Posts tagged somatosensory cortex
Articles and news from the latest research reports.
Neuroscientists challenge long-held understanding of the sense of touch
Different types of nerves and skin receptors work in concert to produce sensations of touch, University of Chicago neuroscientists argue in a review article published Sept. 22, 2014, in the journal Trends in Neurosciences. Their assertion challenges a long-held principle in the field — that separate groups of nerves and receptors are responsible for distinct components of touch, like texture or shape. They hope to change the way somatosensory neuroscience is taught and how the science of touch is studied.
Sliman Bensmaia, PhD, assistant professor of organismal biology and anatomy at the University of Chicago, and Hannes Saal, PhD, a postdoctoral scholar in Bensmaia’s lab, reviewed more than 100 research studies on the physiological basis of touch published over the past 57 years. They argue that evidence once thought to show that different groups of receptors and nerves, or afferents, were responsible for conveying information about separate components of touch to the brain actually demonstrates that these afferents work together to produce the complex sensation.
"Any time you touch an object, all of these afferents are active together," Bensmaia said. "They each convey information about all aspects of an object, whether it’s the shape, the texture, or its motion across the skin."
Three different types of afferents convey information about touch to the brain: slowly adapting type 1 (SA1), rapidly adapting (RA) and Pacinian (PC). According to the traditional view, SA1 afferents are responsible for communicating information about shape and texture of objects, RA afferents help sense motion and grip control, and PC afferents detect vibrations.
In the past, Bensmaia said, this classification system has been supported by experiments using mechanical devices to elicit one or more of these specific components of touch. For example, responses to texture are often generated using a rotating, cylindrical drum covered with a Braille-like pattern of raised dots. Study subjects would place a finger on the drum as it rotated, and scientists recorded the neural responses.
Such experiments showed that SA1 afferents responded very strongly to this artificial stimulus, and RA and PC afferents did not, thus the association of SA1s with texture. However, in experiments in which subjects moved a finger across sandpaper — the quintessential example of the type of textures we encounter in the real world — SA1 afferents did not respond at all.
Bensmaia also pointed out discrepancies in the predominant thinking about how we discern shape. Perception of shapes has generally been tested using devices with raised or embossed letters to test a subject’s ability to interpret text by touch. These experiments also showed that such inputs produced a strong SA1 response, so they were implicated in perception of shape as well.
In the 1980s, however, researchers developed a device meant to help blind people read by generating vibrating patterns in the shape of letters on an array of pins. While the device was not a commercial success, people were able to use it to detect letter shapes and read, although experiments showed that it activated RA and PC afferents, not the supposedly shape-detecting SA1s.
Bensmaia said such experiments show how devices created to generate artificial stimuli focusing on individual components of the sense of touch can result in misleading findings. Some types of afferents are better than others at detecting texture or shape, for example, but all of them respond in their own way and contribute to the overall sensation.
"To get a good picture of how stimulus information is being conveyed in these afferent populations, you have to look at a diverse set of stimuli that spans the range of what you might feel in everyday tactile experience," he said.
Instead of thinking of individual groups of afferents working separately to process different components of the sense of touch, Bensmaia said we should think of all of them working in concert, much like individual musicians in a band to create its overall sound. Each musician contributes in his or her own way. Emphasizing one instrument or removing another can change the character of a song, but no single sound is responsible for the entire performance.
Adopting this new way of thinking will have far-reaching implications for both the study of the sense of touch and the design of future research, Bensmaia said.
"I think it’s going to change neuroscience textbooks, and by extension it’s going to change the way somatosensory neuroscience is taught. It’s really the starting point for everything."
When we learn, we associate a sensory experience either with other stimuli or with a certain type of behaviour. The neurons in the cerebral cortex that transmit the information modify the synaptic connections that they have with the other neurons. According to a generally-accepted model of synaptic plasticity, a neuron that communicates with others of the same kind emits an electrical impulse as well as activating its synapses transiently. This electrical pulse, combined with the signal received from other neurons, acts to stimulate the synapses. How is it that some neurons are caught up in the communication interplay even when they are barely connected? This is the crucial chicken-or-egg puzzle of synaptic plasticity that a team led by Anthony Holtmaat, professor in the Department of Basic Neurosciences in the Faculty of Medicine at UNIGE, is aiming to solve. The results of their research into memory in silent neurons can be found in the latest edition of Nature.
Learning and memory are governed by a mechanism of sustainable synaptic strengthening. When we embark on a learning experience, our brain associates a sensory experience either with other stimuli or with a certain form of behaviour. The neurons in the cerebral cortex responsible for ensuring the transmission of the relevant information, then modify the synaptic connections that they have with other neurons. This is the very arrangement that subsequently enables the brain to optimise the way information is processed when it is met again, as well as predicting its consequences.
Neuroscientists typically induce electrical pulses in the neurons artificially in order to perform research on synaptic mechanisms.
The neuroscientists from UNIGE, however, chose a different approach in their attempt to discover what happens naturally in the neurons when they receive sensory stimuli. They observed the cerebral cortices of mice whose whiskers were repeatedly stimulated mechanically without an artificially-induced electrical pulse. The rodents use their whiskers as a sensor for navigating and interacting; they are, therefore, a key element for perception in mice.
An extremely low signal is enough
By observing these natural stimuli, professor Holtmaat’s team was able to demonstrate that sensory stimulus alone can generate long-term synaptic strengthening without the neuron discharging either an induced or natural electrical pulse. As a result – and contrary to what was previously believed – the synapses will be strengthened even when the neurons involved in a stimulus remain silent.In addition, if the sensory stimulation lasts over time, the synapses become so strong that the neuron in turn is activated and becomes fully engaged in the neural network. Once activated, the neuron can then further strengthen the synapses in a forwards and backwards movement. These findings could solve the brain’s “What came first?” mystery, as they make it possible to examine all the synaptic pathways that contribute to memory, rather than focusing on whether it is the synapsis or the neuron that activates the other.
The entire brain is mobilised
A second discovery lay in store for the researchers. During the same experiment, they were also able to establish that the stimuli that were most effective in strengthening the synapses came from secondary, non-cortical brain regions rather than major cortical pathways (which convey actual sensory information). Accordingly, storing information would simply require the co-activation of several synaptic pathways in the neuron, even if the latter remains silent. These findings may also have important implications both for the way we understand learning mechanisms and for therapeutic possibilities, in particular for rehabilitation following a stroke or in neurodegenerative disorders. As professor Holtmaat explains: “It is possible that sensory stimulation, when combined with another activity (motor activity, for example), works better for strengthening synaptic connections”. The professor concludes: “In the context of therapy, you could combine two different stimuli as a way of enhancing the effectiveness.”
Neural Transplant Reduces Absence Epilepsy Seizures in Mice
New research from North Carolina State University pinpoints the areas of the cerebral cortex that are affected in mice with absence epilepsy and shows that transplanting embryonic neural cells into these areas can alleviate symptoms of the disease by reducing seizure activity. The work may help identify the areas of the human brain affected in absence epilepsy and lead to new therapies for sufferers.
Absence epilepsy primarily affects children. These seizures differ from “clonic-tonic” seizures in that they don’t cause muscle spasms; rather, patients “zone out” or stare into space for a period of time, with no memory of the episode afterward. Around one-third of patients with absence epilepsy fail to respond to medication, demonstrating the complexity of the disease.
NC State neurobiology professor Troy Ghashghaei and colleagues looked at a genetic mouse model for absence epilepsy to determine what was happening in their brains during these seizures. They found that the seizures were accompanied by hyperactivity in the areas of the brain associated with vision and touch – areas referred to as primary visual and primary somatosensory cortices in the occipital and parietal lobes, respectively.
“There are neurons that excite brain activity, and neurons that inhibit activity,” Ghashghaei says. “The inhibitory neurons work by secreting an inhibitory neurotransmitter called gamma-aminobutyric acid, or GABA. The ‘GABAergic’ interneurons were recently shown by others to be defective in the mice with absence seizures, and we surmised that these malfunctioning neurons might be part of the problem, especially in the visual and somatosensory cortical areas.”
Ghashghaei’s team took embryonic neural stem cells from a part of the developing brain that generates GABAergic interneurons for the cerebral cortex. They harvested these cells from normal mouse embryos and transplanted them into the occipital cortex of the genetic mice with absence seizures. Absence seizure activity in treated animals decreased dramatically, and the mice gained more weight and survived longer than untreated mice.
“This is a profound and remarkably effective first result, and adds to the recent body of evidence that these transplantation treatments can work in mouse models of epilepsy. But we still don’t understand the mechanisms behind what the normal inhibitory cells are doing in areas of the visual cortex of absence epileptic mice,” Ghashghaei says. “We know that you can get positive results even when a small number of transplanted neurons actually integrate into the cortex of affected mice, which is very interesting. But we don’t know how the transplanted cells are connecting with other cells in the cortex and how they alleviate the absence seizures in the mouse model we employed.
“Our next steps will be to explore these questions. In addition, we are very interested in methods being devised by multiple labs around the world to ‘reprogram’ cells from transplantation patients to generate normal GABAergic and other types of neurons. Once established, this would eliminate the need for embryonic stem cells for this type of treatment. The ultimate goal is to develop new therapies for humans suffering from various forms of epilepsies, especially those for whom drugs do not work.”
Researchers examine how touch can trigger our emotions
While touch always involves awareness, it also sometimes involves emotion. For example, picking up a spoon triggers no real emotion, while feeling a gentle caress often does. Now, scientists in the Cell Press journal Neuron describe a system of slowly conducting nerves in the skin that respond to such gentle touch. Using a range of scientific techniques, investigators are beginning to characterize these nerves and to describe the fundamental role they play in our lives as a social species—from a nurturing touch to an infant to a reassuring pat on the back. Their work also suggests that this soft touch wiring may go awry in disorders such as autism.
The nerves that respond to gentle touch, called c-tactile afferents (CTs), are similar to those that detect pain, but they serve an opposite function: they relay events that are neither threatening nor tissue-damaging but are instead rewarding and pleasant.
"The evolutionary significance of such a system for a social species is yet to be fully determined," says first author Francis McGlone, PhD, of Liverpool John Moores University in England. "But recent research is finding that people on the autistic spectrum do not process emotional touch normally, leading us to hypothesize that a failure of the CT system during neurodevelopment may impact adversely on the functioning of the social brain and the sense of self."
For some individuals with autism, the light touch of certain fabrics in clothing can cause distress. Temple Grandin, an activist and assistant professor of animal sciences at Colorado State University who has written extensively on her experiences as an individual with autism, has remarked that her lack of empathy in social situations may be partially due to a lack of “comforting tactual input.” Professor McGlone also notes that deficits in nurturing touch during early life could have negative effects on a range of behaviors and psychological states later in life.
Further research on CTs may help investigators develop therapies for autistic patients and individuals who lacked adequate nurturing touch as children. Also, a better understanding of how nerves that relay rewarding sensations interact with those that signal pain could provide insights into new treatments for certain types of pain.
Professor McGlone believes that possessing an emotional touch system in the skin is as important to well-being and survival as having a system of nerves that protect us from harm. “In a world where human touch is becoming more and more of a rarity with the ubiquitous increase in social media leading to non-touch-based communication, and the decreasing opportunity for infants to experience enough nurturing touch from a carer or parent due to the economic pressures of modern living, it is becoming more important to recognize just how vital emotional touch is to all humankind.”
Touching the brain
By examining the sense of touch in stroke patients, a University of Delaware cognitive psychologist has found evidence that the brains of these individuals may be highly plastic even years after being damaged.
The research is published in the March 6 edition of the journal Current Biology, in an article written by Jared Medina, assistant professor of psychology at UD, and Brenda Rapp of Johns Hopkins University’s Department of Cognitive Science. The findings, which are focused on patients who lost the sense of touch in their hands after a stroke, also have potential implications for other impairments caused by brain damage, Medina said.
“Our lab is interested in how the brain represents the body, not just in the sense of touch,” he said. “That involves a lot of different areas of the brain.”
For decades, scientists have been mapping the brain to determine which areas control certain functions, from movement to emotion to memory. In terms of representing the sense of touch, researchers know which specific parts of the brain are associated with representing specific parts of the body, Medina said.
Those scientists also know that, following the brain damage a stroke causes, patients often regain some of what they initially lost due to that damage.
“Even if every neuron has been killed in the part of the brain that represents touch on the hand, that doesn’t mean that you’re never going to feel anything on your hand again,” Medina said. “We’ve known that isn’t the case because the map can reorganize. The brain can change due to injury.”
But what the new research by Medina and Rapp found is that the brains of those stroke patients may change much more easily than the undamaged brains of healthy people — what they call “hyper-lability.”
The researchers worked with people who had had strokes in the past that affected their ability to localize touch. Each research participant, without being able to see his hand, was touched on the wrist and then on the fingertips. When asked to pinpoint the second touch, the stroke patients reported sensing the touch farther down their finger, toward the wrist, rather than in its actual location.
Medina says that likely occurs because the neural map in the brain is shifting based on the earlier wrist touch — a phenomenon termed “experience-dependent plasticity.”
“Now what’s interesting about this is that when you and I [who haven’t had a stroke] are touched on the wrist, then the fingertips, we don’t have these changes that the brain-damaged individuals do,” he said. “This provides the counterintuitive finding that the maps in brain-damaged individuals are actually much more plastic than in you and me.”
Hyper-plasticity has positive and negative implications, he said.
“On the positive side, this plasticity may potentially be harnessed in rehabilitation to improve function” after a stroke or various other types of brain injury, Medina said. But, he added, the brain may also be so plastic in those cases that changes aren’t stable, creating additional problems.
That’s what he expects additional research to address.
“Now that we’ve found that these maps are more plastic than we thought, can certain strategies help the map become more stable and more accurate again? That’s one of the next questions, and we can only answer it by continuing to learn more about how the mind works.”
(Source: udel.edu)
Ultrasound directed to the human brain can boost sensory performance
Whales, bats, and even praying mantises use ultrasound as a sensory guidance system – and now a new study has found that ultrasound can modulate brain activity to heighten sensory perception in humans.
Virginia Tech Carilion Research Institute scientists have demonstrated that ultrasound directed to a specific region of the brain can boost performance in sensory discrimination. The study, published online Jan. 12 in Nature Neuroscience, provides the first demonstration that low-intensity, transcranial-focused ultrasound can modulate human brain activity to enhance perception.
“Ultrasound has great potential for bringing unprecedented resolution to the growing trend of mapping the human brain’s connectivity,” said William “Jamie” Tyler, an assistant professor at the Virginia Tech Carilion Research Institute, who led the study. “So we decided to look at the effects of ultrasound on the region of the brain responsible for processing tactile sensory inputs.”
The scientists delivered focused ultrasound to an area of the cerebral cortex that corresponds to processing sensory information received from the hand. To stimulate the median nerve – a major nerve that runs down the arm and the only one that passes through the carpal tunnel – they placed a small electrode on the wrist of human volunteers and recorded their brain responses using electroencephalography, or EEG. Then, just before stimulating the nerve, they began delivering ultrasound to the targeted brain region.
The scientists found that the ultrasound both decreased the EEG signal and weakened the brain waves responsible for encoding tactile stimulation.
The scientists then administered two classic neurological tests: the two-point discrimination test, which measures a subject’s ability to distinguish whether two nearby objects touching the skin are truly two distinct points, rather than one; and the frequency discrimination task, a test that measures sensitivity to the frequency of a chain of air puffs.
What the scientists found was unexpected.
The subjects receiving ultrasound showed significant improvements in their ability to distinguish pins at closer distances and to discriminate small frequency differences between successive air puffs.
“Our observations surprised us,” said Tyler. “Even though the brain waves associated with the tactile stimulation had weakened, people actually got better at detecting differences in sensations.”
Why would suppression of brain responses to sensory stimulation heighten perception? Tyler speculates that the ultrasound affected an important neurological balance.
“It seems paradoxical, but we suspect that the particular ultrasound waveform we used in the study alters the balance of synaptic inhibition and excitation between neighboring neurons within the cerebral cortex,” Tyler said. “We believe focused ultrasound changed the balance of ongoing excitation and inhibition processing sensory stimuli in the brain region targeted and that this shift prevented the spatial spread of excitation in response to stimuli resulting in a functional improvement in perception.”
To understand how well they could pinpoint the effect, the research team moved the acoustic beam one centimeter in either direction of the original site of brain stimulation – and the effect disappeared.
“That means we can use ultrasound to target an area of the brain as small as the size of an M&M,” Tyler said. “This finding represents a new way of noninvasively modulating human brain activity with a better spatial resolution than anything currently available.”
Based on the findings of the current study and an earlier one, the researchers concluded that ultrasound has a greater spatial resolution than two other leading noninvasive brain stimulation technologies – transcranial magnetic stimulation, which uses magnets to activate the brain, and transcranial direct current stimulation, which uses weak electrical currents delivered directly to the brain through electrodes placed on the head.
“Gaining a better understanding of how pulsed ultrasound affects the balance of synaptic inhibition and excitation in targeted brain regions – as well as how it influences the activity of local circuits versus long-range connections – will help us make more precise maps of the richly interconnected synaptic circuits in the human brain,” said Wynn Legon, the study’s first author and a postdoctoral scholar at the Virginia Tech Carilion Research Institute. “We hope to continue to extend the capabilities of ultrasound for noninvasively tweaking brain circuits to help us understand how the human brain works.”
“The work by Jamie Tyler and his colleagues is at the forefront of the coming tsunami of developing new safe yet effective noninvasive ways to modulate the flow of information in cellular circuits within the living human brain,” said Michael Friedlander, executive director of the Virginia Tech Carilion Research Institute and a neuroscientist who specializes in brain plasticity. “This approach is providing the technology and proof of principle for precise activation of neural circuits for a range of important uses, including potential treatments for neurodegenerative disorders, psychiatric diseases, and behavioral disorders. Moreover, it arms the neuroscientific community with a powerful new tool to explore the function of the healthy human brain, helping us understand cognition, decision-making, and thought. This is just the type of breakthrough called for in President Obama’s BRAIN Initiative to enable dramatic new approaches for exploring the functional circuitry of the living human brain and for treating Alzheimer’s disease and other disorders.”
A team of Virginia Tech Carilion Research Institute scientists – including Tomokazu Sato, Alexander Opitz, Aaron Barbour, and Amanda Williams, along with Virginia Tech graduate student Jerel Mueller of Raleigh, N.C. – joined Tyler and Legon in conducting the research. In addition to his position at the institute, Tyler is an assistant professor of biomedical engineering and sciences at the Virginia Tech–Wake Forest University School of Biomedical Engineering and Sciences. In 2012, he shared a Technological Innovation Award from the McKnight Endowment for Neuroscience to work on developing ultrasound as a noninvasive tool for modulating brain activity.
“In neuroscience, it’s easy to disrupt things,” said Tyler. “We can distract you, make you feel numb, trick you with optical illusions. It’s easy to make things worse, but it’s hard to make them better. These findings make us believe we’re on the right path.”
Keep your friends close, but …
Counterintuitive findings from a new USC study show that the part of the brain that is associated with empathizing with the pain of others is activated more strongly by watching the suffering of hateful people as opposed to likable people.
While one might assume that we would empathize more with people we like, the study may indicate that the human brain focuses more greatly on the need to monitor enemies closely, especially when they are suffering.
“When you watch an action movie and the bad guy appears to be defeated, the moment of his demise draws our focus intensely,” said Lisa Aziz-Zadeh of the Brain and Creativity Institute of the USC Dornsife College of Letters, Arts and Sciences. “We watch him closely to see whether he’s really down for the count because it’s critical for predicting his potential for retribution in the future.”
Aziz-Zadeh, who has a joint appointment with the USC Division of Occupational Science and Occupational Therapy, collaborated with lead author Glenn Fox, a PhD candidate at USC, and Mona Sobhani, formerly a graduate student at USC and who is now a postdoctoral researcher at Vanderbilt University, on a study that appears this month in Frontiers in Psychology.
The study examined activity in the so-called “pain matrix” of the brain, a network that includes the insula cortex, the anterior cingulate and the somatosensory cortices — regions known to activate when an individual watches another person suffer.
The pain matrix is thought to be a related to empathy — allowing us to understand another’s pain. However, this study indicates that the pain matrix may be more involved in processing pain in general and not necessarily tied to empathic processing.
Participants — all of them white, male and Jewish — first watched videos of hateful, anti-Semitic individuals in pain and then other videos of tolerant, nonhateful individuals in pain. Their brains were scanned with functional magnetic resonance imaging (fMRI) to show activity levels in the pain matrix.
Surprisingly, the participants’ pain matrices were more activated by watching the anti-Semites suffer compared to the tolerant individuals.
“The results further revealed the brain’s flexibility in processing complex social situations,” Fox said. “The brain uses the complete context of the situation to mount an appropriate response. In this case, the brain’s response is likely tied to the relative increase in the need to attend to and understand the pain of the hateful person.”
A possible next step for the researchers will be to try to understand how regulating one’s emotional reaction to stimuli such as these alters the resulting patterns of brain activity.
Birth gets the brain ready to sense the world
Neurons that process sensory information such as touch and vision are arranged in precise, well-characterized maps that are crucial for translating perception into understanding. A study published by Cell Press on October 14 in the journal Developmental Cell reveals that the actual act of birth in mice causes a reduction in a brain chemical called serotonin in the newborn mice, triggering sensory maps to form. The findings shed light on the key role of a dramatic environmental event in the development of neural circuits and reveal that birth itself is one of the triggers that prepares the newborn for survival outside the womb.
"Our results clearly demonstrate that birth has active roles in brain formation and maturation," says senior study author Hiroshi Kawasaki of Kanazawa University in Japan. "We found that birth regulates neuronal circuit formation not only in the somatosensory system but also in the visual system. Therefore, it seems reasonable to speculate that birth actually plays a wider role in various brain regions."
Mammals ranging from mice to humans have brain maps that represent various types of sensory information. In a region of the rodent brain known as the barrel cortex, neurons that process tactile information from whiskers are arranged in a map corresponding to the spatial pattern of whiskers on the snout, with neighboring columns of neurons responding to stimulation of adjacent whiskers. Although previous studies have shown that the neurotransmitter serotonin influences the development of sensory maps, its specific role during normal development has not been clear until now.
In this new study, Kawasaki and his team find that the birth of mouse pups leads to a drop in serotonin levels in the newborn’s brain, triggering the formation of neural circuits in the barrel cortex and in the lateral geniculate nucleus (LGN), a brain region that processes visual information. When mice were treated with drugs that either induced preterm birth or decreased serotonin signaling, neural circuits in the barrel cortex as well as in the LGN formed more quickly. Conversely, neural circuits in the barrel cortex failed to form when the mice were treated with a drug that increased serotonin signaling, suggesting that a reduction in levels of this neurotransmitter is crucial for sensory map formation.
Because serotonin also plays a key role in mental disorders, it is possible that abnormalities in birth processes and the effects on subsequent serotonin signaling and brain development could increase the risk of psychiatric diseases. “Uncovering the entire picture of the downstream signaling pathways of birth may lead to the development of new therapeutic methods to control the risk of psychiatric diseases induced by abnormal birth,” Kawasaki says.
(Source: eurekalert.org)
Brain research shows psychopathic criminals do not lack empathy, but fail to use it automatically
Criminal psychopathy can be both repulsive and fascinating, as illustrated by the vast number of books and movies inspired by this topic. Offenders diagnosed with psychopathy pose a significant threat to society, because they are more likely to harm other individuals and to do so again after being released. A brain imaging study in the Netherlands shows individuals with psychopathy have reduced empathy while witnessing the pains of others. When asked to empathize, however, they can activate their empathy. This could explain why psychopathic individuals can be callous and socially cunning at the same time.
Why are psychopathic individuals more likely to hurt others? Individuals with psychopathy characteristically demonstrate reduced empathy with the feelings of others, which may explain why it is easier for them to hurt other people. However, what causes this lack of empathy is poorly understood. Scientific studies on psychopathic subjects are notoriously hard to conduct. “Convicted criminals with a diagnosis of psychopathy are confined to high-security forensic institutions in which state-of-the-art technology to study their brain, like magnetic resonance imaging, is usually unavailable”, explains Professor Christian Keysers, Head of the Social Brain Lab in Amsterdam, and senior author of a study on psychopathy appearing in the Journal Brain this week. “Bringing them to scientific research centres, on the other hand, requires the kind of high-security transportation that most judicial systems are unwilling to finance.”
The Dutch judicial system, however, seems to be an exception. They joined forces with academia to promote a better understanding of psychopathy. As a result, criminals with psychopathy were transported to the Social Brain Lab of the University Medical Center in Groningen (The Netherlands). There, the team could use state of the art high-field functional magnetic resonance imaging to peak into the brain of criminals with psychopathy while they view the emotions of others.
The study, which will appear on the 25th of July in the journal Brain (published by Oxford University Press) and is entitled “Reduced spontaneous but relatively normal deliberate vicarious representations in psychopathy”, included 18 individuals with psychopathy and a control group, and consisted of three parts. “All participants first watched short movie clips of two people interacting with each other, zoomed in on their hands. The movie clips showed one hand touching the other in a loving, a painful, a socially rejecting or a neutral way. At this stage, we asked them to look at these movies just as they would watch one of their favourite films”, Harma Meffert, the first author of the paper, explains. Meffert was a graduate student in the Social Brain Lab while the study was conducted, and is now a post-doctoral fellow at the National Institutes of Mental Health in Bethesda.
Next, the participants watched the same clips again. This time, however, the researchers prompted them explicitly to “empathise with one of the actors in the movie”, that is, they were requested to really try to feel what the actors in the movie were feeling.
"In the third and final part, we performed similar hand interactions with the participants themselves, while they were lying in the scanner, having their brain activity measured", adds Meffert. "We wanted to know to what extent they would activate the same brain regions while they were watching the hand interactions in the movies, as they would when they were experiencing these same hand interactions themselves."
Our brains are equipped with what scientists call a “mirror system”. For example, the motor cortex of the brain normally allows you to move your own body. Your so called somatosensory cortex, when activated, makes you to feel touch on your skin. Your insula, finally, when activated makes you feel emotions like pain or disgust. In the last decades, brain scientists have discovered that when people watch other people move their body, or see those people being touched, or have emotions, these same brain regions are activated. In other words, the actions, touch or emotions of others become your own. This “mirror system” possibly constitutes a crucial part of our ability to empathize with other people, and it has been previously shown, that the less you activate this system, the less you report to empathize with other people. It has been suggested that individuals with psychopathy might somehow suffer from a broken “mirror system”, resulting in a diminished ability to empathize with their victims.
As it turns out, however, the picture seems to be more complex. When asked to just watch the film clips, the individuals with psychopathy indeed did activate their mirror system less. “Regions involved in their own actions, emotions and sensations were less active than that of controls while they saw what happens in others”, summarizes Christian Keysers. “At first, this seems to suggest that psychopathic criminals might hurt others more easily than we do, because they do not feel pain, when they see the pain of their victims.”
As the second part of the study revealed, however, it’s not quite so simple. Instead of generally activating their mirror system less, individuals with psychopathy rather seem not to use this system spontaneously, but they can use it when asked to. “When explicitly asked to empathize, the differences between how strongly the individuals with and without psychopathy activate their own actions, sensations and emotions almost entirely disappeared in their empathic brain”, explains Valeria Gazzola, Assistant Professor at the UMCG and second author of the paper. “Psychopathy may not be so much the incapacity to empathize, but a reduced propensity to empathize, paired with a preserved capacity to empathize when required to do so”. The brain data suggests, that by default, psychopathic individuals feel less empathy than others. If they try to empathize, however, they can switch to ‘empathy mode’.
There might be two sides to these findings. The darker side is that reduced spontaneous empathy together with a preserved capacity for empathy might be the cocktail that makes these individuals so callous when harming their victims and at the same time so socially cunning when they try to seduce their victims. Whether individuals with psychopathy autonomously switch their empathy mode on and off depending on the requirements of a social situation however remains to be established. The brighter side is that the preserved capacity for empathy might be harnessed in therapy. Instead of having to create a capacity for empathy, therapies may need to focus on making the existing capacity more automatic to prevent them from further harming others. How to do so, remains at this stage uncertain.
Problem-solving governs how we process sensory stimuli
Various areas of the brain process our sensory experiences. How the areas of the cerebral cortex communicate with each other and process sensory information has long puzzled neuroscientists. Exploring the sense of touch in mice, brain researchers from the University of Zurich now demonstrate that the transmission of sensory information from one cortical area to connected areas depends on the specific task to solve and the goal-directed behavior. These findings can serve as a basis for an improved understanding of cognitive disorders.
In the mammalian brain, the cerebral cortex plays a crucial role in processing sensory inputs. The cortex can be subdivided into different areas, each handling distinct aspects of perception, decision-making or action. The somatosensory cortex, for instance, comprises the part of the cerebral cortex that primarily processes haptic sensations. The different areas of the cerebral cortex are interconnected and communicate with each other. A central, unanswered question of neuroscience is how exactly do these brain areas communicate to process sensory stimuli and produce appropriate behavior. A team of researchers headed by Professor Fritjof Helmchen at the University of Zurich’s Brain Research Institute now provides an answer: The processing of sensory information depends on what you want to achieve. The brain researchers observed that nerve cells in the sensory cortex that connect to distinct brain areas are activated differentially depending on the task to be solved.
Goal-directed processing of sensory information
In their publication in Nature, the researchers studied how mice use their facial whiskers to explore their environment, much like we do in the dark with our hands and fingers. One mouse group was trained to distinguish coarse and fine sandpapers using their whiskers in order to obtain a reward. Another group had to work out the angle, at which an object – a metal rod – was located relative to their snout. The neuroscientists measured the activity of neurons in the primary somatosensory cortex using a special microscopy technique. With simultaneous anatomical stainings they also identified which of these neurons sent their projections to the more remote secondary somatosensory area and the motor cortex, respectively.
The primary somatosensory neurons with projections to the secondary somatosensory cortex predominantly became active when the mice had to distinguish the surface texture of the sandpaper. Neurons with projections to the motor cortex, on the other hand, were more involved when mice needed to localize the metal rod. These different activity patterns were not evident when mice passively touched sandpaper or metal rods without having been set a task – in other words, when their actions were not motivated by a reward. Thus, the sensory stimuli alone were not sufficient to explain the different pattern of information transfer to the remote brain areas.
Impaired communication in the brain
According to Fritjof Helmchen, the activity in a cortical area can be transmitted to remote areas in a targeted fashion if we have to extract (‘filter’) specific information from the environment to solve a problem. In cognitive disorders such Alzheimer’s disease, Autism, and Schizophrenia, this communication between brain areas is often disrupted. “A better understanding of how these long-range, interconnected networks in the brain operate might help to develop therapies that re-establish this specific cortical communication,” says Helmchen. The aim would be to thereby improve the impaired cognitive abilities of patients.