Visualizing Formation Of A New Synapse.

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ScienceDaily (June 25, 2009) — A protein called neuroligin that is implicated in some forms of autism is critical to the construction of a working synapse, locking neurons together like "molecular Velcro," a study lead by a team of UC Davis researchers has found.

Published online in the June issue of the journal Neural Development, the study is accompanied by groundbreaking images that are the first to show two neurons coming together using neuroligin to construct a new synapse.
"Previous research has suggested that neuroligin is critical for the formation and stabilization of synapses," said Kimberley McAllister, an associate professor of neurology in the UC Davis School of Medicine and a researcher at the UC Davis Center for Neuroscience. "Our work suggests that neuroligin is one of the first molecules to be recruited to new synapses and that it also acts as Velcro to strengthen those new connections."
Neuroligin is a member of a family of four protein molecules that bind to another family of proteins, the β-neurexins, across synapses. During the past decade, scientists have observed that neuroligin is critical for synapse formation and function, but it is only recently that a link between the two synapse-forming molecules and autism has been recognized, McAllister said.
Lead study author and UC Davis postdoctoral fellow Stephanie Barrow said that researchers had hypothesized that neuroligin could facilitate the recruitment of other proteins important in building synapses, but no one had been able to directly visualize the process. That's because synapses are less than 1 micron wide — 100 times narrower than a strand of human hair. To view the process, the researchers cultured neurons taken from newly born rats and flourescently labled the proteins — neuroligin, PSD-95 and NMDA — which are critical to synapse formation.
"We are the first to observe that neuroligin zips around dendrites (the branched projections of neurons) before synapses form and can accumulate very soon after contact between cells," Barrow said.
Barrow described what the team was able to visualize: "Axons of one neuron grow toward the dendrites of neighboring neurons. As they do so, finger-like structures called filopodia extend and retract rapidly from the tip of the axons and eventually make a stable contact with the dendrite. We can then see neuroligin accumulate at these new contact sites very rapidly, possibly stabilizing adhesion between the two cells. After a few minutes, more neuroligin accumulates at this contact site, bringing NMDA receptors in with it, which is then followed by a much slower recruitment of PSD-95."
The images that accompany the study show that, indeed, the two synaptic receptor proteins, PSD-95 and NMDA, are independently recruited to the site of synapse formation once the connections are locked in place by neuroligin.
"Synapses are basically specialized sites of cell adhesion that are initially formed during development of the nervous system. Formation of viable synapses is crucial for establishing neuronal circuits that underlie behavior and cognition," said study senior author Philip Washbourne, a UC Davis postdoctoral fellow when the study was initiated and now an assistant professor of biology at the University of Oregon.
McAllister and Barrow are continuing to capture images of the dynamics of other important molecules during synapse formation. Their goal is to create a virtual cinematic representation that includes many of the molecules that play important roles in the formation of a normal, working synapse.
"Many people think that improper synapse formation leads to the symptoms of autism," McAllister said. "This research will allow us to learn more about how synapses form to better understand what aspects of synapse formation might be altered in the disorder."
Other study authors include Faten El-Sabeawy of UC Davis, Eliana Clark, formerly of UC Davis, and University of Oregon postdoctoral fellow John Constable.
The study was funded by the Pew Charitable Trusts, the National Eye Institute, the John Merck Fund, a UC Davis Vision Science Training Grant, the Whitehall Foundation and Autism Speaks.
Adapted from materials provided by University of California - Davis - Health System.

Social Competition May Be Reason For Bigger Brain

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ScienceDaily (June 23, 2009) — For the past 2 million years, the size of the human brain has tripled, growing much faster than other mammals. Examining the reasons for human brain expansion, University of Missouri researchers studied three common hypotheses for brain growth: climate change, ecological demands and social competition. The team found that social competition is the major cause of increased cranial capacity.

To test the three hypotheses, MU researchers collected data from 153 hominid (humans and our ancestors) skulls from the past 2 million years. Examining the locations and global climate changes at the time the fossil was dated, the number of parasites in the region and estimated population density in the areas where the skulls were found, the researchers discovered that population density had the biggest effect on skull size and thus cranial capacity.
"Our findings suggest brain size increases the most in areas with larger populations and this almost certainly increased the intensity of social competition," said David Geary, Curator's Professor and Thomas Jefferson Professor of Psychosocial Sciences in the MU College of Arts and Science. "When humans had to compete for necessities and social status, which allowed better access to these necessities, bigger brains provided an advantage."
The researchers also found some credibility to the climate-change hypothesis, which assumes that global climate change and migrations away from the equator resulted in humans becoming better at coping with climate change. But the importance of coping with climate was much smaller than the importance of coping with other people.
"Brains are metabolically expensive, meaning they take lots of time and energy to develop and maintain, making it so important to understand why our brains continued to evolve faster than other animals," said Drew Bailey, MU graduate student and co-author of the study. "Our research tells us that competition, whether healthy or not, sets the stage for brain evolution."
Journal reference:
David Geary and Drew Bailey. Hominid Brain Evolution. Human Nature, (in press)
Adapted from materials provided by University of Missouri-Columbia.

Brain Detects Happiness More Quickly Than Sadness

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ScienceDaily (June 21, 2009) — Our brains get a first impression of people's overriding social signals after seeing their faces for only 100 milliseconds (0.1 seconds). Whether this impression is correct, however, is another question. Now an international group of experts has carried out an in-depth study into how we process emotional expressions, looking at the pattern of cerebral asymmetry in the perception of positive and negative facial signals.

The researchers worked with 80 psychology students (65 women and 15 men) to analyze the differences between their cerebral hemispheres using the "divided visual field" technique, which is based on the anatomical properties of the visual system.
"What is new about this study is that working in this way ensures that the information is focused on one cerebral hemisphere or the other", J. Antonio Aznar-Casanova, one of the authors of the study and a researcher at the University of Barcelona (UB), tells SINC.
The results, published in the latest issue of the journal Laterality, show that the right hemisphere performs better in processing emotions. "However, this advantage appears to be more evident when it comes to processing happy and surprised faces than sad or frightened ones", the researcher points out.
"Positive expressions, or expressions of approach, are perceived more quickly and more precisely than negative, or withdrawal, ones. So happiness and surprise are processed faster than sadness and fear", explains Aznar-Casanova.
The two faces of the brain
This research study adds to previous ones, which had revealed asymmetries in the way the brain processes emotions, and enriches the international debate in cognitive-emotional neuroscience in terms of how to define the exact way in which human beings process these facial expressions.
People make deductions from the expressions on people's faces. "These inferences can strongly influence election results or the sentences given in trials, and have been studied before in fields such as criminology and the pseudoscience of physiognomy", the neuroscientist tells SINC.
Two theories are currently "competing" to explain the pattern of cerebral asymmetry in processing emotions. The older one postulates the dominance of the right hemisphere in the processing of emotions, while the second is based on the approach-withdrawal hypothesis, which holds that the pattern of cerebral asymmetry depends upon the emotion in question, in other words that each hemisphere is better at processing particular emotions (the right, withdrawal, and the left, approach).
"Today there is scientific evidence in favour of both these theories, but there is a certain consensus in favour of the lateralisation of emotional processing predicted by the approach-withdrawal hypothesis", concludes Aznar-Casanova.
Journal reference:
Alves et al. Patterns of brain asymmetry in the perception of positive and negative facial expressions. Laterality Asymmetries of Body Brain and Cognition, 2008; 14 (3): 256 DOI: 10.1080/13576500802362927
Adapted from materials provided by Plataforma SINC.

First Image Of Memories Being Made

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ScienceDaily (June 19, 2009) — The ability to learn and to establish new memories is essential to our daily existence and identity; enabling us to navigate through the world. A new study by researchers at the Montreal Neurological Institute and Hospital (The Neuro), McGill University and University of California, Los Angeles has captured an image for the first time of a mechanism, specifically protein translation, which underlies long-term memory formation.

The finding provides the first visual evidence that when a new memory is formed new proteins are made locally at the synapse - the connection between nerve cells - increasing the strength of the synaptic connection and reinforcing the memory. The study published in Science, is important for understanding how memory traces are created and the ability to monitor it in real time will allow a detailed understanding of how memories are formed.
When considering what might be going on in the brain at a molecular level two essential properties of memory need to be taken into account. First, because a lot of information needs to be maintained over a long time there has to be some degree of stability. Second, to allow for learning and adaptation the system also needs to be highly flexible.
For this reason, research has focused on synapses which are the main site of exchange and storage in the brain. They form a vast but also constantly fluctuating network of connections whose ability to change and adapt, called synaptic plasticity, may be the fundamental basis of learning and memory.
"But, if this network is constantly changing, the question is how do memories stay put, how are they formed? It has been known for some time that an important step in long-term memory formation is "translation", or the production, of new proteins locally at the synapse, strengthening the synaptic connection in the reinforcement of a memory, which until now has never been imaged," says Dr. Wayne Sossin, neuroscientist at The Neuro and co-investigator in the study. "Using a translational reporter, a fluorescent protein that can be easily detected and tracked, we directly visualized the increased local translation, or protein synthesis, during memory formation. Importantly, this translation was synapse-specific and it required activation of the post-synaptic cell, showing that this step required cooperation between the pre and post-synaptic compartments, the parts of the two neurons that meet at the synapse. Thus highly regulated local translation occurs at synapses during long-term plasticity and requires trans-synaptic signals."
Long-term memory and synaptic plasticity require changes in gene expression and yet can occur in a synapse-specific manner. This study provides evidence that a mechanism that mediates this gene expression during neuronal plasticity involves regulated translation of localized mRNA at stimulated synapses. These findings are instrumental in establishing the molecular processes involved in long-term memory formation and provide insight into diseases involving memory impairment.
This study was funded by the National Institutes of Health, the WM Keck Foundation and the Canadian Institutes of Health Research.
Adapted from materials provided by McGill University, via EurekAlert!, a service of AAAS.

How Young Mice Phone Home: Study Gives Clue To How Mothers' Brains Screen For Baby Calls

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ScienceDaily (June 11, 2009) — Emory University researchers have identified a surprising mechanism in the brains of mother mice that focuses their awareness on the calls of baby mice. Their study, published June 11 in Neuron, found that the high-frequency sounds of mice pups stand out in a mother's auditory cortex by inhibiting the activity of neurons more attuned to lower frequency sounds.

"Previous research has focused on how the excitation of neurons can detect or interpret sounds, but this study shows the key role that inhibition may play in real situations," said Robert Liu, assistant professor of biology and senior author of the study.
In 2007, Liu and colleagues were the first to demonstrate that the behavioral context in which communication sounds are heard affects the brain's ability to detect, discriminate and respond to them. Specifically, the researchers found that the auditory neurons of female mice that had given birth were better at detecting and discriminating vocalizations from mice pups than auditory neurons in virgin females.
Experiments on awake mice
While that experiment was done with anesthetized mice, the current study by Liu's lab is the first to record the activity of neurons in the auditory cortex of awake mice. Both female mice that had given birth and virgin female mice with no experience caring for mice pups were used in the study.
When exposed to the high-frequency whistles of mice pups, which fall into the 60 to 80 kilohertz range, a large area of neurons in the auditory cortex of the mother mice was more strongly inhibited than in the virgin mice. The pattern of excitation of neurons was similar, however, for both the mothers and virgins.
"Something different is happening in the mothers' brains when they are processing the same sound, and this difference is consistent," Liu said. "The inhibition of neurons appears to be enhancing the contrast in the sound of mice pups, so they stand out more in the acoustic environment."
Showing neural plasticity
Liu's research focuses on how the brain evolves to process sounds in the natural environment. "By understanding normal functioning of the auditory processes in the brain, then we can begin to understand what is breaking down in disease situations, such as following a stroke or brain lesion," he said.
Until recently, it had been widely assumed that the auditory cortex acted simply as a static filter, and that areas downstream in the brain did the complex task of learning to parse meaning from sounds.
"What our experiments help demonstrate is that even at this relatively early stage of cortical sound processing, responses are dynamic," Liu said. "The auditory cortex has plasticity, so that sounds that become behaviorally relevant to us can get optimized."
More research is needed, he added, to determine whether the changes in the brains of mother mice is due to hormonal shifts, the behavioral experience of caring for pups, or both.
The study authors include Edgar Galindo-Leon, a post-doctoral fellow in Liu's lab, and Frank Lin, a graduate student in the lab. Their research was funded by the National Institute for Deafness and Communication Disorders and the NSF Center for Behavioral Neuroscience.
Journal reference:
Edgar E. Galindo-Leon, Frank G. Lin, Robert C. Liu. Inhibitory Plasticity in a Lateral Band Improves Cortical Detection of Natural Vocalizations. Neuron, 2009; DOI: 10.1016/j.neuron.2009.05.001
Adapted from materials provided by Emory University, via EurekAlert!, a service of AAAS.

Can Happiness Be Inherited?

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ScienceDaily (May 14, 2009) — A new study suggests that our feelings in our lifetime can affect our children.

Dr. Halabe Bucay suggests that a wide range of chemicals that our brain generates when we are in different moods could affect 'germ cells' (eggs and sperm), the cells that ultimately produce the next generation. Such natural chemicals could affect the way that specific genes are expressed in the germ cells, and hence how a child develops.
In his article in the latest issue of Bioscience Hypotheses, Dr Alberto Halabe Bucay of Research Center Halabe and Darwich, Mexico, suggested that the hormones and chemicals resulting from happiness, depression and other mental states can affect our eggs and sperm, resulting in lasting changes in our children at the time of their conception.
Brain chemicals such as endorphins, and drugs, such as marijuana and heroin are known to have significant effects on sperm and eggs, altering the patterns of genes that are active in them.
"It is well known, of course, that parental behavior affects children, and that the genes that a child gets from its parents help shape that child's character." said Dr. Halabe Bucay. "My paper suggests a way that the parent's psychology before conception can actually affect the child's genes."
"This is an intriguing idea" commented Dr. William Bains, Editor of Bioscience Hypotheses. "We wanted to publish it to see what other scientists thought, and whether others had data that could support or disprove it. That is what our journal is for, to stimulate debate about new ideas, the more groundbreaking, the better."
Journal reference:
Halabe Bucay et al. Endorphins, personality, and inheritance: Establishing the biochemical bases of inheritance. Bioscience Hypotheses, May 7, 2009; DOI: 10.1016/j.bihy.2009.03.003
Adapted from materials provided by Elsevier, via EurekAlert!, a service of AAAS.

When Senses Intersect: The neurologist Richard Cytowic discusses what synesthesia can teach us about ordinary perception, creativity and V.Nabokov

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Dr. Richard Cytowic is one of the leading researchers of synesthesia, a condition in which two normally separated sensations - such as sight and sound, or touch and taste - occur at the same time. As a result, a synesthetic person might experience the taste of a dish on her fingertips, or be convinced that the letter X is a vibrant turquoise. Mind Matters editor Jonah Lehrer chats with Cytowic about his new book, Wednesday is Indigo Blue, which he co-wrote with David Eagleman.

LEHRER: What first got you interested in synesthesia?
CYTOWIC: It was an accident. I like etymology and so knew the word, whereas my colleagues back in 1979 had never heard of synesthesia. In fact, they refused to believe it could be real, and warned that looking into such “weird” and “New Age” nonsense would ruin my career. Their denial was the typical reaction of orthodoxy to something it can’t explain.
It is said that chance favors the prepared mind, so I guess I was ready when a dinner host apologized that there weren’t “enough points on the chicken.” For Michael Watson, who I later wrote about as “The Man Who Tasted Shapes,” flavor was more than a mouthful. Taste was also a touch sensation felt on his face and in his hands. “With an intense flavor,” he explained, “a feeling sweeps down my arm and I feel weight, shape, texture, and temperature as if I’m actually grasping something.”
Fortunately, I could use university resources to quietly study Michael in depth and write papers. What interested me most was pondering an experience that “wasn’t supposed to be.”
LEHRER: How has our scientific understanding of synesthesia changed in recent years?
CYTOWIC: It has to do with possibilities of how the senses couple in the brain. My first idea that the emotional brain served as the link gave way, based on observations in neonatal synesthesia, to the possibility of faulty pruning. That is, the gene in synesthesia might fail to prune the extra synapses that are normally made in great excess in all newborns. We thought their persistence might plausibly explain why some people are synesthetes.
Today, we know that far from being rare, synesthesia is common––one in 23 individuals has some kind of synesthesia, and one in 90 has colored letters and numerals. That being so, in Wednesday is Indigo Blue David Eagleman and I favor a genetically–determined imbalance between excitation and inhibition. We’ve learned that the normal brain is already highly cross–wired. We think synesthesia occurs due to increased activity in existing wiring rather than the result of extra wiring.
LEHRER: What can synesthetes teach us about the nature of human perception?
CYTOWIC: Far from being a mere curiosity, synesthesia is a consciously elevated form of the perception that everyone already has. Minds that function differently are not so strange after all, and everyone can learn from them.
Synesthesia has opened up a window onto a broad expanse of the brain and perception. Younger researchers are now active in 15 countries. Because the trait runs strongly in families, it is easy to collect DNA from a large number of synesthetic relatives. This means that synesthesia may be the very first perceptual condition for which science can map its gene. This inherited quirk is teaching us that cross–talk among the senses is the rule rather than the exception––we are all inward synesthetes who are outwardly unaware of sensory couplings happening all the time.
For example, sight, sound, and movement normally map to one another so closely that even bad ventriloquists convince us that whatever moves is doing the talking. Likewise, cinema convinces us that dialogue comes from the actors’ mouths rather than the surrounding speakers. Dance is another example of cross–sensory mapping in which body rhythms imitate sound rhythms kinetically and visually. We so take these similarities for granted that we never question them the way we might doubt colored hearing.

LEHRER:In Wednesday Is Indigo Blue, you argue that investigations of synesthesia can help us better understand the neurological basis of metaphor and even creativity. Could you explain?
CYTOWIC: Artists are at ease using metaphors, and we have known for a long time that synesthesia is more common in creative individuals. Famous synesthetes include novelist Vladimir Nabokov, whose mother and son Dmitri also had it; composers Olivier Messiaen, Amy Beech and Billy Joel; and painters David Hockney and Wasily Kandinsky. Dmitri Nabokov, incidentally, wrote a charming afterword about his father and himself for “Indigo Blue.”
There is more to creativity than a capacity for metaphor, of course. Nonetheless, begin with the assumption that the gene for synesthesia lashes together normally unconnected brain areas, thus linking seemingly unrelated qualities such as sound and color. Having one kind of synesthesia gives a person a 50 percent chance of having a second or third kind, meaning that the gene expresses itself in two or three separate areas in that person’s brain. Suppose, however, that brain hyper–connectivity occurred not selectively here and there, but diffusely. One would have a generalized talent for cross connecting apparently unrelated concepts, which is the definition of metaphor: seeing the similar in the dissimilar.
And this is the reason several of us suspect that the synesthesia gene maintains itself at such a high frequency in the population. After all, one in 23 people are walking around with a mutation for an apparently useless trait. It must be doing something of inapparent value in order for evolution to select so strongly in its favor. When the gene expresses itself in sensory parts of the brain, people are outwardly synesthetic. But what are they like when the mutation expresses itself in non–sensory brain parts such as those concerned with memory, planning, or moral reasoning? Might it contribute to increased creativity, thereby making humans smarter as a whole?
We are beginning to find out. The strongest link so far is a region on chromosome 2 that is associated with autism and epilepsy, conditions that occur together with synesthesia more often than chance predicts. The autistic savant Daniel Tammet, whose best–selling autobiography is Born on a Blue Day, has all three conditions––indicating that they might share an underlying genetic mechanism. Tammet first shot to fame in Britain when he set a record for reciting 22,514 digits of pi from memory.
LEHRER: Has there been one case of synesthesia that you've been particularly astonished by?
CYTOWIC: What is astonishing about The Man Who Tasted Shapes is how rare Michael Watson’s type of flavor–touch synesthesia turned out to be in retrospect: less than one percent. So, the odds of him having been the first case were vanishingly small.
One feature that still fascinates me is the “screen” phenomenon that some people with colored hearing have. That is, they see their sound–triggered hues, geometric shapes, and moving configurations projected a foot or so in front of their face as if on a screen. One college professor particularly likes seeing rising and falling lines. Lines that go up are the best. “My favorite music,” she says, “makes the lines go right off the top of the screen.”
In the end, the most astonishing thing I’ve experienced over and over during 30 years of study has been the trust strangers placed in me and their willingness to allow me into their private worlds. That is a brave thing to do when no one has believed you all your life. So it is impossible not to remain fascinated with synesthesia, and even more so synesthetes themselves.
Are you a scientist? Have you recently read a peer-reviewed paper that you want to write about? Then contact Mind Matters editor Jonah Lehrer, the science writer behind the blog The Frontal Cortex and the book Proust Was a Neuroscientist. His latest book is How We Decide.

By Richard Cytowic

Meditation increases brain gray matter

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Push-ups, crunches, gyms, personal trainers -- people have many strategies for building bigger muscles and stronger bones. But what can one do to build a bigger brain? Meditate.

That's the finding from a group of researchers at UCLA who used high-resolution magnetic resonance imaging (MRI) to scan the brains of people who meditate. In a study published in the journal NeuroImage and currently available online (by subscription), the researchers report that certain regions in the brains of long-term meditators were larger than in a similar control group.
Specifically, meditators showed significantly larger volumes of the hippocampus and areas within the orbito-frontal cortex, the thalamus and the inferior temporal gyrus — all regions known for regulating emotions.
"We know that people who consistently meditate have a singular ability to cultivate positive emotions, retain emotional stability and engage in mindful behavior," said Eileen Luders, lead author and a postdoctoral research fellow at the UCLA Laboratory of Neuro Imaging. "The observed differences in brain anatomy might give us a clue why meditators have these exceptional abilities."
Research has confirmed the beneficial aspects of meditation. In addition to having better focus and control over their emotions, many people who meditate regularly have reduced levels of stress and bolstered immune systems. But less is known about the link between meditation and brain structure.
In the study, Luders and her colleagues examined 44 people — 22 control subjects and 22 who had practiced various forms of meditation, including Zazen, Samatha and Vipassana, among others. The amount of time they had practiced ranged from five to 46 years, with an average of 24 years.
More than half of all the meditators said that deep concentration was an essential part of their practice, and most meditated between 10 and 90 minutes every day.
The researchers used a high-resolution, three-dimensional form of MRI and two different approaches to measure differences in brain structure. One approach automatically divides the brain into several regions of interest, allowing researchers to compare the size of certain brain structures. The other segments the brain into different tissue types, allowing researchers to compare the amount of gray matter within specific regions of the brain.

The researchers found significantly larger cerebral measurements in meditators compared with controls, including larger volumes of the right hippocampus and increased gray matter in the right orbito-frontal cortex, the right thalamus and the left inferior temporal lobe. There were no regions where controls had significantly larger volumes or more gray matter than meditators.
Because these areas of the brain are closely linked to emotion, Luders said, "these might be the neuronal underpinnings that give meditators' the outstanding ability to regulate their emotions and allow for well-adjusted responses to whatever life throws their way."
What's not known, she said, and will require further study, are what the specific correlates are on a microscopic level — that is, whether it's an increased number of neurons, the larger size of the neurons or a particular "wiring" pattern meditators may develop that other people don't.
Because this was not a longitudinal study — which would have tracked meditators from the time they began meditating onward — it's possible that the meditators already had more regional gray matter and volume in specific areas; that may have attracted them to meditation in the first place, Luders said.
However, she also noted that numerous previous studies have pointed to the brain's remarkable plasticity and how environmental enrichment has been shown to change brain structure.
Source: University of California - Los Angeles

Brain's Problem-solving Function At Work When We Daydream

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ScienceDaily (May 12, 2009) — A new University of British Columbia study finds that our brains are much more active when we daydream than previously thought.

The study, published in the Proceedings of the National Academy of Sciences, finds that activity in numerous brain regions increases when our minds wander. It also finds that brain areas associated with complex problem-solving – previously thought to go dormant when we daydream – are in fact highly active during these episodes.
"Mind wandering is typically associated with negative things like laziness or inattentiveness," says lead author, Prof. Kalina Christoff, UBC Dept. of Psychology. "But this study shows our brains are very active when we daydream – much more active than when we focus on routine tasks."
For the study, subjects were placed inside an fMRI scanner, where they performed the simple routine task of pushing a button when numbers appear on a screen. The researchers tracked subjects' attentiveness moment-to-moment through brain scans, subjective reports from subjects and by tracking their performance on the task.
The findings suggest that daydreaming – which can occupy as much as one third of our waking lives – is an important cognitive state where we may unconsciously turn our attention from immediate tasks to sort through important problems in our lives.
Until now, the brain's "default network" – which is linked to easy, routine mental activity and includes the medial prefrontal cortex (PFC), the posterior cingulate cortex and the temporoparietal junction – was the only part of the brain thought to be active when our minds wander.
However, the study finds that the brain's "executive network" – associated with high-level, complex problem-solving and including the lateral PFC and the dorsal anterior cingulate cortex – also becomes activated when we daydream.
"This is a surprising finding, that these two brain networks are activated in parallel," says Christoff. "Until now, scientists have thought they operated on an either-or basis – when one was activated, the other was thought to be dormant." The less subjects were aware that their mind was wandering, the more both networks were activated.
The quantity and quality of brain activity suggests that people struggling to solve complicated problems might be better off switching to a simpler task and letting their mind wander.
"When you daydream, you may not be achieving your immediate goal – say reading a book or paying attention in class – but your mind may be taking that time to address more important questions in your life, such as advancing your career or personal relationships," says Christoff.
The research team included members who are now at Stanford University and University of California, Santa Barbara.
Journal reference:
Kalina Christoff, Alan M. Gordon, Jonathan Smallwood, Rachelle Smith, and Jonathan W. Schooler. Experience sampling during fMRI reveals default network and executive system contributions to mind wandering. Proceedings of the National Academy of Sciences, 2009; DOI: 10.1073/pnas.0900234106
Adapted from materials provided by University of British Columbia.

Impaired Brain Plasticity Linked To Angelman Syndrome Learning Deficits

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ScienceDaily (May 10, 2009) — How might disruption of a single gene in the brain cause the severe cognitive deficits associated with Angelman syndrome, a neurogenetic disorder? Researchers at the University of North Carolina at Chapel Hill School of Medicine and Duke University now believe they have the answer: impaired brain plasticity.

"When we have experiences, connections between brain cells are modified so that we can learn," said Benjamin Philpot, Ph.D., professor of cell and molecular physiology at UNC and senior author of the study published online May 10 in Nature Neuroscience. "By strengthening and weakening appropriate connections between brain cells, a process termed 'synaptic plasticity', we are able to constantly learn and adapt to an ever-changing environment."
Angelman syndrome occurs in one in 15,000 live births. The most common genetic defect of the syndrome is the lack of expression of the gene UBE3A on chromosome 15. The syndrome often is misdiagnosed as cerebral palsy or autism. Characteristics of the syndrome include intellectual and developmental delay, severe mental retardation lack of speech (minimal or no use of words), seizures, sleep disturbance, hand flapping and motor and balance disorders.
Philpot and his co-authors studied a mouse model of Angelman syndrome. In these mice, the gene UBE3A is functionally deficient. The study found that brain cells in the mice lacked the ability to appropriately strengthen or weaken their connections in the neocortex, a region of the brain that is important for cognitive abilities.
"If brain cells were unable to modify their connections with new experiences, then we would have difficulty learning," said Michael Ehlers, M.D., Ph.D., professor of neurobiology at Duke and co-senior author of the study. "We have found that a specific form of brain plasticity is severely impaired in a mouse model of Angelman syndrome and this prevents brain circuits from encoding information provided by sensory experiences. In addition, an exciting possibility is that the defect we have found may be a more general feature of other disorders of brain development including autism."
The inability of brain cells to encode information from experiences in the Angelman syndrome model suggests that this is the basis for the learning difficulties in these patients.
"It is difficult to study how experiences lead to changes in the brain in models of mental retardation," said Koji Yashiro, PhD, a former graduate student in Philpot's lab and lead author of the study, now a scientist with Urogenix, Inc. in Research Triangle Park, North Carolina. "Instead of studying a complex learning model, we studied how connections between brain cells change in visual areas of mice exposed to light or kept in darkness. This approach revealed that brain cells in normal mice can modify their connections in response to changes in visual experiences, while the brain cells in Angelman syndrome model mice could not."
An unexpected finding was that the plasticity of the cellular connections could be restored in visual areas of the brain after brief periods of visual deprivation. Philpot said the observation that the brain defect could be reversed "is very encouraging, as it suggests that viable behavioral or pharmacological therapies are likely to exist."
"By showing that brain plasticity can be restored in Angelman syndrome model mice, our findings suggest that brain cells in Angelman syndrome patients maintain a latent ability to express plasticity. We are now collaborating to find a way to tap into this latent plasticity, as this could offer a treatment, or even a cure, for Angelman syndrome," said Philpot.
Philpot added, "This same experimental approach could also reveal how brain cells encode information from experiences in other related disorders, such as autism, and may provide a model to find cures for a variety of neurodevelopmental disorders."
Other authors are, from Philpot's UNC lab: Thorfinn Riday, graduate student; Adam Roberts, Ph.D., postdoctoral fellow; Danilo Bernardo, medical student; and Rohit Prakash, former M.D./Ph.D. rotation student. Kathryn Condon, a graduate student in Ehler's lab and the department of neurobiology at Duke University; and Richard Weinberg, Ph.D., professor of cell and developmental biology at UNC, also participated in the research.
Support for the work came from grants from the National Institutes of Health, the Howard Hughes Medical Institute, the Angelman Syndrome Foundation and the Simons Foundation.
Adapted from materials provided by University of North Carolina School of Medicine, via EurekAlert!, a service of AAAS.