — they couldn’t find the way.
That has to do with the guidance signals – substances that repel or attract interneurons and thus point them in the right direction – encountered by the interneurons on their way to the cerebral cortex. Without Sip1 production, interneurons see things through an overly sharp lens, so to speak. They see too many stop signs and become blocked. That overly sharp lens is Unc5b, a protein. Unc5b is deactivated by Sip1 in healthy mice. There are several known factors that influence the migration of interneurons, but Unc5b is the first protein we’ve isolated that we now know must be switched off in order for interneuron migration to move ahead smoothly.”
The next step is to study this process in the neurons of humans. “Now that there are techniques to create stem cells from skin cells, we can mimic the development of stem cells into interneurons and study what can go wrong. From there, we can test whether certain drugs can reverse the damage. That’s all still on the horizon, but you can see that the focus of research on many brain disorders and diseases is increasingly shifting to early child development because that just might be where a cause can be found.”
New Discovery in Autism-Related Disorder Reveals Key Mechanism in Brain Development and Disease
A new finding in neuroscience for the first time points to a developmental mechanism linking the disease-causing mutation in an autism-related disorder, Timothy syndrome, and observed defects in brain wiring, according to a study led by scientist Ricardo Dolmetsch and published online yesterday in Nature Neuroscience. These findings may be at the heart of the mechanisms underlying intellectual disability and many other brain disorders.
The present study reveals that a mutation of the disease-causing gene throws a key process of neurodevelopment into reverse. That is, the mutation underlying Timothy syndrome causes shrinkage, rather than growth, of the wiring needed for the development of neural circuits that underlie cognition.
“In addition to the implications for autism, what’s really exciting is that we now have a way to get at the core mechanisms tying genes and environmental influences to development and disease processes in the brain,” said Dolmetsch, Senior Director of Molecular Networks at the Allen Institute for Brain Science.
“Imagine what we can learn if we do this hundreds and hundreds of times for many different human genetic variations in a large-scale, systematic way. That’s what we are doing now at the Allen Institute,” Dolmetsch continued.
In normal brain development, brain activity causes branches emanating from neural cells to stretch or expand. In cells with the mutation, these branched extensions, called dendrites, instead retract in response to neural activity, according to this study. This results in abnormal brain circuitry favoring connections with nearby neurons rather than farther-reaching connections. Further, the study identified a previously unknown mode of signaling to uncover the chemical pathway that causes the dendritic retraction.
This finding may have wide-reaching implications in neuroscience, as impaired dendrite formation is a common feature of many neurodevelopmental disorders. Further, the same gene has been implicated in other disorders including bipolar disorder and schizophrenia.
Under Dolmetsch’s leadership, the Molecular Networks program at the Allen Institute, one of three major new initiatives announced by the Institute last March, is using similar methods on a grand scale. The Institute is probing a large number of human genetic variations and many pathways in the brain to untangle the cellular mechanisms of neurodevelopment and disease. In addition to identifying the molecular and environmental rules that shape how the brain is built, the program will create new research tools and data sets that it will share publicly with the global research community.
Timothy syndrome is a neurodevelopmental disorder associated with autism spectrum disorders and caused by a mutation in a single gene. In addition to autism, it is also characterized by cardiac arrhythmias, webbed fingers and toes, and hypoglycemia, and often leads to death in early childhood.
(Image: iStock)
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)
Big Picture: Inside the Brain
The Spring 2013 issue of Big Picture, Inside the Brain, is now available online. This issue, explores the technologies that are helping us to understand the brain, including magnetic resonance imaging (MRI) and computed tomography (CT).
About the cover:
This photograph, taken by Robert Ludlow, shows the surface (cortex) of a human brain belonging to an epileptic patient. The image displays the bright red arteries that supply the brain with nutrients and oxygen and the purple veins that remove deoxygenated blood. This photograph was taken before an intracranial electrode recording procedure for epilepsy, in which electrical activity is measured from the exposed surface of the brain. To find out more about Robert’s image and its creation, view this video on the UCL Institute of Neurology’s website. (Wellcome Image Awards 2012)
What is déjà vu and why does it happen?
Have you ever experienced a sudden feeling of familiarity while in a completely new place? Or the feeling you’ve had the exact same conversation with someone before?
This feeling of familiarity is, of course, known as déjà vu (a French term meaning “already seen”) and it’s reported to occur on an occasional basis in 60-80% of people. It’s an experience that’s almost always fleeting and it occurs at random.
So what is responsible for these feelings of familiarity?
Despite coverage in popular culture, experiences of déjà vu are poorly understood in scientific terms. Déjà vu occurs briefly, without warning and has no physical manifestations other than the announcement: “I just had déjà vu!”
Many researchers propose that the phenomenon is a memory-based experience and assume the memory centres of the brain are responsible for it.
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.
Shakespeare and Wordsworth boost the brain, new research reveals
Scientists, psychologists and English academics at Liverpool University have found that reading the works of the Bard and other classical writers has a beneficial effect on the mind, catches the reader’s attention and triggers moments of self-reflection.
Using scanners, they monitored the brain activity of volunteers as they read works by William Shakespeare, William Wordsworth, T.S Eliot and others.
They then “translated” the texts into more “straightforward”, modern language and again monitored the readers’ brains as they read the words.
Scans showed that the more “challenging” prose and poetry set off far more electrical activity in the brain than the more pedestrian versions.
Scientists were able to study the brain activity as it responded to each word and record how it “lit up” as the readers encountered unusual words, surprising phrases or difficult sentence structure.
This “lighting up” of the mind lasts longer than the initial electrical spark, shifting the brain to a higher gear, encouraging further reading.
The research also found that reading poetry, in particular, increases activity in the right hemisphere of the brain, an area concerned with “autobiographical memory”, helping the reader to reflect on and reappraise their own experiences in light of what they have read. The academics said this meant the classics were more useful than self-help books.
Philip Davis, an English professor who has worked on the study with the university’s magnetic resonance centre, will tell a conference this week: “Serious literature acts like a rocket-booster to the brain.
"The research shows the power of literature to shift mental pathways, to create new thoughts, shapes and connections in the young and the staid alike."
FDA Approves Magnetic Helmet For Treating Depression
The United States Food and Drug Administration approved a device that treats depression using… magnets. About 14.8 million American adults, or 6.7 percent of the U.S. adult population, are diagnosed with major depression in a given year, and antidepressant medications often don’t help.
The technology, known as deep Transcranial Magnetic Stimulation or TMS, involves placing a helmet filled with electromagnetic coils very close to the scalp and zapping them with pulses of electricity, which causes neurons to fire in very specific areas of the brain.
Magnets, How Do They Work?
First the machine is calibrated by placing it over a part of the brain that causes the subject’s hand to move. Then the coils are aimed at the brain region under treatment. The treatment lasts about 15 to 30 minutes, repeated over several weeks, and is noninvasive—all the person feels is a slight buzzing, and there are no side effects. This makes it a more palatable relative of other treatments that also target the brain directly, such as electroconvulsive therapy (formerly electroshock), or surgically implanted electrodes.
Brainsway, a publicly traded Israeli company, has an exclusive license for the technology from the National Institutes of Health, where its two Israeli scientific cofounders developed it. Their device is already approved in Europe for clinical depression, bipolar disorder, schizophrenia (negative symptoms), Parkinson’s diseases, and PTSD. Clinical trials are under way to test how well brain-zapping electromagnets could work to treat a huge range of ailments including cocaine addiction, Tourette’s syndrome, Alzheimer’s, stroke rehabilitation, multiple sclerosis, even ADHD.
(Credit: theloneliestgod)