Gene therapy for hearing loss: Potential and limitations

Regenerating sensory hair cells, which produce electrical signals in response to vibrations within the inner ear, could form the basis for treating age- or trauma-related hearing loss. One way to do this could be with gene therapy that drives new sensory hair cells to grow.

Researchers at Emory University School of Medicine have shown that introducing a gene called Atoh1 into the cochleae of young mice can induce the formation of extra sensory hair cells.

Their results show the potential of a gene therapy approach, but also demonstrate its current limitations. The extra hair cells produce electrical signals like normal hair cells and connect with neurons. However, after the mice are two weeks old, which is before puberty, inducing Atoh1 has little effect. This suggests that an analogous treatment in adult humans would also not be effective by itself.

The findings were published May 9 in the Journal of Neuroscience.

"We've shown that hair cell regeneration is possible in principle," says Ping Chen, PhD, associate professor of cell biology at Emory University School of Medicine. "In this paper, we have identified which cells are capable of becoming hair cells under the influence of Atoh1, and we show that there are strong age-dependent limitations on the effects of Atoh1 by itself."

The first author of the paper, Michael Kelly, now a postdoctoral fellow at the National Institute on Deafness and Other Communication Disorders, was a graduate student in Emory's Neuroscience program.

Kelly and his coworkers engineered mice to turn on the Atoh1 gene in the inner ear in response to the antibiotic doxycycline. Previous experimenters had used a virus to introduce Atoh1 into the cochleae of animals. This approach resembles gene therapy, but has the disadvantage of being slightly different each time, Chen says. In contrast, the mice have the Atoh1 gene turned on in specific cells along the lining of the inner ear, called the cochlear epithelium, but only when fed doxycycline.

Young mice given doxycycline for two days had extra sensory hair cells, in parts of the cochlea where developing hair cells usually appear, and also additional locations (see accompanying image).

The extra hair cells could generate electrical signals, although those signals weren't as strong as mature hair cells. Also, the extra hair cells appeared to attract neuronal fibers, which suggests that those signals could connect to the rest of the nervous system.

"They can generate electrical signals, but we don't know if they can really function in the context of hearing." Chen says. "For that to happen, the hair cells' signals need to be coordinated and integrated."

Although doxycycline could turn on Atoh1 all over the surface of the cochlea, extra sensory hair cells did not appear everywhere. When they removed cochleae from the mice and grew them in culture dishes, her team was able to provoke even more hair cells to grow when they added a drug that inhibits the Notch pathway.

Manipulating the Notch pathway affects several aspects of embryonic development and in some contexts appears to cause cancer, so the approach needs to be refined further. Chen says that it may be possible to unlock the age-related limits on hair cell regeneration by supplying additional genes or drugs in combination with Atoh1, and the results with the Notch drug provide an example.

"Our future goals are to develop approaches to stimulate hair cell formation in older animals, and to examine functional recovery after Atoh1 induction," she says.

Source: Emory University [May 11, 2012]

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Hearing and Touch Have Common Genetic Basis

Vision and hearing are so crucial to our daily lives that any impairments usually become obvious to an affected person. Although a number of known genetic mutations can lead to hereditary defects in these senses, little is known about our sense of touch, where defects might be so subtle that they go unnoticed.

There are good reasons to suspect that hearing and touch might have a common genetic basis. Sound-sensing cells in the ear detect vibrations and transform them into electrical impulses. Likewise, nerves that lie just below the surface of the skin detect movement and changes in pressure, and generate impulses. The similarity suggests that the two systems might have a common evolutionary origin—they may depend on an overlapping set of molecules that transform motion into signals that can be transmitted along nerves to the brain [Credit: © Vladimir Voronin/ Fotolia]

People with good hearing also have a keen sense of touch; people with impaired hearing generally have an impaired sense of touch. Extensive data supporting this hypothesis was presented by Dr. Henning Frenzel and Professor Gary R. Lewin of the Max Delbruck Center for Molecular Medicine (MDC) Berlin-Buch, Germany. The two researchers showed that both senses -- hearing and touch -- have a common genetic basis. In patients with Usher syndrome, a hereditary form of deafness accompanied by impaired vision, the researchers discovered a gene mutation that is also causative for the patients' impaired touch sensitivity.

The examination was preceded by various studies, including studies with healthy identical and non-identical human twins. In total, the researchers assessed sensory function in 518 volunteers.

In all vertebrates, and consequently also in humans, hearing and touch represent two distinct sensory systems that both rely on the transformation of mechanical force into electrical signals. When we hear, sound waves trigger vibrations that stimulate the hair-like nerve endings in the cochlea in the inner ear. These then transform the mechanical stimuli into electrical signals, which are transmitted to the brain via the auditory nerve. When we touch something a similar process takes place: The mechanical stimulus -- sliding the fingers over a rough or smooth surface, the perception of vibrations -- is taken up via sensors in the skin, converted into an electrical stimulus and transmitted to the brain.

Twin study with 100 pairs of twins

In recent years about 70 genes have been identified in humans, mutations in which trigger hearing loss or deafness. "Surprisingly, no genes have been found that negatively influence the sense of touch," Professor Lewin said. To see whether the sense of touch also has a hereditary component, the researchers first studied 100 pairs of twins -- 66 pairs of monozygotic twins and 34 dizygotic pairs of twins. Monozygotic twins are genetically completely identical; dizygotic twins are genetically identical to 50 percent. The tests showed that the touch sensitivity of the subjects was determined to more than 50 percent by genes. Furthermore, hearing and touch tests showed that there is a correlation between the sense of hearing and touch.

The researchers therefore suspected that genes that influence the sense of hearing may also have an influence on the sense of touch. In a next step, they recruited test subjects at a school in Berlin for students with hearing impairments. There they assessed the touch sensitivity in a cohort of 39 young people who suffered from severe congenital hearing impairment. The researchers compared these findings with the data from their twin study and discovered that not all of the young people with hearing loss had impaired tactile acuity. "Strikingly, however, many of these young people did indeed have poor tactile acuity," Professor Lewin explained.

The researchers decided it would take too much time to analyze which of the approximately 70 genes that adversely affect the sense of hearing may also negatively affect the sense of touch. Therefore, the researchers focused specifically on patients with the Usher syndrome, a hereditary form of hearing impairment, in which the patients progressively become blind. Usher syndrome patients have varying degrees of hearing impairment, and the disease is genetically very well studied. There are nine known Usher genes carrying mutations which cause the disease.

The researchers examined one cohort of patients in a special consultation at the Charite -- Universitatsmedizin Berlin for Usher patients from all over Germany. A second cohort was recruited at the university hospital La Fe in Valencia, Spain. The studies revealed that not all patients with Usher-syndrome have poor tactile acuity and touch sensitivity. The researchers showed that only patients with Usher syndrome who have a mutation in the gene USH2A have poor touch sensitivity. This mutation is also responsible for the impaired hearing of 19 patients. The 29 Usher-syndrome patients in whom the mutation could not be detected had a normal sense of touch. The researchers thus demonstrated that there is a common genetic basis for the sense of hearing and touch. They suspect that even more genes will be discovered in the future that influence both mechanosensory traits.

Women hear better than men and have a finer sense of touch

The researchers discovered another interesting detail during their five-year study. "When women complain that their men are not really listening to them, there is some truth in that," Professor Lewin said. "The studies with a total of 518 individuals including 295 women have actually shown that women hear better and they also have a finer sense of touch than men; in short woman hear and feel more than men!"

Source: Helmholtz Association of German Research Centres [May 01, 2012]

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Honeycomb structure responsible for bacteria's extraordinary sense

Cornell researchers have peered into the complex molecular network of receptors that give one-celled organisms like bacteria the ability to sense their environment and respond to chemical changes as small as 1 part in 1,000. 

Honeycomb-like hexagonal lattice formed by the network of receptor molecules (pink), associated enzymes (blue) and coupling proteins (green) in motile bacteria. Such a cooperative lattice arranged across their cell membranes helps bacteria sense their environment with extreme sensitivity. Inset shows the structure of a unit cell of the lattice in detail (top left). [Credit: Crane Lab]

Just as humans use five senses to navigate through surroundings, bacteria employ an intricate structure of thousands of receptor molecules, associated enzymes and linking proteins straddling their cell membranes that trigger responses to external chemical changes. 

Researchers in the lab of Brian Crane, professor of chemistry and chemical biology, with collaborators in the lab of Grant Jensen at the California Institute of Technology, have mapped out the honeycomb-like hexagonal arrangement of these receptor complexes in unprecedented detail. 

They report their discovery in the Feb. 20 issue of the Proceedings of the National Academy of Sciences. 

"The highlight of the paper is that by using a combination of [techniques], we've been able to image these complex arrays in live cells and determine how they are structured -- they are a very unique biological assembly that is conserved across nearly all classes of motile bacteria," said Crane. 

The findings might have potential applications in engineering biologically inspired synthetic molecular devices to detect specific chemicals with high sensitivity over a wide dynamic range; they also could shed light on the pathogenesis of various bacterial diseases like syphilis, cholera and Lyme disease. They may also give some insight into the functioning of the human immune system, where special cells may be employing similar cooperative networks of receptors to recognize and fight against foreign antigens, Crane said. 

Scientists are trying to determine how one receptor -- on detecting nutrients, oxygen or acidity, for example -- triggers communication through multiple enzymes in the complex, setting off a chain reaction. This cooperation leads to a gain or amplification in the signal that is finally communicated to the tails (flagella) of the bacterium, affecting the way they spin. Such a response allows the bacterium to move toward food sources or away from toxic environments.  

The latest work takes a big step toward understanding this mechanism by demonstrating for the first time how the individual pieces of receptors, enzymes and coupling proteins fit together to generate an extended network. It builds on previous work in the Crane lab done in collaboration with Jack Freed, Cornell professor of chemistry and chemical biology. 

"We were able to see how the enzymes and proteins are linked together in the complex array and also their interactions with the receptors," said Xiaoxiao Li, graduate student and joint lead author on the study. 

High-resolution X-ray images of the bacterial membrane receptor complex were obtained after extraction, purification and crystallization at the Cornell High Energy Synchrotron Source (CHESS). The scientists reconstructed the complicated molecular structure of the complex with an accuracy that is within a nanometer (a billionth of a meter). Pictures of the structure were also captured inside living cells, by first "flash-freezing" the cells and then scattering electrons off them. 

The researchers deduced that trimers (groups of three) of receptor molecules are arranged at the vertices of hexagons surrounding rings of enzymes and coupling proteins. These rings linked by proteins form the backbone of the extended honeycomb-like network. 

Author: Vivek Venkataraman | Source: Cornell University [February 20, 2012]

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Right hand or left? How the brain solves a perceptual puzzle

When you see a picture of a hand, how do you know whether it's a right or left hand? This "hand laterality" problem may seem obscure, but it reveals a lot about how the brain sorts out confusing perceptions. Now, a study which will be published in a forthcoming issue of Psychological Science, a journal published by the Association for Psychological Science, challenges the long-held consensus about how we solve this problem. 

"For decades, the theory was that you use your motor imagination," says Shivakumar Viswanathan, who conducted the study with University of California Santa Barbara colleagues Courtney Fritz and Scott T. Grafton. Judging from response times, psychologists thought we imagine flipping a mental image of each of our own hands to find the one matching the picture. These imagined movements were thought to recruit the same brain processes used to command muscles to move—a high-level cognitive feat. 

The study, however, finds that the brain is adept at decoding a left or right hand without these mental gymnastics. Judging laterality is "a low-level sensory problem that uses processes that bring different senses into register"— a process called binding, says Viswanathan. Seeing a hand of unknown laterality leads the brain to bind the seen hand to the correct felt hand. If they are still out of register because of their conflicting positions, an illusory movement arises from the brain's attempt to bring the seen and felt hand into the same position. But "this feeling of moving only comes after you already know which hand it is." 

In the study, participants couldn't see their own hands, which were held palm down. They saw hand shapes tilted at different angles, with a colored dot on them indicating a palm-up or down posture. One group of participants saw the shape first and then the dot; and the other, the dot first. Participants in both groups put the shape and dot together mentally and indicated which hand it was by pushing a button with that hand. 

However, when the shape and dot were shown simultaneously, participants in the first group felt movements of their right hands when seeing a left hand and vice versa; the other group always felt a movement of the correct hand. This behavioral difference (which experimenters gleaned from response time) was due to differences in participants' perception of the seen hand—establishing that an earlier sensory process made the decision. 

In a second experiment, participants were told which hand it was and had to judge whether its palm was down or up, indicating their answer with one hand only. This time, the illusory hand-movement occurred only when the seen hand-shape matched that of the participant's own palm-down responding hand, but not otherwise. Even though no right/left judgments were required, the response was dominated by an automatic binding of the seen and felt hands, and the illusory movement followed, says Viswanathan. 

The study helps us understand the experience of amputees, who sometimes sense an uncontrollable itch or clenching in the "phantom" body part. Showing the opposite hand or leg in a mirror allows the patient to "feel" the absent limb and mentally relieve the discomfort—a "binding" of vision and feeling. 

Source: Association for Psychological Science [February 08, 2012]

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Scientists decode how the brain hears words

US scientists said Wednesday they have found a way to decode how the brain hears words, in what researchers described as a major step toward one day helping people communicate after paralysis or stroke. 

These images courtesy of the Center for Vital Longevity, The University of Texas at Dallas, show positron emission tomography scans of the brains of healthy adults showing low (L) and high (R) levels of beta-amyloid protein. US scientists said Wednesday they have found a way to decode how the brain hears words [Credit: AFP]

By placing electrodes on the brains of research subjects and then having them listen to conversations, scientists were able to analyze the sound frequencies registered and figure out which words they were hearing. 

"We were focused on how the brain processes the sounds of speech," researcher Brian Pasley of the Helen Wills Neuroscience Institute at the University of California Berkeley told AFP. 

"Most of the information in speech is between one to 8,000 hertz. Essentially the brain analyzes those different sound frequencies in somewhat separate locations." 

By tracking how and where the brain registered sounds in the temporal lobe -- the center of the auditory system -- scientists were able to map out the words and then recreate them as heard by the brain. 

"When a particular brain site is being activated, we know that roughly corresponds to some sound frequency that the patient is actually listening to," Pasley said. 

"So we could map that out to an extent that would allow us to use that brain activity to resynthesize the sound from the frequencies we were guessing." 

One word the researchers mapped was "structure." The high-frequency "s" sound showed up as a certain pattern in the brain, while the lower harmonics of the "u" sound appeared as a different pattern. 

"There is to some extent a correspondence between these features of sound and the brain activity that they cause," and putting together the physical registry in the brain helped rebuild the words, Pasley explained. 

The work builds on previous research in ferrets, in which scientists read to the animals and recorded their brain activity. 

They were able to decode which words the creatures heard even though the ferrets themselves didn't understand the words. 

The next step for researchers is to figure out just how similar the process of hearing sounds may be to the process of imagining words and sounds. 

That information could one day help scientists determine what people want to say when they cannot physically speak. 

Some previous research has suggested there may be similarities, but much more work needs to be done, Pasley said. 

"This is huge for patients who have damage to their speech mechanisms because of a stroke or Lou Gehrig's disease and can't speak," co-author Robert Knight, a UC Berkeley professor of psychology and neuroscience, said in a statement. 

"If you could eventually reconstruct imagined conversations from brain activity, thousands of people could benefit." 

Participating researchers came from the University of Maryland, UC Berkeley and Johns Hopkins University in Baltimore, Maryland. 

The study appears in the January 31 edition of the open access journal PLoS Biology. 

Author: Kerry Sheridan | Source: AFP [February 01, 2012]

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'Genetic programming': The mathematics of taste

The design of aromas — the flavors of packaged food and drink and the scents of cleaning products, toiletries and other household items — is a multibillion-dollar business. The big flavor companies spend tens of millions of dollars every year on research and development, including a lot of consumer testing. 

[Graphic: Christine Daniloff]

But making sense of taste-test results is difficult. Subjects’ preferences can vary so widely that no clear consensus may emerge. Collecting enough data about each subject would allow flavor companies to filter out some of the inconsistencies, but after about 40 flavor samples, subjects tend to suffer “smell fatigue,” and their discriminations become unreliable. So companies are stuck making decisions on the basis of too little data, much of it contradictory. 

One of the biggest flavor companies in the world has turned to researchers in MIT’s Computer Science and Artificial Intelligence Laboratory (CSAIL) for help. To analyze taste-test results, the CSAIL researchers are using genetic programming, in which mathematical models compete with each other to fit the available data and then cross-pollinate to produce models that are more accurate still. 

The Swiss flavor company Givaudan asked CSAIL principal research scientist Una-May O’Reilly, postdoc Kalyan Veeramachaneni and the University of Antwerp’s Ekaterina Vladislavleva to help interpret the results of tests in which 69 subjects evaluated 36 different combinations of seven basic flavors, assigning each a score according to its olfactory appeal. 

For each subject, O’Reilly and her colleagues randomly generate mathematical functions that predict scores according to the concentrations of different flavors. Each function is assessed according to two criteria: accuracy and simplicity. A function that, for example, predicts a subject’s preferences fairly accurately using a single factor — say, concentration of butter — could prove more useful than one that yields a slightly more accurate prediction but requires a complicated mathematical manipulation of all seven variables. 

After all the functions have been assessed, those that provide poor predictions are winnowed out. Elements of the survivors are randomly recombined to produce a new generation of functions; those are then evaluated for accuracy and simplicity. The whole process is repeated about 30 times, until it converges on a set of functions that accord well with the preferences of a single subject.  

Because O’Reilly and her colleagues’ method produces profiles of individual test subjects’ tastes, it can sort them into distinct groups. It could be, for instance, that test subjects tend to have strong preferences for either cinnamon or nutmeg but not both. By marketing one product to cinnamon lovers and another to nutmeg lovers, a company could do much better than by marketing one product to both. “For every one of these 36 flavors, someone hated it and someone liked it,” O’Reilly says. “If you try to identify a flavor that the whole panel likes, you end up settling for a little bit less.” 

O’Reilly and her colleagues haven’t had an opportunity to empirically determine whether their models correctly predict subjects’ responses to new flavors. So to try to establish their model’s accuracy, they instead built another model. First, they developed a set of mathematical functions that represent subjects’ true taste preferences. Then they showed that, given the limitations of particular test designs, their algorithms could still divine those preferences. Although they developed the model purely to validate their approach, O’Reilly says, flavor researchers were intrigued by the possibility of using it to develop more accurate and efficient test protocols. 

“People have been playing with these [evolutionary] techniques for decades,” says Lee Spector, a professor of computer science at Hampshire College and editor-in-chief of the journal Genetic Programming and Evolvable Machines, where the MIT researchers’ latest paper appears. “One of the reasons that they haven’t made a big splash until recently is that people haven’t really figured out, I think, where they can pay off big.” Taste preference, Spector says, “is a pretty brilliant area in which to apply the evolutionary methods — and it looks as though they’re working, also, so that’s exciting.” 

Author: Larry Hardesty | Source: Massachusetts Institute of Technology [January 24, 2012]

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Scientists map the frontiers of vision

There's a 3-D world in our brains. It's a landscape that mimics the outside world, where the objects we see exist as collections of neural circuits and electrical impulses. 

Now, scientists at the Salk Institute for Biological Studies are using new tools they developed to chart that world, a key step in revolutionizing research into the neurological basis of vision. 

For the first time, the scientists have produced neuron-by-neuron maps of the regions of the mouse brain that process different kinds of visual information, laying the groundwork for decoding the circuitry of the brain using cutting-edge, genetic research techniques only possible in mice. 

"In the field of cognitive research, this puts the mouse on the map - by putting the map on the mouse," says James Marshel, a Salk research associate. Marshel and Marina Garrett, a graduate student at University of California San Diego, were lead authors on a paper reporting the advance in the December 22 issue of Neuron. 

To understand the extraordinarily complex computations of the human brain, including those behind visual cognition, scientists have mostly relied on studies on primates, such as monkeys, our closest relatives in the animal kingdom, and the most like us in terms of cognitive ability. 

Researchers have identified what portions of the primate brain process different aspects of the sensory information they gather from the outside world. In particular, a great deal is known about what regions of the primate brain process certain visual information, helping them identify objects and follow their movements in three-dimensional space. 

"We've learned a lot about how our eyes feed information to our brains, and a huge portion of our brain is devoted to processing this information," says Edward Callaway, a professor in Salk's Systems Neurobiology Laboratory, whose laboratory conducted the research. "Vision is a terrific system for understanding how the brain works and, ultimately, for studying mental diseases and consciousness." 

Powerful new scientific tools are emerging that could allow scientists to better understand the human brain by studying the relatively simpler brains of mice. These methods allow scientists to alter genes, the instructions in DNA that control the behavior of cells - including the neurons that form brain circuits. By using genetic methods for mapping brain connections and controlling the activity of cells, scientists hope to generate detailed wiring diagrams of the brain and probe how these circuits function. 

"While mice can not replace the work that is being done in monkeys, these research techniques are much further along in mice than in monkeys," Callaway says. "The ability to modify neural activity using genetic tools and to study the resulting changes in brain and nerve activity is revolutionizing neuroscience." 

Although such genetic engineering techniques in mice offer huge potential, little was known about what areas of the mouse visual cortex - the high-level brain region that computes the meaning of signals from the eyes - were responsible for processing different elements of the visual information. 

To remedy this, Callaway and his colleagues set out to chart a map of the mouse's visual processing system. They injected mice with a calcium-sensitive fluorescent dye that glows when exposed to a certain color of light. The amount of calcium in nerve cells varies depending on the activity level of the neurons, so the scientists could measure the activity of brain cells based on how brightly they glowed. 

The scientists then displayed different types of visual stimulus on a television monitor and recorded what parts of the brain glowed. To make the recordings, they used a high-resolution camera capable of discerning the activity of individual nerve cells. 

They found that a mouse's visual field, the area of three-dimensional space visible through its eyes, is represented by a corresponding collection of neurons in its brain. The researchers precisely recorded which neurons were associated with which area of the animal's visual field. 

The scientists studied seven different areas of the animal's visual cortex containing full neuronal "maps" of the visible outside world, and found that each area has a specialized role in processing visual information. For instance, certain areas were more sensitive to the direction objects move in space, while other areas were focused on distinguishing fine detail. 

With these maps of brain function in hand, the Salk researchers and others now have a baseline against which they can compare the brain function of mice in which circuit function is manipulated using genetic methods. Ultimately, Callaway says, understanding in detail how the mouse brain works will illuminate the workings of the human mind. 

"This gives us new ways to explore the neural underpinnings of consciousness and to identify what goes wrong in neural circuits in the case of diseases such as schizophrenia and autism," Callaway said.  

Source: Salk Institute [January 06, 2012]

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Was Darwin wrong about emotions?

Contrary to what many psychological scientists think, people do not all have the same set of biologically "basic" emotions, and those emotions are not automatically expressed on the faces of those around us, according to the author of a new article published in Current Directions in Psychological Science, a journal published by the Association for Psychological Science. This means a recent move to train security workers to recognize "basic" emotions from expressions might be misguided. 

"What I decided to do in this paper is remind readers of the evidence that runs contrary to the view that certain emotions are biologically basic, so that people scowl only when they're angry or pout only when they're sad," says Lisa Feldman Barrett of Northeastern University, the author of the new paper. 

The commonly-held belief is that certain facial muscle movements (called expressions) evolved to express certain mental states and prepare the body to react in stereotyped ways to certain situations. For example, widening the eyes when you're scared might help you take in more information about the scene, while also signaling to the people around you that something dangerous is happening. 

But Barrett (along with a minority of other scientists) thinks that expressions are not inborn emotional signals that are automatically expressed on the face. "When do you ever see somebody pout in sadness? When it's a symbol," she says. "Like in cartoons or very bad movies." People pout when they want to look sad, not necessarily when they actually feel sad, she says. 

Some scientists have proposed that emotions regulate your physical response to a situation, but there's no evidence, for example, that a certain emotion usually produces the same physical changes each time it is experienced, Barrett says. "There's tremendous variety in what people do and what their bodies and faces do in anger or sadness or in fear," she says. People do a lot of things when they're angry. Sometimes they yell; sometimes they smile. 

"Textbooks in introductory psychology says that there are about seven, plus or minus two, biologically basic emotions that have a designated expression that can be recognized by everybody in the world, and the evidence I review in this paper just doesn't support that view," she says. Instead of stating that all emotions fall into a few categories, and everyone expresses them the same way, Barrett says, psychologists should work on understanding how people vary in expressing their emotions. 

This debate isn't purely academic. It has consequences for how clinicians are trained and also for the security industry. In recent years there's been an explosion of training programs that are meant to help security officers of all kinds identify people who are up to something nefarious. But this training might be misguided, Barrett says. "There's a lot of evidence that there is no signature for fear or anger or sadness that you could detect in another person. If you want to improve your accuracy in reading emotion in another person, you have to also take the context into account." 

Incidentally, the theory that emotional expressions evolved for specific functions is normally attributed to Charles Darwin, in his book The Expression of the Emotions in Man and Animals. But Darwin didn't write that emotional expressions are functional. "If you're going to cite Darwin as evidence that you're right, you'd better cite him correctly," Barrett says. Darwin thought that emotional expressions – smiles, frowns, and so on –were akin to the vestigial tailbone – and occurred even though they are of no use. 

Source: Association for Psychological Science [December 13, 2011]

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When errors improve performance: Model describes how experiences influence our perception

During estimation processes we unconsciously make use of recent experiences. Scientists from Ludwig-Maximilians-Universität (LMU) in Munich and the Bernstein Center Munich asked test subjects to estimate distances in a virtual reality environment. The results revealed that estimates tended to approach the mean of all previously experienced distances. For the first time, scientists were able to accurately predict the experimental findings using a mathematical model. The model combines two well-known laws of psychophysics with a theorem from probability theory. The study could be of fundamental relevance to research on perception. 

Why do we perceive identical distances as long in one situation and short in another? It all depends on the distances that we have covered in the immediate past. This might seem a trivial conclusion, but it gives an important insight into how the brain processes signals of different intensities or even abstract elements such as numbers. Dr. Stefan Glasauer (LMU Munich), project leader at the Bernstein Center Munich, and PhD student Frederike Petzschner have investigated this effect both experimentally and theoretically. Test subjects were first asked to perform certain displacements in virtual reality and then to reproduce these displacements as accurately as possible. As in previous studies, the results showed a bias towards the mean of all previously experienced displacements. 

The scientists can now provide a general explanation for this phenomenon. With the help of a mathematical model, they can calculate how previous stimuli affect the current estimate. "The influence of prior experience most probably follows a general principle, and is likely to hold true for the estimation of quantities or sound levels also," says Glasauer. Test subjects whose distance estimates were strongly influenced by prior experience also placed greater weight on prior experience when asked to assess angular displacements. In both cases, they were learning without having received any information about the success or failure of their previous performance. Conventional learning methods, however, presuppose such feedback mechanisms. 

Whether or not a fundamental principle determines the perception of stimulus strengths, such as sound levels, brightness, or even distances, has been a controversial issue. Two important laws of psychophysics, the so-called Weber-Fechner law, published 150 years ago, and the 50-year-old Stevens' power law, seemed to contradict each other. The Munich scientists have now shown that the two laws are in fact compatible, at least for certain cases. By combining the Weber-Fechner law with Bayes' Theorem (1763), a procedure from probability theory that allows evidence to be weighted, they were able to transform it into Stevens' power law. Glasauer is therefore confident that "we have contributed to solving a problem that perception researchers have been studying for more than 50 years now." Next, the researchers want to analyze historical data and determine whether the model also applies to different stimulus modalities, such as sound levels and brightness. 

Source: Ludwig-Maximilians-Universität München [November 25, 2011]

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