The Social Psychology of Nerve Cells

The functional organization of the central nervous system depends upon a precise architecture and connectivity of distinct types of neurons. Multiple cell types are present within any brain structure, but the rules governing their positioning, and the molecular mechanisms mediating those rules, have been relatively unexplored.

A new study by UC Santa Barbara researchers demonstrates that a particular neuron, the cholinergic amacrine cell, creates a “personal space” in much the same way that people distance themselves from one another in an elevator. In addition, the study, published in the Proceedings of the National Academy of Sciences, shows that this feature is heritable and identifies a genetic contributor to it, pituitary tumor-transforming gene 1 (Pttg1).

Patrick Keeley, a postdoctoral scholar in Benjamin Reese’s laboratory at UCSB’s Neuroscience Research Institute, has been using the retina as a model system for exploring such principles of developmental neurobiology. The retina is ideal because this portion of the central nervous system lends itself to such spatial analysis. 

“Populations of neurons in the retina are laid out in single strata within this layered structure, lending themselves to accurate quantitation and statistical analysis,” explained Keeley. “Rather than being distributed as regular lattices of nerve cells, populations in the retina appear to abide by a simple rule, that of minimizing proximity to other cells of the same type. We would like to understand how such populations create and maintain such spacing behavior.”

To address this, Keeley and colleagues quantified the regularity in the population of a particular type of amacrine cell in the mouse retina. They did so in 26 genetically distinct strains of mice and found that every strain exhibited this same self-spacing behavior but that some strains did so more efficiently than others. Amacrine cells are retinal interneurons that form connections between other neurons and regulate bipolar cell output.

“The regularity in the patterning of these amacrine cells showed little variation within each strain, while showing conspicuous variation between the strains, indicating a heritable component to this trait,” said Keeley.

“This itself was something of a surprise, given that the patterning in such populations has an apparently stochastic quality to it,” said Reese, a professor in the Department of Psychological and Brain Sciences. Stochastic systems are random and are analyzed, at least in part, using probability theory.

This strain variation in the regularity of this cellular patterning showed a significant linkage to a location in the genome on chromosome 11, where the researchers identified Pttg1, previously unknown to play any role in the retina.

Working in collaboration with colleagues at the University of Tennessee Health Science Center in Memphis, Keeley’s team demonstrated that the expression of this gene varies across the 26 strains of mice and that there was a positive correlation between gene expression and regularity. They then identified a mutation in this gene that itself correlated with expression levels and with regularity. Working with colleagues at Cedars-Sinai Medical Center in Los Angeles, the team also demonstrated directly that this mutation controlled gene expression.   

“Pttg1 has diverse functions, being an oncogene for pituitary tumors, and is known to have regulatory functions orchestrating gene expression elsewhere in the body,” explained Keeley. “Within this class of retinal neurons, it should be regulating the way in which cells integrate signals from their immediate neighbors, translating that information to position the cell farthest from those neighbors.” Future studies should decipher the genetic network controlled by Pttg1 that mediates such nerve-cell spacing.

Running, Combined with Visual Experience, Restores Brain Function

In a new study by UC San Francisco scientists, running, when accompanied by visual stimuli, restored brain function to normal levels in mice that had been deprived of visual experience in early life.

In addition to suggesting a novel therapeutic strategy for humans with blindness in one eye caused by a congenital cataract, droopy eyelid, or misaligned eye, the new research—the latest in a series of UCSF studies exploring effects of locomotion on brain function—suggests that the adult brain may be far more capable of rewiring and repairing itself than previously thought.

In 2010, Michael P. Stryker, PhD, the W.F. Ganong Professor of Physiology, and postdoctoral fellow Cris Niell, PhD, now at the University of Oregon, made the surprising discovery that neurons in the visual area of the mouse brain fired much more robustly whenever the mice walked or ran.

Earlier this year, postdoctoral fellow Yu Fu, PhD, Stryker and a number of colleagues built on these findings, identifying and describing the neural circuit responsible for this locomotion-induced “high-gain state” in the visual cortex of the mouse brain.

Neither of these studies made clear, however, whether this circuit might have broader functional or clinical significance.

It has been known since the 1960s that visual areas of the brain do not develop normally if deprived of visual input during a “critical period” of brain development early in life. For example, in humans, if amblyopia (“lazy eye”) or other major eye problems are not surgically corrected in infancy, vision will never be normal in the affected eye—if such individuals lose sight in their “good” eye in later life, they are blind.

In the new research, published June 26, 2014 in the online journal eLife, Stryker and UCSF postdoctoral fellow Megumi Kaneko, MD, PhD, closed one eyelid of mouse pups at about 20 days after birth, and that eye was kept closed until the mice reached about five months of age.

As expected, the mice in which one eye had been closed during the critical developmental period showed sharply reduced neural activity in the part of the brain responsible for vision in that eye.

As in the previous UCSF experiments in this area, some mice were allowed to run freely on Styrofoam balls suspended on a cushion of air while recordings were made from their brains.

Little improvement was seen in the mice that had been deprived of visual input either when they were simply allowed to run or when they received visual training with the deprived eye not accompanied by walking or running.

But when the mice were exposed to the visual stimuli while they were running or walking, the results were dramatic: within a week the brain responses to those stimuli from the deprived eye were nearly identical to those from the normal eye, indicating that the circuits in the visual area of the brain representing the deprived eye had undergone a rapid reorganization, known in neuroscience as “plasticity.”

Interestingly, this recovery was stimulus-specific: if the brain activity of the mice was tested using a stimulus other than that they had seen while running, little or no recovery of function was apparent.

“We have no idea yet whether running puts the human cortex into a high-gain state that enhances plasticity, as it does the visual cortex of the mouse,” Stryker said, “but we are designing experiments to find out.”

Early life stress can leave lasting impacts on the brain

For children, stress can go a long way. A little bit provides a platform for learning, adapting and coping. But a lot of it — chronic, toxic stress like poverty, neglect and physical abuse — can have lasting negative impacts.

A team of University of Wisconsin-Madison researchers recently showed these kinds of stressors, experienced in early life, might be changing the parts of developing children’s brains responsible for learning, memory and the processing of stress and emotion. These changes may be tied to negative impacts on behavior, health, employment and even the choice of romantic partners later in life.

The study, published in the journal Biological Psychiatry, could be important for public policy leaders, economists and epidemiologists, among others, says study lead author and recent UW Ph.D. graduate Jamie Hanson.

"We haven’t really understood why things that happen when you’re 2, 3, 4 years old stay with you and have a lasting impact," says Seth Pollak, co-leader of the study and UW-Madison professor of psychology.

Yet, early life stress has been tied before to depression, anxiety, heart disease, cancer, and a lack of educational and employment success, says Pollak, who is also director of the UW Waisman Center’s Child Emotion Research Laboratory.

"Given how costly these early stressful experiences are for society … unless we understand what part of the brain is affected, we won’t be able to tailor something to do about it," he says.

For the study, the team recruited 128 children around age 12 who had experienced either physical abuse, neglect early in life or came from low socioeconomic status households.

Researchers conducted extensive interviews with the children and their caregivers, documenting behavioral problems and their cumulative life stress. They also took images of the children’s brains, focusing on the hippocampus and amygdala, which are involved in emotion and stress processing. They were compared to similar children from middle-class households who had not been maltreated.

Hanson and the team outlined by hand each child’s hippocampus and amygdala and calculated their volumes. Both structures are very small, especially in children (the word amygdala is Greek for almond, reflecting its size and shape in adults), and Hanson and Pollak say the automated software measurements from other studies may be prone to error.

Indeed, their hand measurements found that children who experienced any of the three types of early life stress had smaller amygdalas than children who had not. Children from low socioeconomic status households and children who had been physically abused also had smaller hippocampal volumes. Putting the same images through automated software showed no effects.

Behavioral problems and increased cumulative life stress were also linked to smaller hippocampus and amygdala volumes.

Why early life stress may lead to smaller brain structures is unknown, says Hanson, now a postdoctoral researcher at Duke University’s Laboratory for NeuroGenetics, but a smaller hippocampus is a demonstrated risk factor for negative outcomes. The amygdala is much less understood and future work will focus on the significance of these volume changes.

"For me, it’s an important reminder that as a society we need to attend to the types of experiences children are having," Pollak says. "We are shaping the people these individuals will become."

But the findings, Hanson and Pollak say, are just markers for neurobiological change; a display of the robustness of the human brain, the flexibility of human biology. They aren’t a crystal ball to be used to see the future.

"Just because it’s in the brain doesn’t mean it’s destiny," says Hanson.

Hearing with the skull

The ear is an important organ that allows us to perceive the world around us. However, very few of us are aware that not only the ear cup but also our skull bone can receive and conduct sounds. Tatjana Tchumatchenko from the Max Planck Institute for Brain Research in Frankfurt and Tobias Reichenbach from Imperial College London have now developed a new model explaining how the vibrations of the surrounding bone and the basilar membrane are coupled. These new results can be important for the development of new headphones and hearing devices.

Our sense of hearing, which is the ability to perceive sounds, arises exclusively in the inner ear. When sound waves travel through the air and reach our ear canal they cause different regions of the basilar membrane in the inner ear to vibrate. Which regions of the membrane they vibrate depends on their frequency. It is these microscopic vibrations of the membrane that we perceive as sound. However, the inner ear is surrounded by a bone that can also vibrate.

With the help of fluid dynamics calculations Tchumatchenko and Reichenbach have now discovered that the vibrations of the bone and basilar membrane are coupled. In other words, they can also mutually excite each other.

This gives rise to fascinating phenomena which, thanks to the new model, can now be understood: For example, two sounds with slightly different frequencies that arrive in the inner ear at the same time can overlap and excite the same regions on the basilar membrane. In this case, combination tones, or so-called otoacoustic emissions, are produced in the inner ear through the nonlinearity of the membrane. Precisely how these sounds leave the inner ear and how they spread inside the cochlea is currently a matter of scientific debate. “In our study we have shown that the combination tones can leave the inner ear in the form of a fast wave along the bone surface, and not, as previously assumed, by a wave along the basilar membrane,” explains Tatjana Tchumatchenko from the Max Planck Institute for Brain Research.

Moreover, the new model proves that the travelling waves along the basilar membrane can be generated by both the vibrations of the cochlear bone and the vibrations of the air inside the ear canal. “Our results provide an elegant explanation for this long-known but poorly understood observation,” says Tobias Reichenbach from Imperial College London.

These results will help advance our understanding of the complex interaction between the dynamics of fluids and the mechanics of the bone. This understanding can prove essential for ever more fascinating future clinical and commercial applications of bone conduction, such new-generation hearing aids and combinations between headphones and glasses.

Bad learning

University of Iowa researchers have discovered a new form of neurotransmission that influences the long-lasting memory created by addictive drugs, like cocaine and opioids, and the subsequent craving for these drugs of abuse. Loss of this type of neurotransmission creates changes in brains cells that resemble the changes caused by drug addiction.

The findings, published June 22 in the journal Nature Neuroscience, suggest that targeting this type of neurotransmission might lead to new therapies for treating drug addiction.

“Molecular therapies for drug addiction are pretty much non-existent,” says Collin Kreple, UI graduate student and co-first author of the study. “I think this finding at least provides the possibility of a new molecular target.”

The new form of neurotransmission involves proteins called acid-sensing ion channels (ASICs), which have previously been shown to promote learning and memory, and which are abundant in a part of the brain that is involved in drug addiction. The researchers, led by John Wemmie, professor of psychiatry in the UI Carver College of Medicine, reasoned that disrupting ASIC activity in this brain region (the nucleus accumbens) should reduce learned addiction-related behaviors. However, their experiments showed that loss of ASIC signaling actually increases learned drug-seeking in mice.

When mice learned to associate one side of a chamber with receiving cocaine, animals that lacked the ASIC protein developed an even stronger preference for the “cocaine side” than control mice, suggesting that loss of ASIC had increased addiction behavior. The same result was seen for morphine, another drug of abuse, which has a different mechanism of action than cocaine.

"Always before, the data suggested that when you get rid of ASICs, learning and memory are impaired," Wemmie says. "So we expected the same trend when we studied reward-related learning and behavior and we were surprised to find the opposite."

In a second experiment, rats learned to press a lever to self-administer cocaine. Blocking or removing ASIC in the rat brains caused the animals to self-administer more cocaine than control animals. Conversely, increasing the amount of ASIC by over-expressing the protein seemed to decrease the animals’ craving for cocaine.

"There are many forms of addiction," says Wemmie, who also holds appointments in the UI Departments of Molecular Physiology and Biophysics and Neurosurgery, and with the Iowa City VA Medical Center. "We’d like to see if these mechanisms also apply to other addictions besides cocaine and morphine. And, we want to move forward to see if this pathway can be used to target addiction."

Novel neurotransmission

As the name suggests, acid-sensing ion channels are activated by acid, in the form of protons. This research and a second UI study recently published in PNAS show that protons and ASICs form a previously unrecognized neurotransmitter pair that helps neurons communicate in a novel way; and appear to influence several forms of learning and memory, including fear, as well as addiction.

Manipulating the activity of ASICs or the level of protons (acidity) may provide a new way to treat addiction.

"We are still a long way from using these findings to create a therapy," notes Yuan Lu, co-first author and UI postdoctoral scholar. "The key significance of this study is that we have found new, different targets [that might allow us to inhibit the addiction behavior].”

Drugs change the brain

Previous research has shown that drug abuse and addiction physically alter the connections between neurons (synapses) that are important for the creation and storage of memories. Although normal learning requires synapses to be dynamic and plastic, exposure to addictive drugs abnormally increases synaptic plasticity in a way that is thought to underlie drug-related learning and addiction behaviors. The UI study found that absence of ASIC-proton mediated neurotransmission also increased synaptic plasticity in a way that resembled the changes created by addiction and drug withdrawal.

"It seemed like everything we looked at (physiology and structural changes) really paralleled what you would see in an animal undergoing drug withdrawal, even though these animals missing ASIC had never been exposed to drugs," Kreple says.

Overall the study findings suggest that ASIC-related neurotransmission in the nucleus accumbens may play a role in reducing synaptic plasticity and appropriately stabilizing synapses.

Research gives unprecedented 3-D view of important brain receptor

Researchers with Oregon Health & Science University’s Vollum Institute have given science a new and unprecedented 3-D view of one of the most important receptors in the brain — a receptor that allows us to learn and remember, and whose dysfunction is involved in a wide range of neurological diseases and conditions, including Alzheimer’s, Parkinson’s, schizophrenia and depression.

The unprecedented view provided by the OHSU research, published online June 22 in the journal Nature, gives scientists new insight into how the receptor — called the NMDA receptor — is structured. And importantly, the new detailed view gives vital clues to developing drugs to combat the neurological diseases and conditions.

"This is the most exciting moment of my career," said Eric Gouaux, a senior scientist at the Vollum Institute and a Howard Hughes Medical Institute investigator. "The NMDA receptor is one of the most essential, and still sometimes mysterious, receptors in our brain. Now, with this work, we can see it in fascinating detail."

Receptors facilitate chemical and electrical signals between neurons in the brain, allowing those neurons to communicate with each other. The NMDA (N-methyl-D-aspartate) receptor is one of the most important brain receptors, as it facilitates neuron communication that is the foundation of memory, learning and thought. Malfunction of the NMDA receptor occurs when it is increasingly or decreasingly active and is associated with a wide range of neurological disorders and diseases. Alzheimer’s disease, Parkinson’s disease, depression, schizophrenia and epilepsy are, in many instances, linked to problems with NMDA activity.

Scientists across the world study the NMDA receptor; some of the most notable discoveries about the receptor during the past three decades have been made by OHSU Vollum scientists.

The NMDA receptor makeup includes receptor “subunits” — all of which have distinct properties and act in distinct ways in the brain, sometimes causing neurological problems. Prior to Gouaux’s study, scientists had only a limited view of how those subtypes were arranged in the NMDA receptor complex and how they interacted to carry out specific functions within the brain and central nervous system.

Gouaux’s team of scientists – Chia-Hsueh Lee, Wei Lu, Jennifer Michel, April Goehring, Juan Du and Xianqiang Song – created a 3-D model of the NMDA receptor through a process called X-ray crystallography. This process throws x-ray beams at crystals of the receptor; a computer calibrates the makeup of the structure based on how those x-ray beams bounce off the crystals. The resulting 3-D model of the receptor, which looks something like a bouquet of flowers, shows where the receptor subunits are located, and gives unprecedented insight into their actions.

"This new detailed view will be invaluable as we try to develop drugs that might work on specific subunits and therefore help fight or cure some of these neurological diseases and conditions," Gouaux said. "Seeing the structure in more detail can unlock some of its secrets — and may help a lot of people."

Researchers find clue to stopping Alzheimer’s-like diseases

Tiny differences in mice that make them peculiarly resistant to a family of conditions that includes Alzheimer’s, Parkinson’s and Creutzfeldt-Jakob Disease may provide clues for treatments in humans.

Amyloid diseases are often incurable because drug designers cannot identify the events that cause them to start.

Professor Sheena Radford, Astbury Professor of Biophysics at the University of Leeds, said: “Amyloid diseases are associated with the build-up of fibrous plaques out of long strings of ‘misfolding’ proteins, but it is not clear what kicks the process off. That means the normal approach of designing a drug to destroy or disable the species that start the disease process does not work.

“We have to take a completely different tack: instead of targeting the cause of the disease, we need to disrupt the plaque building process.”

The University of Leeds-led team’s study, published in the journal Molecular Cell, looked to mice for a way forward.

“We already knew that mice were not prone to the build up of some of these plaques. This study, for the first time, observed the building happening and saw the differences between the mice proteins and their almost identical human equivalents,” Professor Radford said.

She added: “We mixed the mice and human proteins and found that the mice protein actually stopped the formation of the plaque-forming fibrils by the human protein.”

The research was conducted completely in the test-tube using human and mice beta-2 microglobulin proteins produced in the laboratory. Plaques made up of beta-2 microglobulin are associated with Dialysis Related Amyloidosis (DRA). Instead of being a neurodegenerative condition like Alzheimer’s or Parkinson’s, DRA primarily affects the joints of people on kidney dialysis.

The team observed differences in the formation of the plaque-forming fibrils in samples containing only mice protein, samples with only the human protein and samples containing mixtures of the two.

The lead researcher, Dr Theodoros Karamanos, said: “These two versions of the proteins are almost exactly the same, with very slight differences in structure, but the outcomes are completely different. If I put a misfolding-prone protein in the human sample, I see the formation of fibrils in two days in the right conditions. If I do the same in the mouse sample, I can leave it for weeks and there are no fibrils.

Dr Karamanos added: “The exciting thing is that if you mix the proteins—with only one mouse protein for every five human proteins—you see a significant disruption of the formation of fibrils.”

The study used Nuclear Magnetic Resonance spectroscopy to look at a molecular level at the interactions of the different proteins and identified tiny differences in the physical and chemical properties of the surfaces that made a great difference to whether plaques are formed.

The results showed that the mouse protein binds to the human protein more tightly than the human protein binds to its misfolded form. Interestingly, subtle differences in the driving forces of binding (i.e. the balance of hydrophobic and charge-charge interactions) in the binding interface govern the outcome of assembly.

Dr Karamanos said: “We can’t just load up a syringe and inject mouse protein into patients. But if we know the properties of the interface between the two proteins that are responsible for the inhibition effect, we can ask the chemists to design small molecule drugs which mimic what the mouse protein does to the human protein. That may be a key insight into how to stop the plaque building process.”

Controlling movement with light

For the first time, MIT neuroscientists have shown they can control muscle movement by applying optogenetics — a technique that allows scientists to control neurons’ electrical impulses with light — to the spinal cords of animals that are awake and alert.  

Led by MIT Institute Professor Emilio Bizzi, the researchers studied mice in which a light-sensitive protein that promotes neural activity was inserted into a subset of spinal neurons. When the researchers shone blue light on the animals’ spinal cords, their hind legs were completely but reversibly immobilized. The findings, described in the June 25 issue of PLoS One, offer a new approach to studying the complex spinal circuits that coordinate movement and sensory processing, the researchers say.

In this study, Bizzi and Vittorio Caggiano, a postdoc at MIT’s McGovern Institute for Brain Research, used optogenetics to explore the function of inhibitory interneurons, which form circuits with many other neurons in the spinal cord. These circuits execute commands from the brain, with additional input from sensory information from the limbs.

Previously, neuroscientists have used electrical stimulation or pharmacological intervention to control neurons’ activity and try to tease out their function. Those approaches have revealed a great deal of information about spinal control, but they do not offer precise enough control to study specific subsets of neurons.

Optogenetics, on the other hand, allows scientists to control specific types of neurons by genetically programming them to express light-sensitive proteins. These proteins, called opsins, act as ion channels or pumps that regulate neurons’ electrical activity. Some opsins suppress activity when light shines on them, while others stimulate it.

“With optogenetics, you are attacking a system of cells that have certain characteristics similar to each other. It’s a big shift in terms of our ability to understand how the system works,” says Bizzi, who is a member of MIT’s McGovern Institute.

Muscle control

Inhibitory neurons in the spinal cord suppress muscle contractions, which is critical for maintaining balance and for coordinating movement. For example, when you raise an apple to your mouth, the biceps contract while the triceps relax. Inhibitory neurons are also thought to be involved in the state of muscle inhibition that occurs during the rapid eye movement (REM) stage of sleep.

To study the function of inhibitory neurons in more detail, the researchers used mice developed by Guoping Feng, the Poitras Professor of Neuroscience at MIT, in which all inhibitory spinal neurons were engineered to express an opsin called channelrhodopsin 2. This opsin stimulates neural activity when exposed to blue light. They then shone light at different points along the spine to observe the effects of neuron activation.

When inhibitory neurons in a small section of the thoracic spine were activated in freely moving mice, all hind-leg movement ceased. This suggests that inhibitory neurons in the thoracic spine relay the inhibition all the way to the end of the spine, Caggiano says. The researchers also found that activating inhibitory neurons had no effect on the transmission of sensory information from the limbs to the brain, or on normal reflexes.

“The spinal location where we found this complete suppression was completely new,” Caggiano says. “It has not been shown by any other scientists that there is this front-to-back suppression that affects only motor behavior without affecting sensory behavior.”

“It’s a compelling use of optogenetics that raises a lot of very interesting questions,” says Simon Giszter, a professor of neurobiology and anatomy at Drexel University who was not part of the research team. Among those questions is whether this mechanism behaves as a global “kill switch,” or if the inhibitory neurons form modules that allow for more selective suppression of movement patterns.

Now that they have demonstrated the usefulness of optogenetics for this type of study, the MIT team hopes to explore the roles of other types of spinal cord neurons. They also plan to investigate how input from the brain influences these spinal circuits.

“There’s huge interest in trying to extend these studies and dissect these circuits because we tackled only the inhibitory system in a very global way,” Caggiano says. “Further studies will highlight the contribution of single populations of neurons in the spinal cord for the control of limbs and control of movement.”

Gestures that speak

When you gesticulate you don’t just add a “note of colour” that makes your speech more pleasant: you convey information on sentence structure and make your meanings clearer. A study carried out at SISSA in Trieste demonstrates that gestures and “prosody” (the intonation and rhythm of spoken language) form  a  single “communication system” at the cognitive level, and that we speak using our “whole  body” and not only our vocal tract.

Have you ever found yourself gesticulating and felt a bit stupid for it while talking on the phone?

You’re not alone: it happens very often that people accompany their speech with hand gestures, sometimes even when no one can see them. Why can’t we keep still while speaking? “Because gestures and words very probably form a single “communication system”, which ultimately serves to enhance expression intended as the ability to make oneself understood”, explains Marina Nespor, a neuroscientist at the International School for Advanced Studies (SISSA) of Trieste. Nespor, together with Alan Langus, a SISSA research fellow, and Bahia Guellai from the Université Paris Ouest Nanterre La Défence, who conducted the investigation at SISSA, has just published a study in Frontiers in Psychology which demonstrates the role of gestures in speech “prosody”.

Linguists define prosody as the intonation and rhythm of spoken language, features that help to highlight sentence structure and therefore make the message easier to understand. For example, without prosody, nothing would distinguish the declarative statement “this is an apple” from the surprise question “this is an apple?” (in this case the difference lies in the intonation).

According to Nespor and colleagues, even hand gestures are part of prosody: “the prosody that accompanies speech is not ‘modality specific” explains Langus. “Prosodic information, for the person receiving the message, is a combination of auditory and visual cues. The ‘superior’ aspects (at the cognitive processing level) of spoken language are mapped to the motor‐programs responsible for the production of both speech sounds and accompanying hand gestures”.

Nespor, Langus and Guellai had 20 Italian speakers listen to a series of “ambiguous” utterances, which could be said with different prosodies corresponding to two different meanings. Examples of utterances were “come sicuramente hai visto la vecchia sbarra la porta” where, depending on meaning, “vecchia” can be the subject of the main verb (sbarrare, to block) or an adjective qualifying the subject (sbarra, bar) (‘As you for sure have seen the old lady blocks the door’ versus ‘As you for sure have seen the old bar carries it’). The utterances could be simply listened to (“audio only” modality) or be presented in a video, where the participants could both listen to the sentences and see the accompanying gestures. In the “video” stimuli, the condition could be “matched” (gestures corresponding to the meaning conveyed by speech prosody) or “mismatched” (gestures matching the alternative meaning).

“In the matched conditions there was no improvement ascribable to gestures: the  participants’ performance was very good both in the video and in the “audio only” sessions. It’s in the mismatched condition that the effect of hand gestures became apparent”, explains Langus. “With these stimuli the subjects were much more likely to make the wrong choice (that is, they’d choose the meaning indicated in the gestures rather than in the speech) compared to matched or audio only conditions. This means that gestures affect how meaning is interpreted, and we believe this points to the existence of a common cognitive system for gestures, intonation and rhythm of spoken language”.

“In human communication, voice is not sufficient: even the torso and in particular hand movements are involved, as are facial expressions”, concludes Nespor.