Posts tagged psychology

ScienceDaily (July 6, 2012) — In a forthcoming issue of Topics in Cognitive Science researchers from the University of Amsterdam (UvA) argue that at least two, seemingly trivial musical skills can be considered fundamental to the evolution of music: relative pitch — the skill to recognise a melody independent of its pitch level — and beat induction — the skill to pick up regularity (the beat) from a varying rhythm. Both are considered cognitive mechanisms that are essential to perceive, make and appreciate music, and, as such, could be argued to be conditional to the origin of music.

While it recently became quite popular to address the study of the origins of music from an evolutionary perspective, there is still little agreement on the idea that music is in fact an adaptation, that it influenced our survival, or that it made us sexually more attractive. Music appears to be of little use. It doesn’t quell our hunger, nor do we live a day longer because of it. So why argue that music is an adaptation? There are even researchers who claim that studying the evolution of cognition is virtually impossible (Lewontin, 1998; Bolhuis & Wynne, 2009).

Distinguishing between music and musicality

The alternative that Henkjan Honing and Annemie Ploeger of the UvA propose is, first, to distinguish between the notion of ‘music’ and ‘musicality’, with musicality being defined as a natural, spontaneously developing trait based on and constrained by our cognitive system, and music as a social and cultural construct based on that very musicality. And secondly, to collect accumulative evidence from a variety of sources (e.g., psychological, physiological, genetic, phylogenetic, and cross-cultural evidence) to be able to show that a specific cognitive trait is indeed an adaptation.

Both relative pitch and beat induction are suggested as primary candidates for such cognitive traits, musical skills that are considered trivial by most humans, but that turn out to be quite special in the rest of the animal world.

Once these fundamental cognitive mechanisms are identified, it becomes possible to see how these might have evolved. In short: the study of the evolution of music cognition is conditional on a characterisation of the basic mechanisms that make up musicality.

Source: Science Daily

ScienceDaily (July 6, 2012) — If you’re concerned about losing your hearing because of noise exposure (earbud deafness syndrome), a new discovery published online in the FASEB Journal offers some hope. That’s because scientists from Germany and Canada show that the protein, AMPK, which protects cells during a lack of energy, also activates a channel protein in the cell membrane that allows potassium to leave the cell. This activity is important because this mechanism helps protect sensory cells in the inner ear from permanent damage following acoustic noise exposure.

This information could lead to new strategies and therapies to prevent and treat trauma resulting from extreme noise, especially in people with AMPK gene variants that may make them more vulnerable to hearing loss.

"Future research on the basis of the present study may lead to the development of novel strategies preventing noise-induced hearing loss or accelerating recovery from acoustic trauma," said Florian Lang, Ph.D., a researcher involved in the work from the Department of Physiology at the University of Tübingen, in Tübingen, Germany.

To make this discovery, Lang and colleagues compared two groups of mice. The first group was normal and the second lacked the AMPK protein. Hearing of the mice was tested by measuring sound-induced brain activity. All mice were exposed to well-defined noise causing an acoustic trauma and leading to hearing impairment. Prior to noise exposure, the hearing ability was similar in normal mice and mice lacking AMPK. After exposure, the hearing of the normal mice mostly recovered after two weeks, but the recovery of hearing in AMPK-deficient mice remained significantly impaired.

"When it comes to preventing hearing loss, keeping the volume down is still the best strategy, and this discovery doesn’t prevent loud music from beating on our ear drums," said Gerald Weissmann, M.D., Editor-in-Chief of the FASEB Journal. “This discovery does help explain why some people seem more likely to lose their hearing than others. At the same time, it also provides a target for new preventive strategies — and perhaps even a treatment — for earbud deafness syndrome.”

Source: Science Daily

July 6, 2012

(Medical Xpress) — Researchers decode a molecular mechanism that sheds light on how trauma can become engraved in the brain

Scientists at the Universities of Bonn and Berlin have discovered a mechanism which stops the process of forgetting anxiety after a stress event. In experiments they showed that feelings of anxiety don’t subside if too little dynorphin is released into the brain. The results can help open up new paths in the treatment of trauma patients. The study has been published in the current edition of the Journal of Neuroscience.

Feelings of anxiety very effectively prevent people from getting into situations that are too dangerous. Those who have had a terrible experience initially tend to avoid the place of tragedy out of fear. If no other oppressive situation arises, normally the symptoms of fear gradually subside. “The memory of the terrible events is not just erased.” states first author, PD Dr. Andras Bilkei Gorzo, from the Institute for Molecular Psychiatry at the University of Bonn. “Those impacted learn rather via an active learning process that they no longer need to be afraid because the danger has passed.” But following extreme psychical stress resulting from wars, hostage-takings, accidents or catastrophes chronic anxiety disorders can develop which even after months don’t subside.

Body’s own dynorphin weakens fears

Why is it that in some people terrible events are deeply engraved in their memory, while after a while others seem to have completely put aside any anxiety related to the incident? Scientists in the fields of psychiatry, molecular psychiatry and radiology at the University of Bonn are all involved in probing this issue. “We were able to demonstrate by way of a series of experiments that dynorphin plays an important role in weakening anxiety,” says Prof. Dr. Andreas Zimmer, Director of the Institute for Molecular Psychiatry at the University of Bonn. The substance group in question is opiods which also includes, for instance, endorphins. The latter are released by the body of athletes and have an analgesic and euphoric effect. The reverse, however, is true of dynorphins: They are known for putting a damper on emotional moods.

Mice with disabled gene exhibit persistent anxiety

The team working with Prof. Zimmer tested the exact impact of dynorphins on the brain using mice whose gene for the formation of this substance had been disabled. After being exposed to a brief and unpleasant electric shock, the animals exhibited persistent anxiety symptoms, even if they hadn’t been confronted with the negative stimulus over a longer time. Mice exhibiting a normal amount of released dynorphin were anxious to begin with as well, but the symptoms quickly subsided. “This behavior is the same in humans: If you burn your hand on the stove once, you don’t forget the incident that quickly,” explains Prof. Zimmer. “Learning vocabulary, on the other hand, typically tends to be more tedious because it’s not tied to emotions.”

Results are transferrable to people

Next the researchers showed that these results can be transferred to people. “We took advantage of the fact that people exhibit natural variations of the dynorphin gene that lead to different levels of this substance being released in the brain,” reports Prof. Dr. Henrik Walter, Director of the Research Area Mind and Brain at the Psychiatric University Clinic at the Charité in Berlin, who also used to perform research in this area at the University Clinic in Bonn. A total of 33 healthy probands were divided into two groups: One with the genetically stronger dynorphin release and the other which exhibits less gene activity.

Unpleasant stimulus leads to stress reactions in the probands

Equipped with computer glasses the probands observed blue and green squares which appeared and then disappeared again in a magnetic resonance tomograph (MRT). When the green square was visible the scientists repeatedly gave probands an unpleasant stimulus on the hand using a laser. Scientists were able to prove that these negative stimuli actually led to a stress reaction given the increased sweat on the skin. At the same time, researchers recorded the activities of various brain areas with the tomograph. After this conditioning stage came part two of the experiment: The researchers showed the colored squares without any unpleasant stimuli and recorded how long the stress reaction acquired earlier lasted. The next day the experiment was continued without the laser stimulus in an effort to monitor the longer-term development.

New paths in the treatment of trauma patients

It became apparent that, as in mice human, probands with lower gene activity for dynorphin exhibited stress reactions lasting considerably longer than those probands who released considerably more. Moreover, in brain scans it could be observed that the amygdala – a brain structure in the temporal lobes that processes emotional contents - was also active even if in later testing rounds a green square was shown without the subsequent laser stimulus.

“After the negative laser stimulus stopped this amygdala activity gradually became weaker. This means that the acquired anxiety reaction to the stimulus was forgotten,” reports Prof. Walter. This effect was not as pronounced in the group with less dynorphin activity and prolonged anxiety. “But the ‘forgetting’ of acquired anxiety reactions isn’t a fading, but, rather, an active process which involves the ventromedial prefrontal cortex,” emphasizes Prof. Walter. To corroborate this, researchers found that in the group with less dynorphin activity there was reduced coupling between the prefrontal cortex and the amygdala. “In all likelihood dynorphins affect fear forgetting in a crucial way through this structure,” says Prof. Walter. The scientists now hope that by using the results they will be able to develop long-term approaches for new strategies when it comes to the treatment of trauma patients.

Provided by University of Bonn

Source: medicalxpress.com

ScienceDaily (July 5, 2012) — A gene whose mutation results in malformed faces and skulls as well as mental retardation has been found by scientists.

They looked at patients with Potocki-Shaffer syndrome, a rare disorder that can result in significant abnormalities such as a small head and chin and intellectual disability, and found the gene PHF21A was mutated, said Dr. Hyung-Goo Kim, molecular geneticist at the Medical College of Georgia at Georgia Health Sciences University.

The scientists confirmed PHF21A’s role by suppressing it in zebrafish, which developed head and brain abnormalities similar to those in patients. “With less PHF21A, brain cells died, so this gene must play a big role in neuron survival,” said Kim, lead and corresponding author of the study published in The American Journal of Human Genetics. They reconfirmed the role by giving the gene back to the malformed fish — studied for their adeptness at regeneration — which then became essentially normal. They also documented the gene’s presence in the craniofacial area of normal mice.

While giving the normal gene unfortunately can’t cure patients as it does zebrafish, the scientists believe the finding will eventually enable genetic screening and possibly early intervention during fetal development, including therapy to increase PHF21A levels, Kim said. It also provides a compass for learning more about face, skull and brain formation.

The scientists zeroed in on the gene by using a distinctive chromosomal break found in patients with Potocki-Shaffer syndrome as a starting point. Chromosomes — packages of DNA and protein — aren’t supposed to break, and when they do, it can damage genes in the vicinity.

"We call this breakpoint mapping and the breakpoint is where the trouble is," said Dr. Lawrence C. Layman, study co-author and Chief of the MCG Section of Reproductive Endocrinology, Infertility and Genetics. Damaged genes may no longer function optimally; in PHF21A’s case it’s about half the norm.

"When you see the chromosome translocation, you don’t know which gene is disrupted," Layman said. "You use the break as a focus then use a bunch of molecular techniques to zoom in on the gene." Causes of chromosomal breaks are essentially unknown but likely are environmental and/or genetic, Kim said.

Little was known about PHF21A other than its role in determining how tightly DNA is wound in a package with proteins called histones. How tightly DNA is wound determines whether proteins called transcription factors have the access needed to regulate gene expression, which is important, for example, when a gene needs to be expressed only at a specific time or tissue. PHF21A is believed to primarily work by suppressing other genes, for example, ensuring that genes that should be expressed only in brain cells don’t show up in other cell types, Kim said.

Next steps include using PHF21A as a sort of geographic positioning system to identify other “depressor” genes it regulates then screening patients to look for mutations in those genes as well. “We want to find other people with different genes causing the same problem,” Layman said, and they suspect the genes PHF21A interacts with or regulates are the most likely suspects. It’s too early to know what percentage of Potocki-Shaffer syndrome patients have the PHF21A mutation, Kim noted. “Now that we know the causative gene, we can sequence the gene in more patients and see if they have a mutation,” Layman said.

They also want to look at less-severe forms of mental deficiency, including autism, for potentially milder mutations of PHF21A. More than a dozen of the 25,000 human genes are known to cause craniofacial defects and mental retardation, which often occur together, Kim said.

Source: Science Daily

ScienceDaily (July 5, 2012) — Sensory substitution devices (SSDs) use sound or touch to help the visually impaired perceive the visual scene surrounding them. The ideal SSD would assist not only in sensing the environment but also in performing daily activities based on this input. For example, accurately reaching for a coffee cup, or shaking a friend’s hand. In a new study, scientists trained blindfolded sighted participants to perform fast and accurate movements using a new SSD, called EyeMusic. Their results are published in the July issue of Restorative Neurology and Neuroscience.

Left: An illustration of the EyeMusic SSD, showing a user with a camera mounted on the glasses, and scalp headphones, hearing musical notes that create a mental image of the visual scene in front of him. He is reaching for the red apple in a pile of green ones. Top right: close-up of the glasses-mounted camera and headphones; bottom right: hand-held camera pointed at the object of interest. (Credit: Maxim Dupliy, Amir Amedi and Shelly Levy-Tzedek)

The EyeMusic, developed by a team of researchers at the Hebrew University of Jerusalem, employs pleasant musical tones and scales to help the visually impaired “see” using music. This non-invasive SSD converts images into a combination of musical notes, or “soundscapes.”

The device was developed by the senior author Prof. Amir Amedi and his team at the Edmond and Lily Safra Center for Brain Sciences (ELSC) and the Institute for Medical Research Israel-Canada at the Hebrew University. The EyeMusic scans an image and represents pixels at high vertical locations as high-pitched musical notes and low vertical locations as low-pitched notes according to a musical scale that will sound pleasant in many possible combinations. The image is scanned continuously, from left to right, and an auditory cue is used to mark the start of the scan. The horizontal location of a pixel is indicated by the timing of the musical notes relative to the cue (the later it is sounded after the cue, the farther it is to the right), and the brightness is encoded by the loudness of the sound.

The EyeMusic’s algorithm uses different musical instruments for each of the five colors: white (vocals), blue (trumpet), red (reggae organ), green (synthesized reed), yellow (violin); Black is represented by silence. Prof. Amedi mentions that “The notes played span five octaves and were carefully chosen by musicians to create a pleasant experience for the users.” Sample sound recordings are available at http://brain.huji.ac.il/em/.

"We demonstrated in this study that the EyeMusic, which employs pleasant musical scales to convey visual information, can be used after a short training period (in some cases, less than half an hour) to guide movements, similar to movements guided visually," explain lead investigators Drs. Shelly Levy-Tzedek, an ELSC researcher at the Faculty of Medicine, Hebrew University, Jerusalem, and Prof. Amir Amedi. "The level of accuracy reached in our study indicates that performing daily tasks with an SSD is feasible, and indicates a potential for rehabilitative use."

The study tested the ability of 18 blindfolded sighted individuals to perform movements guided by the EyeMusic, and compared those movements to those performed with visual guidance. At first, the blindfolded participants underwent a short familiarization session, where they learned to identify the location of a single object (a white square) or of two adjacent objects (a white and a blue square).

In the test sessions, participants used a stylus on a digitizing tablet to point to a white square located either in the north, the south, the east or the west. In one block of trials they were blindfolded (SSD block), and in the other block (VIS block) the arm was placed under an opaque cover, so they could see the screen but did not have direct visual feedback from the hand. The endpoint location of their hand was marked by a blue square. In the SSD block, they received feedback via the EyeMusic. In the VIS block, the feedback was visual.

"Participants were able to use auditory information to create a relatively precise spatial representation," notes Dr. Levy-Tzedek.

The study lends support to the hypothesis that representation of space in the brain may not be dependent on the modality with which the spatial information is received, and that very little training is required to create a representation of space without vision, using sounds to guide fast and accurate movements. “SSDs may have great potential to provide detailed spatial information for the visually impaired, allowing them to interact with their external environment and successfully make movements based on this information, but further research is now required to evaluate the use of our device in the blind ” concludes Dr. Levy-Tzedek. These results demonstrate the potential application of the EyeMusic in performing everyday tasks — from accurately reaching for the red (but not the green!) apples in the produce aisle, to, perhaps one day, playing a Kinect / Xbox game.

Source: Science Daily

July 5, 2012

Feeling full involves more than just the uncomfortable sensation that your waistband is getting tight. Investigators reporting online on July 5th in the Cell Press journal Cell have now mapped out the signals that travel between your gut and your brain to generate the feeling of satiety after eating a protein-rich meal. Understanding this back and forth loop between the brain and gut may pave the way for future approaches in the treatment and/or prevention of obesity.

Feeling full involves more than just the uncomfortable sensation that your waistband is getting tight. Investigators reporting online on July 5th in the Cell Press journal Cell have now mapped out the signals that travel between your gut and your brain to generate the feeling of satiety after eating a protein-rich meal. Understanding this back and forth loop between the brain and gut may pave the way for future approaches in the treatment and/or prevention of obesity. Credit: Duraffourd et al., Cell

Food intake can be modulated through mu-opioid receptors (MORs, which also bind morphine) on nerves found in the walls of the portal vein, the major blood vessel that drains blood from the gut. Specifically, stimulating the receptors enhances food intake, while blocking them suppresses intake. Investigators have now found that peptides, the products of digested dietary proteins, block MORs, curbing appetite. The peptides send signals to the brain that are then transmitted back to the gut to stimulate the intestine to release glucose, suppressing the desire to eat.

Mice that were genetically engineered to lack MORs did not carry out this release of glucose, nor did they show signs of ‘feeling full’, after eating high-protein foods. Giving them MOR stimulators or inhibitors did not affect their food intake, unlike normal mice.

Because MORs are also present in the neurons lining the walls of the portal vein in humans, the mechanisms uncovered here may also take place in people.

"These findings explain the satiety effect of dietary protein, which is a long-known but unexplained phenomenon,” says senior author Dr. Gilles Mithieux of the Université de Lyon, in France. “They provide a novel understanding of the control of food intake and of hunger sensations, which may offer novel approaches to treat obesity in the future,” he adds.

Provided by Cell Press

Source: medicalxpress.com

ScienceDaily (July 5, 2012) — The widely used diabetes drug metformin comes with a rather unexpected and alluring side effect: it encourages the growth of new neurons in the brain. The study reported in the July 6th issue of Cell Stem Cell, a Cell Press publication, also finds that those neural effects of the drug also make mice smarter.

New research finds that the widely used diabetes drug metformin comes with a rather unexpected and alluring side effect: it encourages the growth of new neurons in the brain. (Credit: iStockphoto/Guido Vrola)

The discovery is an important step toward therapies that aim to repair the brain not by introducing new stem cells but rather by spurring those that are already present into action, says the study’s lead author Freda Miller of the University of Toronto-affiliated Hospital for Sick Children. The fact that it’s a drug that is so widely used and so safe makes the news all that much better.

Earlier work by Miller’s team highlighted a pathway known as aPKC-CBP for its essential role in telling neural stem cells where and when to differentiate into mature neurons. As it happened, others had found before them that the same pathway is important for the metabolic effects of the drug metformin, but in liver cells.

"We put two and two together," Miller says. If metformin activates the CBP pathway in the liver, they thought, maybe it could also do that in neural stem cells of the brain to encourage brain repair.

The new evidence lends support to that promising idea in both mouse brains and human cells. Mice taking metformin not only showed an increase in the birth of new neurons, but they were also better able to learn the location of a hidden platform in a standard maze test of spatial learning.

While it remains to be seen whether the very popular diabetes drug might already be serving as a brain booster for those who are now taking it, there are already some early hints that it may have cognitive benefits for people with Alzheimer’s disease. It had been thought those improvements were the result of better diabetes control, Miller says, but it now appears that metformin may improve Alzheimer’s symptoms by enhancing brain repair.

Miller says they now hope to test whether metformin might help repair the brains of those who have suffered brain injury due to trauma or radiation therapies for cancer.

Source: Science Daily

ScienceDaily (July 5, 2012) — Although many areas of the human brain are devoted to social tasks like detecting another person nearby, a new study has found that one small region carries information only for decisions during social interactions. Specifically, the area is active when we encounter a worthy opponent and decide whether to deceive them.

(Credit: © wtamas / Fotolia)

A brain imaging study conducted by researchers at the Duke Center for Interdisciplinary Decision Science (D-CIDES) put human subjects through a functional MRI brain scan while playing a simplified game of poker against a computer and human opponents. Using computer algorithms to sort out what amount of information each area of the brain was processing, the team found only one brain region — the temporal-parietal junction, or TPJ — carried information that was unique to decisions against the human opponent.

Some of the time, the subjects were dealt an obviously weak hand. The researchers wanted to see whether they could watch the player calculate whether to bluff his opponent. The brain signals in the TPJ told the researchers whether the subject would soon bluff against a human opponent, especially if that opponent was judged to be skilled. But against a computer, signals in the TPJ did not predict the subject’s decisions.

The TPJ is in a boundary area of the brain, and may be an intersection for two streams of information, said lead researcher McKell Carter, a postdoctoral fellow at Duke. It brings together a flow of attentional information and biological information, such as “is that another person?”

Carter observed that in general, participants paid more attention to their human opponent than their computer opponent while playing poker, which is consistent with humans’ drive to be social.

Throughout the poker game experiment, regions of the brain that are typically thought to be social in nature did not carry information specific to a social context. “The fact that all of these brain regions that should be specifically social are used in other circumstances is a testament to the remarkable flexibility and efficiency of our brains,” said Carter.

"There are fundamental neural differences between decisions in social and non-social situations," said D-CIDES Director Scott Huettel, the Hubbard professor of psychology & neuroscience at Duke and senior author of the study. "Social information may cause our brain to play by different rules than non-social information, and it will be important for both scientists and policymakers to understand what causes us to approach a decision in a social or a non-social manner.

"Understanding how the brain identifies important competitors and collaborators — those people who are most relevant for our future behavior — will lead to new insights into social phenomena like dehumanization and empathy," Huettel added.

Source: Science Daily