Posts tagged science
Articles and news from the latest research reports.
Recognising movement and its direction is one of the first and most important processing steps in any visual system. By this way, nearby predators or prey can be detected and even one’s own movements are controlled. More than fifty years ago, a mathematical model predicted how elementary motion detectors must be structured in the brain. However, which nerve cells perform this job and how they are actually connected remained a mystery. Scientists at the Max Planck Institute of Neurobiology in Martinsried have now come one crucial step closer to this “holy grail of motion vision”: They identified the cells that represent these so-called “elementary motion detectors” in the fruit fly brain. The results show that motion of an observed object is processed in two separate pathways. In each pathway, motion information is processed independently of one another and sorted according to its direction.
Ramón y Cajal, the famous neuroanatomist, was the first to examine the brains of flies. Almost a century ago, he thus discovered a group of cells he described as “curious elements with two tufts”. About 50 years later, German physicist Werner Reichardt postulated from his behavioural experiments with flies that they possess “elementary motion detectors”, as he referred to them. These detectors compare changes in luminance between two neighbouring photoreceptor units, or facets, in the fruit fly’s eye for every point in the visual space. The direction of a local movement is then calculated from this. At least, that is what the theory predicts. Since that time, the fruit fly research community has been speculating about whether these “two-tufted cells” described by Cajal are the mysterious elementary motion detectors.
The answer to this question has been slow in coming, as the tufted cells are extremely small – much too small for sticking an electrode into them and capturing their electrical signals. Now, Alexander Borst and his group at the Max Planck- Institute of Neurobiology have succeeded in making a breakthrough with the aid of a calcium indicator. These fluorescent proteins are formed by the neurons themselves and change their fluorescence when the cells are active. It thus finally became possible for the scientists to observe and measure the activity of the tufted cells under the microscope. The results prove that these cells actually are the elementary motion detectors predicted by Werner Reichardt.
As further experiments have shown, the tufted cells can be divided into two groups. One group (T4 cells) only reacts to a transition from dark to light caused by motion, while the other group (T5 cells) reacts oppositely – only for light-to-dark edges. In every group there are four subgroups, each of which only responds to movements in a specific direction – to the right, left, upwards or downwards. The neurons in these directionally selective groups release their information into layers of subsequent nerve tissue that are completely separated from one another. There, large neurons use these signals for visual flight control, generating the appropriate commands for the flight musculature, for example. This could be impressively proven by the scientists: When they blocked the T4 cells, the neurons connected downstream and the fruit flies themselves were shown in behavioural tests to be blind to motions caused by dark-to-light edges. When the T5 cells were blocked, light-to-dark edges could no longer be perceived.
In discussions about their research results, which have just been published in the scientific journal Nature, both lead authors, Matt Maisak and Jürgen Haag, were very impressed with the “cleanly differentiated, yet highly ordered” motion information within the brains of the fruit flies. Alexander Borst, head of the study, adds: “That was real teamwork – almost all of the members in my department took part in the experiments. One group carried out the calcium measurements, another worked on the electrophysiology, and a third made the behavioural measurements. They all pulled together. It was a wonderful experience.” And it should continue like this, since the scientists are already turning to the next mammoth challenge: they would now like to identify the neurons that deliver the input signals to the elementary motion detectors. According to Reichardt, the two signals coming from neighbouring photoreceptors in the eye have to be delayed in relation to one another. “That is going to be really exciting!” says Alexander Borst.
Study Reveals That Overthinking Can Be Detrimental to Human Performance
Trying to explain riding a bike is difficult because it is an implicit memory. The body knows what to do, but thinking about the process can often interfere. So why is it that under certain circumstances paying full attention and trying hard can actually impede performance? A new UC Santa Barbara study, published today in the Journal of Neuroscience, reveals part of the answer.
There are two kinds of memory: implicit, a form of long-term memory not requiring conscious thought and expressed by means other than words; and explicit, another kind of long-term memory formed consciously that can be described in words. Scientists consider these distinct areas of function both behaviorally and in the brain.
Long-term memory is supported by various regions in the prefrontal cortex, the newest part of the brain in terms of evolution and the part of the brain responsible for planning, executive function, and working memory. “A lot of people think the reason we’re human is because we have the most advanced prefrontal cortex,” said the study’s lead author, Taraz Lee, a postdoctoral scholar working in UCSB’s Action Lab.
Two previous brain studies have shown that taxing explicit memory resources improved recognition memory without awareness. The results suggest that implicit perceptual memory can aid performance on recognition tests. So Lee and his colleagues decided to test whether the effects of the attentional control processes associated with explicit memory could directly interfere with implicit memory.
Lee’s study used continuous theta-burst transcranial magnetic stimulation (TMS) to temporarily disrupt the function of two different parts of the prefrontal cortex, the dorsolateral and ventrolateral. The dorsal and ventral regions are close to each other but have slightly different functions. Disrupting function in two distinct areas provided a direct causal test of whether explicit memory processing exerts control over sensory resources –– in this case, visual information processing –– and in doing so indirectly harms implicit memory processes.
Participants were shown a series of kaleidoscopic images for about a minute, then had a one-minute break before being given memory tests containing two different kaleidoscopic images. They were then asked to distinguish images they had seen previously from the new ones. “After they gave us that answer, we asked whether they remembered a lot of rich details, whether they had a vague impression, or whether they were blindly guessing,” explains Lee. “And the participants only did better when they said they were guessing.”
The results of disrupting the function of the dorsolateral prefrontal cortex shed light on why paying attention can be a distraction and affect performance outcomes. “If we ramped down activity in the dorsolateral prefrontal cortex, people remembered the images better,” said Lee.
When the researchers disrupted the ventral area of the prefrontal cortex, participants’ memory was just slightly worse. “They would shift from saying that they could remember a lot of rich details about the image to being vaguely familiar with the images,” Lee said. “It didn’t actually make them better at the task.”
Lee’s fascination with the effect of attentional processes on memory stems from his extensive sports background. As he pointed out, there are always examples of professional golfers who have the lead on the 18th hole, but when it comes down to one easy shot, they fall apart. “That should be the time when it all comes out the best, but you just can’t think about that sort of thing,” he said. “It just doesn’t help you.”
His continuing studies at UCSB’s Action Lab will focus on dissecting the process of choking under pressure. Lee’s work will use brain scans to examine why people who are highly incentivized to do well often succumb to pressure and how the prefrontal cortex and these attentional processes interfere with performance.
"I think most researchers who look at prefrontal cortex function are trying to figure out what it does to help you and how that explains how the brain works and how we act," said Lee. "I look at it at the opposite. If we can figure out the ways in which activity in this part of the brain hurts you, then this also informs how your brain works and can give us some clues to what’s actually going on."
Cognitive decline with age is normal, routine – but not inevitable
If you forget where you put your car keys and you can’t seem to remember things as well as you used to, the problem may well be with the GluN2B subunits in your NMDA receptors.
And don’t be surprised if by tomorrow you can’t remember the name of those darned subunits.
They help you remember things, but you’ve been losing them almost since the day you were born, and it’s only going to get worse. An old adult may have only half as many of them as a younger person.
Research on these biochemical processes in the Linus Pauling Institute at Oregon State University is making it clear that cognitive decline with age is a natural part of life, and scientists are tracking the problem down to highly specific components of the brain. Separate from some more serious problems like dementia and Alzheimer’s disease, virtually everyone loses memory-making and cognitive abilities as they age. The process is well under way by the age of 40 and picks up speed after that.
But of considerable interest: It may not have to be that way.
“These are biological processes, and once we fully understand what is going on, we may be able to slow or prevent it,” said Kathy Magnusson, a neuroscientist in the OSU Department of Biomedical Sciences, College of Veterinary Medicine, and professor in the Linus Pauling Institute. “There may be ways to influence it with diet, health habits, continued mental activity or even drugs.”
The processes are complex. In a study just published in the Journal of Neuroscience, researchers found that one protein that stabilizes receptors in a young animal – a good thing conducive to learning and memory – can have just the opposite effect if there’s too much of it in an older animal.
But complexity aside, progress is being made. In recent research, supported by the National Institutes of Health, OSU scientists used a genetic therapy in laboratory mice, in which a virus helped carry complementary DNA into appropriate cells and restored some GluN2B subunits. Tests showed that it helped mice improve their memory and cognitive ability.
The NMDA receptor has been known of for decades, Magnusson said. It plays a role in memory and learning but isn’t active all the time – it takes a fairly strong stimulus of some type to turn it on and allow you to remember something. The routine of getting dressed in the morning is ignored and quickly lost to the fog of time, but the day you had an auto accident earns a permanent etching in your memory.
Within the NMDA receptor are various subunits, and Magnusson said that research keeps pointing back to the GluN2B subunit as one of the most important. Infants and children have lots of them, and as a result are like a sponge in soaking up memories and learning new things. But they gradually dwindle in number with age, and it also appears the ones that are left work less efficiently.
“You can still learn new things and make new memories when you are older, but it’s not as easy,” Magnusson said. “Fewer messages get through, fewer connections get made, and your brain has to work harder.”
Until more specific help is available, she said, some of the best advice for maintaining cognitive function is to keep using your brain. Break old habits, do things different ways. Get physical exercise, maintain a good diet and ensure social interaction. Such activities help keep these “subunits” active and functioning.
Gene therapy such as that already used in mice would probably be a last choice for humans, rather than a first option, Magnusson said. Dietary or drug options would be explored first.
“The one thing that does seem fairly clear is that cognitive decline is not inevitable,” she said. “It’s biological, we’re finding out why it happens, and it appears there are ways we might be able to slow or stop it, perhaps repair the NMDA receptors. If we can determine how to do that without harm, we will.”
(Source: oregonstate.edu)
This is your brain on Vivaldi and Beatles
Listening to music activates large networks in the brain, but different kinds of music are processed differently. A team of researchers from Finland, Denmark and the UK has developed a new method for studying music processing in the brain during a realistic listening situation. Using a combination of brain imaging and computer modeling, they found areas in the auditory, motor, and limbic regions to be activated during free listening to music. They were furthermore able to pinpoint differences in the processing between vocal and instrumental music. The new method helps us to understand better the complex brain dynamics of brain networks and the processing of lyrics in music. The study was published in the journal NeuroImage.
Using functional magnetic resonance imaging (fMRI), the research team, led by Dr. Vinoo Alluri from the University of Jyväskylä, Finland, recorded the brain responses of individuals while they were listening to music from different genres, including pieces by Antonio Vivaldi, Miles Davis, Booker T. & the M.G.’s, The Shadows, Astor Piazzolla, and The Beatles. Following this, they analyzed the musical content of the pieces using sophisticated computer algorithms to extract musical features related to timbre, rhythm and tonality. Using a novel cross-validation method, they subsequently located activated brain areas that were common across the different musical stimuli.
The study revealed that activations in several areas in the brain belonging to the auditory, limbic, and motor regions were activated by all musical pieces. Notable, areas in the medial orbitofrontal region and the anterior cingulate cortex, which are relevant for self-referential appraisal and aesthetic judgments, were found to be activated during the listening. A further interesting finding was that vocal and instrumental music were processed differently. In particular, the presence of lyrics was found to shift the processing of musical features towards the right auditory cortex, which suggests a left-hemispheric dominance in the processing of the lyrics. This result is in line with previous research, but now for the first time observed during continuous listening to music.
"The new method provides a powerful means to predict brain responses to music, speech, and soundscapes across a variety of contexts", says Dr. Vinoo Alluri.
A ‘Rocking’ Receptor: Crucial Brain-Signaling Molecule Requires Coordinated Motion to Turn On
Study could help yield new drugs for brain disorders
Johns Hopkins biophysicists have discovered that full activation of a protein ensemble essential for communication between nerve cells in the brain and spinal cord requires a lot of organized back-and-forth motion of some of the ensemble’s segments. Their research, they say, may reveal multiple sites within the protein ensemble that could be used as drug targets to normalize its activity in such neurological disorders as epilepsy, schizophrenia, Parkinson’s and Alzheimer’s disease.
The glutamate-binding segments (blue, yellow) of ionotropic glutamate receptors undergo a “rocking” motion during activation by glutamate (red). (The dotted line provides a point of reference.)
A summary of the results, published online in the journal Neuron on Aug. 7, shows that full activation of so-called ionotropic glutamate receptors is more complex than previously envisioned. In addition to the expected shape changes that occur when the receptor “receives” and clamps down on glutamate messenger molecules, the four segments of the protein ensemble also rock back and forth in relation to each other when fewer than four glutamates are bound.
“We believe that our study is the first to show the molecular architecture and behavior of a prominent neural receptor protein ensemble in a state of partial activation,” says Albert Lau, Ph.D., assistant professor of biophysics and biophysical chemistry at the Johns Hopkins University School of Medicine.
Glutamate receptors reside in the outer envelope of every nerve cell in the brain and spinal cord, Lau notes, and are responsible for changing chemical information — the release of glutamate molecules from a neighboring nerve cell — into electrical information, the flow of charged particles into the receiving nerve cell. There would be sharply reduced communication between nerve cells in our brains if these receptors were disabled, he added, and thought and normal brain function in general would be severely compromised. Malfunctioning receptors, says Lau, have been linked with numerous neurological disorders and are therefore potential targets for drug therapies.
Lau explained that each glutamate receptor is a united group of four protein segments that has a pocket for clamping down on glutamate like a Venus fly trap snaring a bug. Below the glutamate-binding segments are four other segments embedded in the cell’s outer envelope to form a channel for charged particles to flow through. When no glutamates are bound to the receptor, the channel is closed; full activation of the receptor and full opening of the channel occur when four glutamates are bound, each to a difference pocket.
Previously, Lau says, investigators thought that the level of receptor activation simply corresponded to the degree to which each glutamate-binding segment changed shape during the glutamate-binding process. Using a combination of computer modeling, biophysical “imaging” of molecular structure, biochemical analysis and electrical monitoring of individual cells, the researchers teased apart some of the steps in between zero activation and full activation. They were able to show that the four glutamate-binding segments, in addition to clamping down on glutamate, also rock back and forth in pairs when fewer than four glutamates are bound.
“It isn’t clear yet how this rocking motion affects receptor function, but we now know that activation depends on more than how much each glutamate-binding segment clamps down,” says Lau. Previous development of drugs targeting the receptor focused on the four glutamate-binding pockets. “Our discovery of this molecular motion could aid the development of drugs by revealing additional drug-binding sites on the receptor,” he adds.
(Source: hopkinsmedicine.org)
Scientists Find Key Signal that Guides Brain Development
Scientists at The Scripps Research Institute (TSRI) have decoded an important molecular signal that guides the development of a key region of the brain known as the neocortex. The largest and most recently evolved region of the brain, the neocortex is particularly well developed in humans and is responsible for sensory processing, long-term memory, reasoning, complex muscle actions, consciousness and other functions.
“The mammalian neocortex has a distinctive structure featuring six layers of neurons, and our finding helps explain how this layered structure is generated in early life,” said Ulrich Mueller, chair of TSRI’s Department of Molecular and Cellular Neuroscience and director of the Dorris Neuroscience Center at TSRI.
The discovery, which appears in the August 7,2013 issue of Neuron, also is likely to aid research on autism, schizophrenia and other psychiatric conditions. “With studies such as this one, we’re starting to understand the normal functions of molecules whose disruption by gene mutations can cause developmental brain disorders,” Mueller said.
Finding Their Proper Place
The signal uncovered by Mueller’s team is one that helps guide the migration of baby neurons through the developing neocortex. Such neurons are born from stem-like cells at the bottom of the neocortex, where it wraps around a large, fluid-filled space in the brain called ventricle. The newborn neurons then migrate upward, or radially away from the ventricle, being directed to their proper places in the neocortex’s six-layered, columnar structure by—among others—special guide cells called Cajal-Retzius (CR) cells.
Decades ago, scientists discovered a key signaling protein, reelin, which CR cells secrete and baby neocortical neurons must detect to migrate properly. (Mutant mice that lack a functional form of the protein show, among other abnormalities, a reeling gait—thus the name.) There have been hints since then that CR cells and baby neocortical neurons exchange other molecular signals, too. “But in many years of study, no one has been able to find these other signals,” said Mueller.
However, in a study published in 2011, Mueller and his laboratory colleagues found a significant clue. Reelin, they discovered, guides neuronal migration at least in part by boosting baby neurons’ expression of a generic cell-adhesion molecule, cadherin2 (Cdh2). Since Cdh2 can be expressed by almost any cell type in the developing neocortex, the team then began to look for other factors that would account for the specificity of the interaction between CR cells and migrating baby neurons.
An Interesting Pattern
One set of candidates were the nectins—cell-adhesion proteins known to work with cadherins in other contexts. Lead author Cristina Gil-Sanz, a senior research associate in the Mueller laboratory, mapped the expression levels of the four known types of mammalian nectin proteins in the developing mouse cortex and found an interesting pattern. “We observed that nectin1 is expressed specifically by CR cells and nectin3 by migrating neurons,” said Gil-Sanz. “At the same time, we knew from previous research that nectin1 and nectin3 are preferred binding partners.”
Gil-Sanz and her colleagues followed up with other experiments and soon confirmed that the hookup of nectin1 on CR cells with nectin3 on baby neurons is essential for proper neuronal migration. “This showed for the first time the importance of direct contacts between CR cells and migrating neurons,” Gil-Sanz said.
The experiments also showed that this direct nectin-to-nectin connection is effectively part of the reelin signaling pathway, since reelin’s promotion of Cdh2’s function in migrating neurons turns out to work largely via nectin3. “This helps explain how the interaction occurs specifically between neurons and CR cells, and doesn’t involve other nearby cells that also express Cdh2,” she said.
New Possibilities
The finding points to the possibility of other cell-specific pairings that work via generic Cdh2-to-Cdh2 adhesions in brain development. “We know that there are four nectin proteins, plus a slew of nectin-like molecules,” said Mueller. “We think that there are others that do this as well, and we’re hoping to find them.”
The new study represents a big step toward the full scientific understanding of neuronal migration in the neocortex, and it is likely to be relevant to the study of developmental brain diseases too. Reelin-signaling abnormalities in humans have been linked to autism, depression, schizophrenia and even Alzheimer’s, and, in recent years, cadherin protein mutations also have been linked to disorders including schizophrenia and autism. “Studies like ours provide insight into such findings, by showing that these molecules, in cooperation with nectins, regulate key developmental processes such as the positioning of neurons in the neocortex,” said Mueller.
What Color is Your Night Light? It May Affect Your Mood
Study Finds Red Light Least Harmful, While Blue Light is Worst
When it comes to some of the health hazards of light at night, a new study suggests that the color of the light can make a big difference.
In a study involving hamsters, researchers found that blue light had the worst effects on mood-related measures, followed closely by white light.
But hamsters exposed to red light at night had significantly less evidence of depressive-like symptoms and changes in the brain linked to depression, compared to those that experienced blue or white light.
The only hamsters that fared better than those exposed to red light were those that had total darkness at night.
The findings may have important implications for humans, particularly those whose work on night shifts makes them susceptible to mood disorders, said Randy Nelson, co-author of the study and professor of neuroscience and psychology at The Ohio State University.
“Our findings suggest that if we could use red light when appropriate for night-shift workers, it may not have some of the negative effects on their health that white light does,” Nelson said.
The study appears in the Aug. 7, 2013, issue of The Journal of Neuroscience.
The research examined the role of specialized photosensitive cells in the retina — called ipRGCs — that don’t have a major role in vision, but detect light and send messages to a part of the brain that helps regulate the body’s circadian clock. This is the body’s master clock that helps determine when people feel sleepy and awake.
Other research suggests these light-sensitive cells also send messages to parts of the brain that play a role in mood and emotion.
“Light at night may result in parts of the brain regulating mood receiving signals during times of the day when they shouldn’t,” said co-author Tracy Bedrosian, a former graduate student at Ohio State who is now a postdoctoral researcher at the Salk Institute. “This may be why light at night seems to be linked to depression in some people.”
What people experience as different colors of light are actually lights of different wavelengths. The ipRGCs don’t appear to react to light of different wavelengths in the same way.
“These cells are most sensitive to blue wavelengths and least sensitive to red wavelengths,” Nelson said. “We wanted to see how exposure to these different color wavelengths affected the hamsters.”
In one experiment, the researchers exposed adult female Siberian hamsters to four weeks each of nighttime conditions with no light, dim red light, dim white light (similar to that found in normal light bulbs) or dim blue light.
They then did several tests with the hamsters that are used to check for depressive-like symptoms. For example, if the hamsters drink less-than-normal amounts of sugar water — a treat they normally enjoy — that is seen as evidence of a mood problem.
Results showed that hamsters that were kept in the dark at night drank the most sugar water, followed closely by those exposed to red light. Those that lived with dim white or blue light at night drank significantly less of the sugar water than the others.
After the testing, the researchers then examined the hippocampus regions of the brains of the hamsters.
Hamsters that spent the night in dim blue or white light had a significantly reduced density of dendritic spines compared to those that lived in total darkness or that were exposed to only red light. Dendritic spines are hairlike growths on brain cells that are used to send chemical messages from one cell to another.
A lowered density of these dendritic spines has been linked to depression, Nelson said.
“The behavior tests and changes in brain structure in hamsters both suggest that the color of lights may play a key role in mood,” he said.
“In nearly every measure we had, hamsters exposed to blue light were the worst off, followed by those exposed to white light,” he said. “While total darkness was best, red light was not nearly as bad as the other wavelengths we studied.”
Nelson and Bedrosian said they believe these results may be applicable to humans.
In addition to shift workers, others may benefit from limiting their light at night from computers, televisions and other electronic devices, they said. And, if light is needed, the color may matter.
“If you need a night light in the bathroom or bedroom, it may be better to have one that gives off red light rather than white light,” Bedrosian said.
Emotional behavior of adults could be triggered in the womb
Adults could be at greater risk of becoming anxious and vulnerable to poor mental health if they were deprived of certain hormones while developing in the womb according to new research by scientists at Cardiff and Cambridge universities.
New research in mice has revealed the role of the placenta in long-term programming of emotional behaviour and the first time scientists have linked changes in adult behaviour to alterations in placental function.
Insulin-like growth factor-2 has been shown to play a major role in foetal and placental development in mammals, and changes in expression of this hormone in the placenta and foetus are implicated in growth restriction in the womb.
"The growth of a baby is a very complex process and there are lots of control mechanisms which make sure that the nutrients required by the baby to grow can be supplied by the mother," according to Professor Lawrence Wilkinson, a behavioural neuroscientist from Cardiff University’s School of Psychology who led the research.
"We were interested in how disrupting this balance could influence emotional behaviours a long time after being born, as an adult," he added.
In order to explore how a mismatch between supply and demand of certain nutrients might affect humans, Professor Wilkinson and his colleagues Dr Trevor Humby, Mikael Mikaelsson - both also from Cardiff University – and Dr Miguel Constancia of Cambridge University, examined the behaviour of adult mice with a malfunctioned supply of a vital hormone.
Dr Humby added: “We achieved this by damaging a hormone called Insulin-like growth factor-2, important for controlling growth in the womb. What we found when we did this was an imbalance in the supply of nutrients controlled by the placenta, and that this imbalance had major effects on how subjects were during adulthood – namely, that subject became more anxious later in life.
"These symptoms were accompanied by specific changes in brain gene expression related to this type of behaviour. This is the first example of what we have termed ‘placental-programming’ of adult behaviour. We do not know exactly how these very early life events can cause long-range effects on our emotional predispositions, but we suspect that our research findings may indicate that the seeds of our behaviour, and possibly vulnerability to brain and mental health disorders, are sown much earlier than previously thought."
Although these studies were carried out in mice, the findings may have wider implications for human development. Further studies are planned to investigate the brain mechanisms linking early life events, placental dysfunction and the emotional state of adults.
(Source: eurekalert.org)
Sleep deprivation linked to junk food cravings
A sleepless night makes us more likely to reach for doughnuts or pizza than for whole grains and leafy green vegetables, suggests a new study from UC Berkeley that examines the brain regions that control food choices. The findings shed new light on the link between poor sleep and obesity.
Using functional magnetic resonance imaging (fMRI), UC Berkeley researchers scanned the brains of 23 healthy young adults, first after a normal night’s sleep and next, after a sleepless night. They found impaired activity in the sleep-deprived brain’s frontal lobe, which governs complex decision-making, but increased activity in deeper brain centers that respond to rewards. Moreover, the participants favored unhealthy snack and junk foods when they were sleep deprived.
“What we have discovered is that high-level brain regions required for complex judgments and decisions become blunted by a lack of sleep, while more primal brain structures that control motivation and desire are amplified,” said Matthew Walker, a UC Berkeley professor of psychology and neuroscience and senior author of the study published today (Tuesday, Aug. 6) in the journal Nature Communications.
Moreover, he added, “high-calorie foods also became significantly more desirable when participants were sleep-deprived. This combination of altered brain activity and decision-making may help explain why people who sleep less also tend to be overweight or obese.”
Previous studies have linked poor sleep to greater appetites, particularly for sweet and salty foods, but the latest findings provide a specific brain mechanism explaining why food choices change for the worse following a sleepless night, Walker said.
“These results shed light on how the brain becomes impaired by sleep deprivation, leading to the selection of more unhealthy foods and, ultimately, higher rates of obesity,” said Stephanie Greer, a doctoral student in Walker’s Sleep and Neuroimaging Laboratory and lead author of the paper. Another co-author of the study is Andrea Goldstein, also a doctoral student in Walker’s lab.
In this newest study, researchers measured brain activity as participants viewed a series of 80 food images that ranged from high-to low-calorie and healthy and unhealthy, and rated their desire for each of the items. As an incentive, they were given the food they most craved after the MRI scan.
Food choices presented in the experiment ranged from fruits and vegetables, such as strawberries, apples and carrots, to high-calorie burgers, pizza and doughnuts. The latter are examples of the more popular choices following a sleepless night.
On a positive note, Walker said, the findings indicate that “getting enough sleep is one factor that can help promote weight control by priming the brain mechanisms governing appropriate food choices.”
Researchers uncover brain molecule regulating human emotion, mood
A RIKEN research team has discovered an enzyme called Rines that regulates MAO-A, a major brain protein controlling emotion and mood. The enzyme is a potentially promising drug target for treating diseases associated with emotions such as depression.
Monoamine oxidase A (MAO-A) is an enzyme that breaks down serotonin, norephinephrine and dopamine, neurotransmitters well-known for their influence on emotion and mood. Nicknamed the “warrior gene”, a variant of the MAOA gene has been associated with increased risk of violent and anti-social behavior.
While evidence points to a link between MAO-A levels and various emotional patterns, however, the mechanism controlling MAO-A levels in the brain has remained unknown.
Now, a research team headed by Jun Aruga at the RIKEN Brain Science Institute has shown for the first time that a ligase named Rines (RING finger-type E3 ubiquitin ligase) regulates these levels. Their research shows that mice without the Rines gene exhibit impaired stress responses and enhanced anxiety, controlled in part through the regulation of MAO-A levels. The study is published today in Journal of Neuroscience.
As the first study to demonstrate regulation of MAO-A protein via the ubiquitin proteasomal system, this research presents a promising new avenue for analyzing the role of MAO-A in brain function. Further research promises insights into the treatment of anxiety, stress-related disorders and impaired social functions.
Reference:
Miyuki Kabayama, Kazuto Sakoori, Kazuyuki Yamada, Veravej G. Ornthanalai, Maya Ota, Naoko Morimura, Kei-ichi Katayama, Niall P. Murphy, and Jun Aruga. “Rines E3 Ubiquitin Ligase Regulates MAO-A Levels and Emotional Responses.” The Journal of Neuroscience, 2013.