Posts tagged neuroscience
Articles and news from the latest research reports.
Brain’s dynamic duel underlies win-win choices
People choosing between two or more equally positive outcomes experience paradoxical feelings of pleasure and anxiety, feelings associated with activity in different regions of the brain, according to research led by Amitai Shenhav, an associate research scholar at the Princeton Neuroscience Institute at Princeton University.
In one experiment, 42 people rated the desirability of more than 300 products using an auction-like procedure. Then they looked at images of paired products with different or similar values and were asked to choose between them. Their brain activity was scanned using functional magnetic resonance imaging (fMRI). After the scan, participants reported their feelings before and during each choice. They received one of their choices at the end of the study.
Choices between two highly valued items (high-high), such as a digital camera and a camcorder, were associated with the most positive feelings and the greatest anxiety, compared with choices between items of low value (low-low), like a desk lamp and a water bottle, or between items of different values (low-high). Functional MRI scans showed activity in two regions of the brain, the striatum and the prefrontal cortex, both known to be involved in decision-making. Interestingly, lower parts of both regions were more active when subjects felt excited about being offered the choice, while activity in upper parts was strongly tied to feelings of anxiety.
This evidence that parallel brain circuits are associated with opposing emotional reactions helps to answer a puzzling question, according to Shenhav: “Why isn’t our positivity quelled by our anxiety, or our anxiety quelled by the fact that we’re getting this really good thing at the end? This suggests that it’s because these circuits evolved for two different reasons,” he said. “One of them is about evaluating the thing we’re going to get, and the other is about guiding our actions and working out how difficult the choice will be.”
The study, “Neural correlates of dueling affective reactions to win-win choices,” was published July 14 in the Proceedings of the National Academy of Sciences. Shenhav conducted the research as a graduate student at Harvard University, along with Professor of Psychology and Neuroscience Randy Buckner, the study’s senior author.
A second fMRI experiment showed that the same patterns of emotional reactions and brain activity persisted even when the participants were told before each choice how similarly they had valued the items. Their anxiety didn’t abate, despite knowing how little they stood to lose by making a “wrong” choice. In a third experiment, Shenhav and Buckner tested whether giving people more than two choices increased their levels of anxiety. Indeed, they found that providing six options led to higher levels of anxiety than two options, particularly when all six of the options were highly valued items. But positive feelings about being presented with the choice were similar for two or six options.
This suggests that the anxiety stems from the conflict of making the decision, rather than the opportunity cost of the choice — an economic concept that refers to the lost value of the second-best option. The opportunity cost should be the same, regardless of the number of choices. In addition, subjects in this final study were given an unlimited amount of time to make a decision, compared with 1.5 seconds in the first two studies. The results showed that time pressure was not the main source of anxiety during the choices.
At the end of each study, participants had a surprise opportunity to reverse their earlier choices. Higher activity in a part of the brain called the anterior cingulate cortex around the time of an initial choice predicted whether that decision would later be reversed. Previous work has shown that this brain region is involved in assessing how conflicted an individual feels over a particular choice; this result suggests that some choices may have continued to elicit conflict after the participant made a decision, Shenhav said. The researchers also found that people who reported more anxiety in their daily lives were more likely to change their minds.
This work could explain why ostensibly positive options can evoke a mixture of positive and negative responses, which are not explained by purely economic analyses of choice. “Rationally, there’s no reason why when you put one good thing with another good thing, you should feel worse about the situation,” said Brian Knutson, an associate professor of psychology and neuroscience at Stanford University, who is familiar with the work but was not involved in it. “The neuroimaging tells us that these different mechanisms are fighting with each other,” he said. “Understanding that dynamic can help us understand why decisions that we think should make us feel better can actually make us feel worse.”
According to Shenhav, this research could shed light on the neural processes that can make more momentous choices so paralyzing for some people — for instance, deciding where to go to college or which job offer to take. But he admits that even more trivial decisions can be tough for him. “I probably experience more win-win choice anxiety than the average person,” he said. “I’m even terrible at choosing where to eat dinner.”
Choice bias: A quirky byproduct of learning from reward
The price of learning from rewarding choices may be just a touch of self-delusion, according to a new study in Neuron.
The research by Brown University brain scientists links a fundamental problem in neuroscience called “credit assignment” — how the brain reinforces learning only in the exact circuits that caused the rewarding choice — to an oft-observed quirk of behavior called “choice bias” – we value the rewards we choose more than equivalent rewards we don’t choose. The researchers used computational modeling and behavioral and genetic experiments to discover evidence that choice bias is essentially a byproduct of credit assignment.
“We weren’t looking to explain anything about choice bias to start off with,” said lead author Jeffrey Cockburn, a graduate student in the research group of senior author Michael Frank, associate professor of cognitive, linguistic, and psychological sciences. “This just happened to be the behavioral phenomenon we thought would emerge out of this credit assignment model.”
So the next time a friend raves about the movie he chose and is less enthusiastic about the just-as-good one that you chose, you might be able to chalk it up to his basic learning circuitry and a genetic difference that affects it.
Modeled mechanism
The model, developed by Frank, Cockburn, and co-author Anne Collins, a postdoctoral researcher, was based on prior research on the function of the striatum, a part of the brain’s basal ganglia (BG) that is principally involved in representing reward values of actions and picking one. “An interaction between three key BG regions moderates that decision-making process. When a rewarding choice has been made, the substantia nigra pars compacta (SNc) releases dopamine into the striatum to reinforce connections between cortex and striatum, so that rewarded actions are more likely to be repeated. But how does the SNc reinforce just the circuits that made the right call? The authors proposed a mechanism by which another part of the subtantia nigra, the SNr, detects when actions are worth choosing and then simultaneously amplifies any dopamine signal coming from the SNc.”
“The novel part here is that we have proposed a mechanism by which the BG can detect when it has selected an action and should therefore amplify the dopamine reinforcing event specifically at that time,” Frank said. “When the SNr decides that striatal valuation signals are strong enough for one action, it releases the brakes not only on downstream structures that allow actions to be executed, but also on the SNc dopamine system, so any unexpected rewards are amplified.”
Specifically, dopamine provides reinforcement by enhancing the responsiveness of connections between cells so that a circuit can more easily repeat its rewarding behavior in the future. But along with that process of reinforcing the action of choosing, the value placed on the resulting reward becomes elevated compared to rewards not experienced this way.
Experimental evidence
That prediction seemed intriguing, but it still had to be tested. The authors identified both behavioral and genetic tests that would be telling.
They recruited 80 people at Brown and elsewhere in Providence to play a behavioral game and to donate some saliva for genetic testing.
The game first presented the subjects pictures of arbitrary Japanese characters that would have different probabilities of rewards if chosen ranging from a 20 percent to 80 percent chance of winning a point or losing a point. For some characters, the player could choose a character to discover its resulting reward or penalty, whereas for others, its result was simply given to them. After that learning phase, the subjects were then presented the characters in pairs and instructed to pick the one they thought had the highest chance of winning based on what they had learned.
The researchers built the game so that for every character a player could choose, there was an equally rewarding one that had merely been given to them. On average, players showed a clear choice bias in that they were more likely to prefer rewarding characters that they had chosen over equally rewarding characters they had been given.
Notably, they exhibited no choice bias between unrewarding characters suggesting that choice bias emerges only in relation to reward, one of the key predictions of their model. But they wanted to test further whether the impact of reward on choice bias was related to the proposed biological mechanism, that striatal dopaminergic learning is enhanced to chosen rewards.
The genetic tests focused on single-letter differences in a gene called DARPP-32, which governs how well cells in the striatum respond to the reinforcing influence of dopamine.
People with one version of the gene have been shown in previous research to be less able to learn from rewards, while people with other versions were less driven by reward in learning.
“The reason why this gene is interesting is because we know something about the biology of what it does and where it is expressed in the brain,” Frank said. “It’s predominant in the striatum and specifically affects synaptic plasticity induced by dopamine signaling. It’s related to the imbalance by which you learn from really good things or not so good things.
“The logic was if the mechanism that we think describes this choice bias and credit assignment problem is accurate then that gene should predict the impact of how good something was on this choice bias phenomenon,” he said.
Indeed, that’s what the data showed. People with the form of the gene that predisposed them to be responsive to big rewards also showed more choice bias from the most strongly rewarded characters. Interestingly, the other people also showed choice bias, but more strongly for those characters that were more mediocre. This pattern was mirrored by the authors’ model when it simulated the effects of DARPP-32 on reward learning imbalances from positive vs. negative outcomes.
For some people, the plums are sweeter if they picked them.
(Image caption: Granule cells connect with other cells via long projections (dendrites). The actual junctions (synapses) are located on thorn-like protuberances called “spines”. Spines are shown in green in the computer reconstruction. Credit: DZNE/Michaela Müller)
A protein couple controls flow of information into the brain’s memory center
Neuroscientists in Bonn and Heidelberg have succeeded in providing new insights into how the brain works. Researchers at the DZNE and the German Cancer Research Center (DKFZ) analyzed tissue samples from mice to identify how two specific proteins, ‘CKAMP44’ and ‘TARP Gamma-8’, act upon the brain’s memory center. These molecules, which have similar counterparts in humans, affect the connections between nerve cells and influence the transmission of nerve signals into the hippocampus, an area of the brain that plays a significant role in learning processes and the creation of memories. The results of the study have been published in the journal Neuron.
Brain function depends on the active communication between nerve cells, known as neurons. For this purpose, neurons are woven together into a dense network where they constantly relay signals to one another. However, neurons do not form direct contacts with each other. Instead they are separated by an extremely narrow gap, known as the synapse. This gap is bridged by ‘neurotransmitters’, which carry nerve signals from one cell to the next.
Docking stations
Specific molecular complexes in the cell’s outer shell, so-called ‘receptors’, receive the signal by binding the neurotransmitters. This triggers an electrical impulse in the receptor-bearing cell and thus the nerve signal has moved on one neuron further.
In the current study, a team led by Dr Jakob von Engelhardt focused on the AMPA receptors. These bind the neurotransmitter glutamate and are particularly common in the brain. “We looked at AMPA receptors in an area of the brain, which constitutes the main entrance to the hippocampus,” explains von Engelhardt, who works for the DZNE and DKFZ. “The hippocampus is responsible for learning and memory formation. Among other things it processes and combines sensory perception. We therefore asked ourselves how the flow of information into the hippocampus is controlled.”
A pair of helpers
Dr von Engelhardt’s research team specifically focused on two protein molecules: ‘CKAMP44’ and ‘TARP Gamma-8’. These proteins are present, along with AMPA receptors, in the ‘granule’ cells, which are neurons that receive signals from areas outside of the hippocampus. It was already known that these proteins form protein complexes with AMPA receptors. “We have now found out that they exert a significant influence on the functioning of glutamate receptors. Each in its own way, as chemically they are completely different,” says the neuroscientist. “We identified that the ability of a nerve cell to receive signals doesn’t depend solely on the actual receptors; CKAMP44 and TARP Gamma-8 are just as important. Their function cannot be separated from that of the receptors.”
This was the result of an analysis in which the researchers compared brain tissue from mice with a natural genotype with brain tissue from genetically modified mice. Neurons in the genetically modified animals were not able to produce either CKAMP44 or TARP Gamma-8 or both.
Long-term effect
The researchers discovered, among other things, that both proteins promote the transportation of glutamate receptors to the cell surface. “This means they influence how receptive the nerve cell is to incoming signals,” says von Engelhardt.
However, the number of receptors and thus the signal reception can be altered by neuronal activity. The von Engelhardt group found that in this regard the auxiliary molecules have different effects: TARP Gamma-8 is essential to ensure that more AMPA receptors are integrated into the synapse following a plasticity induction protocol, whereas CKAMP44 plays no role in this context. “Synapses alter their communication depending on their activity. This ability is called plasticity. Some of the changes involved are only temporary, others may last longer,” explains von Engelhardt. “TARP Gamma-8 influences long-term plasticity. It makes the cell able to strengthen synaptic communication for a prolonged time-period. The larger the number of receptors on the receiving side of the synapse, the better the neuronal connection.”
The number of receptors doesn’t change suddenly, but remains largely stable for a certain amount of time. “This condition may last for hours, days or even longer. This long-term effect is essential for the creation of memories. We can only remember things if the connections between neurons undergo a long-lasting change,” says the scientist.
Fast sequence of signals
However, CKAMP44 and TARP Gamma-8 also act over shorter periods of time. The research team discovered that the molecules affect how quickly the AMPA receptors return to a receptive state. “If glutamate has docked on to a receptor, it takes a while until the receptor can react to the next neurotransmitter. CKAMP44 lengthens this period. In contrast, TARP Gamma-8 helps the receptor to recover more quickly,” says von Engelhardt.
Hence, CKAMP44 temporarily weakens the synaptic connection, while TARP Gamma-8 strengthens it. Through the interplay of these proteins the synapse is able to tune its sensitivity to a specific level. This condition can last from milliseconds to a few seconds before the strength of the connection is again adapted. Specialists refer to this as “short-term plasticity”.
“These molecules ultimately influence how well the nerve cell is able to react to a rapid succession of signals,” the scientist summarises the findings. “Such a rapid firing enables neuronal networks to synchronize their activity, which is a common process in the brain.”
Sensitive balance
Much to the researchers’ surprise, it turned out that the two proteins influence not only the synapse but also the shape of the nerve cells. In the absence of these auxiliary molecules, the neurons have fewer dendrites to establish contact with other nerve cells. “The organism can use CKAMP44 and TARP Gamma-8 molecules to regulate neuronal connections in a number of ways,” von Engelhardt says. “This ability depends on the balance between the partners, as to some extent they have a contrary effect. The way in which the neurons of the hippocampus react to signals from other regions of the brain is therefore highly dependent on the presence and the expression ratio of these molecules.”
Since the two molecules act directly on the structure and function of synapses of granule cells, Jakob von Engelhardt considers it probable that they also have an influence on learning and memory.
Researchers find new mechanism for neurodegeneration
A research team led by Jackson Laboratory Professor and Howard Hughes Investigator Susan Ackerman, Ph.D., has pinpointed a surprising mechanism behind neurodegeneration in mice, one that involves a defect in a key component of the cellular machinery that makes proteins, known as transfer RNA or tRNA.
The researchers report in the journal Science that a mutation in a gene that produces tRNAs operating only in the central nervous system results in a “stalling” or pausing of the protein production process in the neuronal ribosomes. When another protein the researchers identified, GTPBP2, is also missing, neurodegeneration results.
“Our study demonstrates that individual tRNA genes can be tissue-specifically expressed in vertebrates,” Ackerman says, “and mutations in such genes may cause disease or modify other phenotypes. This is a new area to look for disease mechanisms.”
Neurodegeneration—the process through which mature neurons decay and ultimately die—is poorly understood, yet it underlies major human diseases, such as Alzheimer’s disease, Parkinson’s disease, Huntington’s disease and ALS (amyotrophic lateral sclerosis, also known as Lou Gehrig’s disease).
While the causes of neurodegeneration are still coming to light, there is mounting evidence that neurons are exquisitely sensitive—much more so than other types of cells—to disruptions in how proteins are made and how they fold.
tRNAs are critical in translating the genetic code into proteins, the workhorses of the cell. tRNAs possess a characteristic cloverleaf shape with two distinct “business” ends—one that reads out the genetic code in three-letter increments (or triplets), and another that transports the protein building block specified by each triplet (known as an amino acid).
In higher organisms, tRNAs are strikingly diverse. For example, while there are 61 distinct triplets that are recognized by tRNAs in humans, the human genome contains roughly 500 tRNA genes. To date little is known about why they are so numerous, whether they carry out overlapping or redundant functions, or whether they possibly have roles beyond the making of proteins.
“Multiple genes encode almost all tRNA types,” Ackerman says. “In fact, AGA codons are decoded by five tRNAs in mice. Until now, this apparent redundancy has caused us to completely overlook the disease-causing potential of mutations in tRNAs, as well as other repetitive genes.”
Ackerman and her colleagues at The Jackson Laboratory in Bar Harbor, Maine, and Farmington, Conn., The Scripps Research Institute in LaJolla, Calif., and Kumamoto University in Japan pinpointed a mutation in the tRNA gene n-Tr20 as a genetic culprit behind the neurodegeneration observed in mice lacking GTPBP2.
Remarkably, the tRNA’s activity is confined to the brain and other parts of the central nervous system, in both mice and humans. The tRNA encoded by n-Tr20 recognizes the triplet code, AGA (which specifies the amino acid arginine).
The n-Tr20 defect disrupts how proteins are made. Specifically, it causes the “factories” responsible for synthesizing proteins, called ribosomes, to stall when they encounter an AGA triplet.
Such stalling can be largely overcome, thanks to the work of a partner protein called GTPBP2. But when this partner is missing—as it is in the mutant mice that Ackerman and her colleagues studied—the stalling intensifies. This is thought to be a driving force behind the neurodegeneration seen in these mice.
(Source: jax.org)
Neymar’s brain on auto-pilot
Brazilian superstar Neymar’s brain activity while dancing past opponents is less than 10 per cent the level of amateur players, suggesting he plays as if on auto-pilot, according to Japanese neurologists.
Results of brain scans conducted on Neymar indicate minimal cerebral function when he rotates his ankle and point to the Barcelona striker’s wizardry being uncannily natural.
"From MRI images, we discovered Neymar’s brain activity to be less than 10 per cent of an amateur player," researcher Eiichi Naito said on Friday.
"It is possible genetics is a factor, aided by the type of training he does."
The findings were published in the Swiss journal Frontiers in Human Neuroscience following a series of motor skills tests carried out on the 22-year-old Neymar and several other athletes in Barcelona in February.
(Image: Sergio Moraes / REUTERS)
Targeting the brain to treat obesity
Unlocking the secrets to better treating the pernicious disorders of obesity and dementia reside in the brain, according to a paper from American University’s Center for Behavioral Neuroscience. In the paper, researchers make the case for treating obesity with therapies aimed at areas of the brain responsible for memory and learning. Furthermore, treatments that focus on the hippocampus could play a role in reducing certain dementias.
"In the struggle to treat these diseases, therapies and preventive measures often fall short. This is a new way for providers who treat people with weight problems and for researchers who study dementias to think about obesity and cognitive decline," said Prof. Terry Davidson, center director and lead study author.
In the paper, published in the journal Physiology & Behavior, Davidson and colleague Ashley A. Martin review research findings linking obesity with cognitive decline, including the center’s findings about the “vicious cycle” model, which explains how weight-challenged individuals who suffer from particular kinds of cognitive impairment are more susceptible to overeating.
Obesity, Memory Deficits and Lasting Effects
It is widely accepted that overconsumption of dietary fats, sugar and sweeteners can cause obesity. These types of dietary factors are also linked to cognitive dysfunction. Foods that are risk factors for cognitive impairment (i.e., foods high in saturated fats and simple carbohydrates that make up the modern Western diet) are so widespread and readily available in today’s food environment, their consumption is all but encouraged, Davidson said.
Across age groups, evidence reveals links between excess food intake, body weight and cognitive dysfunction. Childhood obesity and consumption of the Western diet can have lasting effects, as seen through the normal aging process, cognitive deficits and brain pathologies. Several analyses of cases of mild cognitive impairment progressing to full-blown cases of Alzheimer’s disease show that the first signs of brain disease can occur at least 50 years prior to the emergence of serious cognitive dysfunction. These signs originate in the hippocampus, the area of the brain where memory, learning, decision making, behavior control and other cognitive functions come into play.
Still, most research on the role of the brain in obesity focuses on areas thought to be involved with hunger motivation (e.g., hypothalamus), taste (e.g., brain stem), reinforcement (e.g., striatum) and reward (e.g., nucleus accumbens) or with hormonal or metabolic disorders. This research has not yet been successful in generating therapies that are effective in treating or preventing obesity, Davidson says.
Vicious Cycle
Experiments in rats by Davidson and colleagues show that overconsumption of the Western diet can damage or change the blood-brain barrier, the tight network of blood vessels protecting the brain and substrates for cognition. Certain kinds of dementias are known to arise from the breakdown in these brain substrates.
"Breakdown in the blood-brain barrier is more rationale for treating obesity as a learning and memory disorder," Davidson said. "Treating obesity successfully may also reduce the incidence of dementias, because the deterioration in the brain is often produced by the same diets that promote obesity."
The “vicious cycle” model AU researchers put forth says eating a Western diet high in saturated fats, sugar and simple carbohydrates produces pathologies in brain structures and circuits, ultimately changing brain pathways and disrupting cognitive abilities.
It works like this: People become less able to resist temptation when they encounter environmental cues (e.g., food itself or the sight of McDonald’s Golden Arches) that remind them of the pleasures of consumption. They then eat more of the same type of foods that produce the pathological changes in the brain, leading to progressive deterioration in those areas and impairments in cognitive processes important for providing control over one’s thoughts and behaviors. These cognitive impairments can weaken a person’s ability to resist thinking about food, making them more easily distracted by food cues in the environment and more susceptible to overeating and weight gain.
"People have known at least since the time of Hippocrates that one key to a healthy life is to eat in moderation. Yet many of us are unable to follow that good advice," Davidson said. "Our work suggests that new therapeutic interventions that target brain regions involved with learning and memory may lead to success in controlling both the urge to eat, as well as the undesirable consequences produced by overeating."
(Source: eurekalert.org)
Missing sleep may hurt your memory
Lack of sleep, already considered a public health epidemic, can also lead to errors in memory, finds a new study by researchers at Michigan State University and the University of California, Irvine.
The study, published online in the journal Psychological Science, found participants deprived of a night’s sleep were more likely to flub the details of a simulated burglary they were shown in a series of images.
Distorted memory can have serious consequences in areas such as criminal justice, where eyewitness misidentifications are thought to be the leading cause of wrongful convictions in the United States.
“We found memory distortion is greater after sleep deprivation,” said Kimberly Fenn, MSU associate professor of psychology and co-investigator on the study. “And people are getting less sleep each night than they ever have.”
The Centers for Disease Control and Prevention calls insufficient sleep an epidemic and said it’s linked to vehicle crashes, industrial disasters and chronic diseases such as hypertension and diabetes.
The researchers conducted experiments at MSU and UC-Irvine to gauge the effect of insufficient sleep on memory. The results: Participants who were kept awake for 24 hours – and even those who got five or fewer hours of sleep – were more likely to mix up event details than participants who were well rested.
“People who repeatedly get low amounts of sleep every night could be more prone in the long run to develop these forms of memory distortion,” Fenn said. “It’s not just a full night of sleep deprivation that puts them at risk.”
Study Links Autistic Behaviors to Enzyme
Fragile X syndrome (FXS) is a genetic disorder that causes obsessive-compulsive and repetitive behaviors, and other behaviors on the autistic spectrum, as well as cognitive deficits. It is the most common inherited cause of mental impairment and the most common cause of autism.
Now biomedical scientists at the University of California, Riverside have published a study that sheds light on the cause of autistic behaviors in FXS. Appearing online today (July 23) in the Journal of Neuroscience, and highlighted also on the cover in this week’s print issue of the journal, the study describes how MMP-9, an enzyme, plays a critical role in the development of autistic behaviors and synapse irregularities, with potential implications for other autistic spectrum disorders.
MMP-9 is produced by brain cells. Inactive, it is secreted into the spaces between cells of the brain, where it awaits activation. Normal brains have quite a bit of inactive MMP-9, and the activation of small amounts has significant effects on the connections between neurons, called synapses. Too much MMP-9 activity causes synapses in the brain to become unstable, leading to functional deficits.
“Our study targets MMP-9 as a potential therapeutic target in Fragile X and shows that genetic deletion of MMP-9 favorably impacts key aspects of FXS-associated anatomical alterations and behaviors in a mouse model of Fragile X,” said Iryna Ethell, a professor of biomedical sciences in the UC Riverside School of Medicine, who co-led the study. “We found that too much MMP-9 activity causes synapses to become unstable, which leads to functional deficits that depend on where in the brain that occurs.”
Ethell explained that mutations in FMR1, a gene, have been known for more than a decade to cause FXS, but until now it has been unclear how these mutations cause unstable synapses and characteristic physical features of this disorder. The new findings expand on earlier work by the research group that showed that an MMP-9 inhibitor, minocycline, can reduce behavioral aspects of FXS, which then led to its use to treat FXS.
To further establish a causative role for MMP-9 in the development of FXS-associated features, including autistic behaviors, the authors generated mice that were missing both FMR1 and MMP-9. They found that while mice with a single FMR1 mutation showed autistic behaviors and macroorchidism (abnormally large testes), mice that also lacked MMP-9 showed no autistic behaviors.
“Our work points directly to MMP-9 over-activation as a cause for synaptic irregularities in FXS, with potential implications for other autistic spectrum disorders and perhaps Alzheimer’s disease,” said Doug Ethell, the head of Molecular Neurobiology at the Western University of Health Sciences, Pomona, Calif., and a coauthor on the study.
The research paper represents many years of bench work and effort by a dedicated team led by the Ethells. The work was primarily done in mice, but human tissue samples were also analyzed, with findings found to be consistent. Specifically, the work involved assessing behaviors, biochemistry, activity and anatomy of synaptic connections in the brain of a mouse model of FXS, as well as the creation of a new mouse line that lacked both the FXS gene and MMP-9.
FXS affects both males and females, with females often having milder symptoms than males. It is estimated that about 1 in 5,000 males are born with the disorder.
The Ethells were joined in the study by UCR’s Harpreet Sidhu (first author of the research paper), Lorraine E. Dansie, and Peter Hickmott. Sidhu and Dansie are neuroscience graduate students; Hickmott is an associate professor of psychology.
Next, the researchers plan to understand how MMP-9 regulates synapse stability inside the neurons. They also plan to find drugs that specifically target MMP-9 without side effects such as new tetracycline derivatives that are potent inhibitors of MMP-9 but lack antibiotic properties.
“Although minocycline was successfully used in clinical trial in FXS, it has some side effects associated with its antibiotic properties, such gastrointestinal irritation,” Iryna Ethell said. “We, therefore, plan to test new non-antibiotic minocycline derivatives. These compounds lack antibiotic activity but still act as non-competitive inhibitors of MMP-9 similar to minocycline.”
Rhymes can inspire reasoning during the third trimester in the womb
Mozart, Beethoven or even Shakespeare — pregnant mothers have been known to expose their babies to many forms of auditory stimulation. But according to researchers at the University of Florida, all a baby really needs is the music of mom’s voice.
Research published in the most recent issue of the journal Infant Behavior and Development shows that babies in utero begin to respond to the rhythm of a nursery rhyme — showing evidence of learning — by 34 weeks of pregnancy and are capable of remembering a set rhyme until just prior to birth. Nursing researcher Charlene Krueger and her team studied pregnant women who recited a rhyme to their babies three times a day for six weeks, beginning at 28 weeks’ gestational age, which is the start of the third trimester of pregnancy.
“The mother’s voice is the predominant source of sensory stimulation in the developing fetus,” said Krueger, an associate professor in the UF College of Nursing. “This research highlights just how sophisticated the third trimester fetus really is and suggests that a mother’s voice is involved in the development of early learning and memory capabilities. This could potentially affect how we approach the care and stimulation of the preterm infant.”
Krueger’s team recruited 32 pregnant women during their 28th week of pregnancy, as determined by fetal ultrasound. The participants were between 18 and 39 years of age, spoke English as a primary language and were pregnant with their first baby. Once recruited, the women were randomly assigned to either an experimental or a control group. The mean age of the women in the group was 25. In addition, 68 percent of the women were white, 28 percent were black and 4 percent were of another race or ethnicity.
From 28 to 34 weeks of pregnancy, all mothers in the study recited a passage or nursery rhyme out loud twice a day and then came in for testing at 28, 32, 33 and 34 weeks’ gestation. To determine whether the fetus could remember the pattern of speech at 34 weeks of age, all mothers were asked to stop speaking the passage. Then the fetuses were tested again at 36 and 38 weeks’ gestational age.
During testing, researchers used a fetal heart monitor, similar to what is used during traditional labor and delivery, to record heart rate and determine any changes. Researchers interpret a small heart rate deceleration in the fetus as an indicator of learning or familiarity with a stimulus.
At testing, the fetuses in the experimental group were played a recording of the same rhyme their mother had been reciting at home but spoken by a female stranger. Those in the control group heard a different rhyme also spoken by a stranger. This was to help determine if the fetus was responding simply to its mother’s voice or to a familiar pattern of speech, which is a more difficult task, Krueger said.
The researchers found that the fetus’ heart rate began to respond to the familiar rhyme recited by a stranger’s voice by 34 weeks of gestational age — once the mother had spoken the rhyme out loud at home for six weeks. They continued to respond with a small cardiac deceleration for as long as four weeks after the mother had stopped saying the rhyme until about 38 weeks. At 38 weeks, there was a statistically significant difference between the two groups in responding to the strangers’ recited rhymes — the experimental group who heard the original rhyme responded with a deeper and more sustained cardiac deceleration, whereas the control group who heard a new rhyme responded with a cardiac acceleration.
Further research is needed to more fully understand how ongoing development affects learning and memory, Krueger said. Her aim is to recognize how this type of research can influence care in preterm infants and their long-term outcomes.
“This study helped us understand more about how early a fetus could learn a passage of speech and whether the passage could be remembered weeks later even without daily exposure to it,” Krueger said. “This could have implications to those preterm infants who are born before 37 weeks of age and the impact an intervention such as their mother’s voice may have on influencing better outcomes in this high-risk population.”
(Source: news.ufl.edu)
Children as young as three recognise ‘cuteness’ in faces of people and animals
Children as young as three are able to recognise the same ‘cute’ infantile facial features in humans and animals which encourage caregiving behaviour in adults, new research has shown.
A study investigating whether youngsters can identify baby-like characteristics – a set of traits known as the ‘baby schema’ – across different species has revealed for the first time that even pre-school children rate puppies, kittens and babies as cuter than their adult counterparts.
The discovery that young children are influenced by the baby schema – a round face, high forehead, big eyes and a small nose and mouth – is a significant step towards understanding why humans are more attracted to infantile features, the study authors believe.
The baby schema has been proven to engender protective, care-giving behaviour and a decreased likelihood of aggression toward infants from adults.
The research was carried out by PhD student Marta Borgi and Professor Kerstin Meints, members of the Evolution and Development Research Group in the School of Psychology at the University of Lincoln, UK.
Marta said: “This study is important for several reasons. We already knew that adults experience this baby schema effect, finding babies with more infantile features cuter.
“Our results provide the first rigorous demonstration that a visual preference for these traits emerges very early during development. Independently of the species viewed, children in our study spent more time looking at images with a higher degree of these baby-like features.
“Interestingly, while participants gave different cuteness scores to dogs, cats and humans, they all found the images of adult dog faces cuter than both adult cats and human faces.”
The researchers carried out two experiments with children aged between three and six years old: one to track eye movements to see which facial areas the children were drawn to, and a second to assess how cute the children rated animals and humans with infantile traits.
Pictures of human adults and babies, dogs, puppies, cats and kittens were digitally manipulated to appear ‘cuter’ by applying baby schema characteristics. The same source images were also made less cute by giving the subjects more adult-like features: a narrow face, low forehead, small eyes, and large nose and mouth – making this study more rigorous than previous work.
The children rated how cute they thought each image was and their eye movements were analysed using specialist eye-tracking software developed by the University of Lincoln.
The research could also lead to improved education in teaching children about safe behaviour with dogs.
Professor Kerstin Meints, Professor in Developmental Psychology at Lincoln’s School of Psychology, supervised the research.
She said: “We have also demonstrated that children are highly attracted to dogs and puppies, and we now need to find out if that attractiveness may override children’s ability to recognise stress signalling in dogs.”
“This study will also lead to further research with an impact on real life, namely whether the ‘cuteness’ of an animal in rescue centres makes them more or less likely to be adopted.”
This research was published in the scientific journal Frontiers in Psychology.