Couch Potatoes May Be Genetically Predisposed to Being Lazy

Studies show 97 percent of American adults get less than 30 minutes of exercise a day, which is the minimum recommended amount based on federal guidelines. New research from the University of Missouri suggests certain genetic traits may predispose people to being more or less motivated to exercise and remain active. Frank Booth, a professor in the MU College of Veterinary Medicine, along with his post-doctoral fellow Michael Roberts, were able to selectively breed rats that exhibited traits of either extreme activity or extreme laziness. They say these rats indicate that genetics could play a role in exercise motivation, even in humans.

“We have shown that it is possible to be genetically predisposed to being lazy,” Booth said. “This could be an important step in identifying additional causes for obesity in humans, especially considering dramatic increases in childhood obesity in the United States. It would be very useful to know if a person is genetically predisposed to having a lack of motivation to exercise, because that could potentially make them more likely to grow obese.”

In their study published in the American Journal of Physiology: Regulatory, Integrative and Comparative Physiology on April 3, 2013, Roberts and Booth put rats in cages with running wheels and measured how much each rat willingly ran on their wheels during a six-day period. They then bred the top 26 runners with each other and bred the 26 rats that ran the least with each other. They repeated this process through 10 generations and found that the line of running rats chose to run 10 times more than the line of “lazy” rats.

Once the researchers created their “super runner” and “couch potato” rats, they studied the levels of mitochondria in muscle cells, compared body composition and conducted thorough genetic evaluations through RNA deep sequencing of each rat.

“While we found minor differences in the body composition and levels of mitochondria in muscle cells of the rats, the most important thing we identified were the genetic differences between the two lines of rats,” Roberts said. “Out of more than 17,000 different genes in one part of the brain, we identified 36 genes that may play a role in predisposition to physical activity motivation.”

Now that the researchers have identified these specific genes, they plan on continuing their research to explore the effects each gene has on motivation to exercise.

Neuroscientists show ’jumping genes’ may contribute to aging-related brain defects

As the body ages, the physical effects are notable; wrinkles in the skin appear, physical exertion becomes harder. But there are also less visible processes going on. Inside aging brains there is another phenomenon at work, which may contribute to age-related brain defects.

In a paper published in the journal Nature Neuroscience CSHL Associate Professor Joshua Dubnau and colleagues show that so-called “jumping genes,” or transposons, increase in abundance and activity in the brains of fruit flies as they age.

Originally discovered at CSHL by Professor Barbara McClintock while working on maize (corn) in the 1940s, transposons are typically repeat DNA sequences that insert themselves into the DNA of an animal or plant.

The moniker “jumping genes” comes from the fact that when activated they can reinsert themselves, or transpose, into another part of the genome. In the course of doing so they are thought to either provide variations in genetic function or, especially in the germline, induce potentially fatal disruptive defects.

Jumping genes in the brains of fruit flies

The median lifespan of a fruit fly can be measured in days. The average fly lives for somewhere between 40-50 days. But they provide a powerful model with which to get at the genetics of things like aging and brain function, including memory.

Dubnau’s interest was piqued by an experiment in which his team showed that when the activity of a protein called Ago2 (Argonaute 2) was perturbed, so was long-term memory—which was tested using a trained Pavolvian response to smell. “This is a neurodegenerative defect that gets profoundly more apparent with age of the flies,” notes Dubnau.

Since Ago2 is known to be involved in protecting against transposon activity in fruit flies, Dubnau and colleagues in his lab, including Wanhe Li and Lisa Prazak, were compelled to look for transposons.

Though transposons have been shown to be active during normal brain development, they are silenced soon afterward. The implication is that they have some functional role in development.

When Dubnau’s group looked for transposons they found that there is a marked increase in transposon levels in the brain cells, or neurons, by 21 days of age in normal fruit flies. The levels were observed to increase steadily with age. These transposons, including one in particular called gypsy, were highly active, jumping from place to place in the genome.

When they blocked Ago2 from being expressed in fruit flies, transposons accumulated at a much younger age. In fact the levels of transposons in young Ago2 “knock-out” flies were equivalent to those in much older normal flies, and increased further still as the Ago2 knock-out flies aged.

Accompanying this transposon accumulation were defects in long-term memory that mirrored those usually seen in much older flies, as well as a much-reduced lifespan. “Essentially the Ago2 knock out flies have no long-term memory by the time they are 20 days old, while normal flies have a normal long-term memory at the same age,” Dubnau reports.

In a previous paper the Dubnau lab, in collaboration with CSHL Assistant Professor Molly Hammell, established a connection between transposons and devastating neurodegenerative diseases such ALS (amyotrophic lateral sclerosis, or Lou Gehrig’s disease) and FTLD (frontotemporal lobar degeneration). The link was the protein TDP-43, which they showed controls transposon activity.

Taken together with the results in his team’s new paper, Dubnau proposes that a “transposon storm” may be responsible for age-related neurodegeneration as well as the pathology seen in some neurodegenerative disorders.

However, his studies so far don’t address whether transposons are the cause or an effect of aging-related brain defects. “The next step will be to activate transposons by genetically manipulating fruit flies and ask whether they are a direct cause of neurodegeneration,” Dubnau says.

Fatheads: How neurons protect themselves against excess fat

We’re all fatheads. That is, our brain cells are packed with fat molecules, more of them than almost any other cell type. Still, if the brain cells’ fat content gets too high, they’ll be in trouble. In a recent study in mice, researchers at Johns Hopkins pinpointed an enzyme that keeps neurons’ fat levels under control, and may be implicated in human neurological diseases. Their findings are published in the May 2013 issue of Molecular and Cellular Biology.

"There are known connections between problems with how the body’s cells process fats and neurodegenerative diseases such as Alzheimer’s, Parkinson’s and amyotrophic lateral sclerosis," says Michael Wolfgang, Ph.D., an assistant professor in the Department of Biological Chemistry at the Johns Hopkins University School of Medicine’s Institute for Basic Biomedical Sciences. "Now we’ve taken a step toward better understanding that connection by identifying an enzyme that lets neurons get rid of excess fat that would otherwise be toxic."

Wolfgang says one clue to the reason for the neurodegeneration/fat-processing connection is that neurons, unlike most cells in the body, seemingly can’t break down fats for energy. Instead, brain cells use fats for tasks such as building cell membranes and communicating information. At the same time, he says, they must prevent the buildup of unneeded fats. Neurons’ fat-loss strategy is rooted in the fact that a fat molecule attached to a chemical group called coenzyme A will be trapped inside the cell, while the coenzyme A-free version can easily cross the cell membrane and escape. With this in mind, Wolfgang, along with colleagues Jessica Ellis, Ph.D., and G. William Wong, Ph.D., focused their study on an enzyme, called ACOT7, which is plentiful in the brain and lops coenzyme A off of certain fat molecules.

The team created mice with a non-working gene for ACOT7 and compared them with normal mice. The scientists saw no obvious differences between the two types of mice as long as they had ready access to food, Wolfgang says. But when food was taken away overnight, so that the mice’s cells would start to break down their fat stores and release fat molecules into the bloodstream for use as energy, ACOT7’s role began to emerge. While the normal fasting mice were merely hungry, the mice lacking ACOT7 had poor coordination, a sign of neurodegeneration. More differences emerged when the researchers dissected the mice; most strikingly, the livers of mice missing ACOT7 were “stark white” with excess fat, Wolfgang says.

Wolfgang cautions that his group’s results are not quite a smoking gun for ACOT7’s involvement in human neurological disease, but says they add to existing circumstantial evidence pointing in that direction. He notes that a special diet that changes the levels of fats and sugars in the bloodstream – the so-called ketogenic diet – can prevent seizures in epileptics; in addition, one study found that patients with epilepsy have less of the ACOT7 enzyme than healthy people.

"We think ACOT7’s purpose is to protect neurons from toxicity and death by allowing excess fat to escape the cells," Ellis says. "Our next step will be to see whether this enzyme does indeed play a role in human neurological disease."

(Image: Courtesy of Sabrina Diano)

Non-Invasive Mapping Helps to Localize Language Centers Before Brain Surgery

A new functional magnetic resonance imaging (fMRI) technique may provide neurosurgeons with a non-invasive tool to help in mapping critical areas of the brain before surgery, reports a study in the April issue of Neurosurgery, official journal of the Congress of Neurological Surgeons. The journal is published by Lippincott Williams & Wilkins, a part of Wolters Kluwer Health.

Evaluating brain fMRI responses to a “single, short auditory language task” can reliably localize critical language areas of the brain—in healthy people as well as patients requiring brain surgery for epilepsy or tumors, according to the new research by Melanie Genetti, PhD, and colleagues of Geneva University Hospitals, Switzerland.

Brief fMRI Task for Functional Brain Mapping
The researchers designed and evaluated a quick and simple fMRI task for use in functional brain mapping. Functional MRI can show brain activity in response to stimuli (in contrast to conventional brain MRI, which shows anatomy only). Before neurosurgery for severe epilepsy or brain tumors, functional brain mapping provides essential information on the location of critical brain areas governing speech and other functions.

The standard approach to brain mapping is direct electrocortical stimulation (ECS)—recording brain activity from electrodes placed on the brain surface. However, this requires several hours of testing and may not be applicable in all patients. Previous studies have compared fMRI techniques with ECS, but mainly for determining the side of language function (lateralization) rather than the precise location (localization).

The new fMRI task was developed and evaluated in 28 healthy volunteers and in 35 patients undergoing surgery for brain tumors or epilepsy. The test used a brief (eight minutes) auditory language stimulus in which the patients heard a series of sense and nonsense sentences.

Functional MRI scans were obtained to localize the brain areas activated by the language task—activated areas would “light up,” reflecting increased oxygenation. A subgroup of patients also underwent ECS, the results of which were compared to fMRI.

Non-invasive Test Accurately Localizes Critical Brain Areas
Based on responses to the language stimulus, fMRI showed activation of the anterior and posterior (front and rear) language areas of the brain in about 90 percent of subjects—neurosurgery patients as well as healthy volunteers. Functional MRI activation was weaker and the language centers more spread-out in the patient group. These differences may have reflected brain adaptations to slow-growing tumors or longstanding epilepsy.

Five of the epilepsy patients also underwent ECS using brain electrodes, the results of which agreed well with the fMRI findings. Two patients had temporary problems with language function after surgery. In both cases, the deficits were related to surgery or complications (bleeding) in the language area identified by fMRI.

Functional brain mapping is important for planning for complex neurosurgery procedures. It provides a guide for the neurosurgeon to navigate safely to the tumor or other diseased area, while avoiding damage to critical areas of the brain. An accurate, non-invasive approach to brain mapping would provide a valuable alternative to the time-consuming ECS procedure.

"The proposed fast fMRI language protocol reliably localized the most relevant language areas in individual subjects," Dr. Genetti and colleagues conclude. In its current state, the new test probably isn’t suitable as the only approach to planning surgery—too many areas "light up" with fMRI, which may limit the surgeon’s ability to perform more extensive surgery with necessary confidence. The researchers add, "Rather than a substitute, our current fMRI protocol can be considered as a valuable complementary tool that can reliably guide ECS in the surgical planning of epileptogenic foci and of brain tumors."

Mind over matter? Study led by NUS researcher reveals for the first time that core body temperature can be controlled by the brain

A team of researchers led by Associate Professor Maria Kozhevnikov from the Department of Psychology at the National University of Singapore (NUS) Faculty of Arts and Social Sciences showed, for the first time, that it is possible for core body temperature to be controlled by the brain. The scientists found that core body temperature increases can be achieved using certain meditation techniques (g-tummo) which could help in boosting immunity to fight infectious diseases or immunodeficiency.

Published in science journal PLOS ONE in March 2013, the study documented reliable core body temperature increases for the first time in Tibetan nuns practising g-tummo meditation. Previous studies on g-tummo meditators showed only increases in peripheral body temperature in the fingers and toes. The g-tummo meditative practice controls “inner energy” and is considered by Tibetan practitioners as one of the most sacred spiritual practices in the region. Monasteries maintaining g-tummo traditions are very rare and are mostly located in the remote areas of eastern Tibet.

The researchers collected data during the unique ceremony in Tibet, where nuns were able to raise their core body temperature and dry up wet sheets wrapped around their bodies in the cold Himalayan weather (-25 degree Celsius) while meditating. Using electroencephalography (EEG) recordings and temperature measures, the team observed increases in core body temperature up to 38.3 degree Celsius. A second study was conducted with Western participants who used a breathing technique of the g-tummo meditative practice and they were also able to increase their core body temperature, within limits.

Applications of the research findings

The findings from the study showed that specific aspects of the meditation techniques can be used by non-meditators to regulate their body temperature through breathing and mental imagery. The techniques could potentially allow practitioners to adapt to and function in cold environments, improve resistance to infections, boost cognitive performance by speeding up response time and reduce performance problems associated with decreased body temperature.

The two aspects of g-tummo meditation that lead to temperature increases are “vase breath” and concentrative visualisation. “Vase breath” is a specific breathing technique which causes thermogenesis, which is a process of heat production. The other technique, concentrative visualisation, involves focusing on a mental imagery of flames along the spinal cord in order to prevent heat losses. Both techniques work in conjunction leading to elevated temperatures up to the moderate fever zone.

Assoc Prof Kozhevnikov explained, “Practicing vase breathing alone is a safe technique to regulate core body temperature in a normal range. The participants whom I taught this technique to were able to elevate their body temperature, within limits, and reported feeling more energised and focused. With further research, non-Tibetan meditators could use vase breathing to improve their health and regulate cognitive performance.”

Further research into controlling body temperature

Assoc Prof Kozhevnikov will continue to explore the effects of guided imagery on neurocognitive and physiological aspects. She is currently training a group of people to regulate their body temperature using vase breathing, which has potential applications in the field of medicine. Furthermore, the use of guided mental imagery in conjunction with vase breathing may lead to higher body temperature increases and better health.

Study finds that hot and cold senses interact

A study from the University of North Carolina School of Medicine offers new insights into how the nervous system processes hot and cold temperatures. The research led by neuroscientist Mark J. Zylka, PhD, associate professor of cell biology and physiology, found an interaction between the neural circuits that detect hot and cold stimuli: cold perception is enhanced when nerve circuitry for heat is inactivated.

“This discovery has implications for how we perceive hot and cold temperatures and for why people with certain forms of chronic pain, such as neuropathic pain, or pain arising as  direct consequence of a nervous system injury or disease, experience heightened responses to cold temperatures,” says Zylka, a member of the UNC Neuroscience Center.

The study also has implications for why a promising new class of pain relief drugs known as TRPV1 antagonists (they block a neuron receptor protein) cause many patients to shiver and “feel cold” prior to the onset of hyperthermia, an abnormally elevated body temperature. Enhanced cold followed by hyperthermia is a major side effect that has limited the use of these drugs in patients with chronic pain associated with multiple sclerosis, cancer, and osteoarthritis.

Zylka’s research sheds new light on how the neural circuits that regulate temperature sensation bring about these responses, and could suggest ways of reducing such side-effects associated with TRPV1 antagonists and related drugs.

The research was selected by the journal Neuron as cover story for the April 10, 2013 print edition and was available in the April 4, 2013 advanced online edition.

This new study used cutting edge cell ablation technology to delete the nerve circuit that encodes heat and some forms of itch while preserving the circuitry that sense cold temperatures. This manipulation results in animals  that were practically “blind” to heat, meaning they could no longer detect hot temperatures, Zylka explains. “Just like removing heat from a room makes us feel cold (such as with an air conditioner), removing the circuit that animals use to sense heat made them hypersensitive to cold. Physiological studies indicated that these distinct circuits regulate one another in the spinal cord.”

TRPV1 is a receptor for heat and is found in the primary sensory nerve circuit that Zylka studied. TRPV1 antagonists make patients temporarily blind to heat, which Zylka speculates is analogous to what happened when his lab deleted the animals’ circuit that detects heat: cold hypersensitivity.

Zylka emphasizes that future studies will be needed to confirm that TRPV1 antagonists affect cold responses in a manner similar to what his lab found with nerve circuit deletion.

First trial to investigate magic mushrooms as a treatment for depression delayed by UK and EU regulations

The world’s first clinical trial to explore the use of the hallucinogenic ingredient in magic mushrooms to treat depression is being delayed due to the UK and EU rules on the use of illegal drugs in research.

Professor David Nutt, president of the British Neuroscience Association and Professor of Neuropsychopharmacology at Imperial College London (UK), will tell the BNA’s Festival of Neuroscience today (Sunday) that although the UK’s Medical Research Council has awarded a grant for the trial, the Government’s regulations controlling the licensing of illegal drugs in research and the EU’s guidelines on Good Manufacturing Practice (GMP) have stalled the start of the trial, which was expected to start this year. He is calling for a change to the regulations.

He will tell the meeting at the Barbican in London, that his research has shown that psilocybin, the psychedelic ingredient in magic mushrooms, has the potential to alleviate severe forms of depression in people who have failed to respond fully to other anti-depressant treatments. However, psilocybin is illegal in the UK; the United Nations 1971 Convention on Psychotropic Substances classifies it as a Schedule 1 drug, one that has a high potential for abuse with no recognised medical use, and the UK has classified it as a Class A drug, the classification used for the most dangerous drugs. This means that a special licence has to be obtained to use magic mushrooms in research in the UK, and the manufacture of a synthetic form of psilocybin for use in patients is tightly controlled by EU regulations.

Prof Nutt will say: “The law for the control of drugs like psilocybin as a Schedule 1 Class A drug makes it almost impossible to use them for research and the reason we haven’t started the study is because finding companies who could manufacture the drug and who are prepared to go through the regulatory hoops to get the licence, which can take up to a year and triple the price, is proving very difficult. The whole situation is bedevilled by this primitive, old-fashioned attitude that Schedule 1 drugs could never have therapeutic potential, and so they have to be made impossible to access.”

“The knock-on effect is this profound impairment of research. We are the first people ever to have done a psilocybin study in the UK, but we are still hunting for a company that can manufacture the drug to GMP standards for the clinical trial, even though we’ve been trying for a year to find one. We live in a world of insanity in terms of regulating drugs at present. The whole field is so bogged down by these intransient regulations, so that even if you have a good idea, you may never get it into the clinic.”

He will say that the regulations need to be changed. “Even if I do this study and I show it’s a really useful treatment for some people with depression, there’s only four hospitals in this country that have a licence to hold this drug, so you couldn’t roll out the treatment if it worked because the regulations would make it difficult to use,” he said.

Prof Nutt and his team at Imperial College London (UK) have shown that when healthy volunteers are injected with psilocybin, the drug switched off a front part of the brain called the anterior cingulate cortex, which is known from previous imaging studies to be over-active in depression. “We found that, even in normal people, the more that part of the brain was switched off under the influence of the drug, the better they felt two weeks later. So there was a relationship between that transient switching off of the brain circuit and their subsequent mood,” he will explain. “This is the basis on which we want to run the trial, because this is what you want to do in depression: you want to switch off that over-active part of the brain.

“The other thing we discovered is that the major site of action of the magic mushrooms is to turn down a circuit in the brain called the ‘default mode network’, which the anterior cingulate cortex is part of. The default mode network is a part of the brain between the front and back. It is active when you are thinking about you; it coordinates the thinking and emotional aspects of you.”

The researchers discovered that the ‘default mode network’ had the highest density of 5HT2A receptors in the brain. These are known to be involved in depression and are the targets for a number of existing anti-depressive drugs that aim to improve levels of serotonin – the neurotransmitter [1] that gives people a sense of well-being and happiness. Psilocybin also acts on these receptors.

“We have found that people with depression have over-active default mode networks, and they are continually locked into a mode of thinking about themselves. So they ruminate on themselves, on their incompetencies, on their badness, that they’re worthless, that they’ve failed; these things are not true, and sometimes they reach delusional levels. This negative rumination may be due to a lack of serotonin and what psilocybin is doing is going in and rapidly replacing the missing serotonin, switching them back into a mind state where they are less ruminating and less depressed,” Prof Nutt will say.

The proposed trial will be for patients with depression who have failed two previous treatments for the condition. Thirty patients will be given a synthetic form of psilocybin and 30 patients will be given a placebo. The drug (or placebo) will be given during two, possibly three, carefully controlled and prepared 30-60 minute sessions. The first session will be a low dose to check there are no adverse responses, the second session will give a higher, therapeutic dose, and then patients can have a third, booster dose in a later session if it’s considered necessary. While they are under the influence of the drug, the patients will have guided talking therapy to enable them to explore their negative thinking and issues that are troubling them. The doctors will follow up the patients for at least a year.

“What we are trying to do is to tap into the reservoir of under-researched ‘illegal’ drugs to see if we can find new and beneficial uses for them in people whose lives are often severely affected by illnesses such as depression. The current legislation is stopping the benefits of these drugs being explored and for the last 40 years we have missed really interesting opportunities to help patients.”

Ethical approval for the trial was granted in March and Prof Nutt says he hopes to be able to start the trial within the next six months – so long as he can find a manufacturer for the drug.

(Image: coolchaser.com)

New research shows how our bodies interact with our minds in response to fear and other emotions

New research has shown that the way our minds react to and process emotions such as fear can vary according to what is happening in other parts of our bodies.

In two different presentations today (Monday) at the British Neuroscience Association Festival of Neuroscience (BNA2013) in London, researchers have shown for the first time that the heart’s cycle affects the way we process fear, and that a part of the brain that responds to stimuli, such as touch, felt by other parts of the body also plays a role.

Dr Sarah Garfinkel, a postdoctoral fellow at the Brighton and Sussex Medical School (Brighton, UK), told a news briefing: “Cognitive neuroscience strives to understand how biological processes interact to create and influence the conscious mind. While neural activity in the brain is typically the focus of research, there is a growing appreciation that other bodily organs interact with brain function to shape and influence our perceptions, cognitions and emotions.

“We demonstrate for the first time that the way in which we process fear is different dependent on when we see fearful images in relation to our heart.”

Dr Garfinkel and her colleagues hooked up 20 healthy volunteers to heart monitors, which were linked to computers. Images of fearful faces were shown on the computers and the electrocardiography (ECG) monitors were able to communicate with the computers in order to time the presentation of the faces with specific points in the heart’s cycle.

“Our results show that if we see a fearful face during systole (when the heart is pumping) then we judge this fearful face as more intense than if we see the very same fearful face during diastole (when the heart is relaxed). To look at neural activity underlying this effect, we performed this experiment in an MRI [magnetic resonance imaging] scanner and demonstrated that a part of the brain called the amygdala influences how our heart changes our perception of fear.

“From previous research, we know that if we present images very fast then we have trouble detecting them, but if an image is particularly emotional then it can ‘pop’ out and be seen. In a second experiment, we exploited our cardiac effect on emotion to show that our conscious experience is affected by our heart. We demonstrated that fearful faces are better detected at systole (when they are perceived as more fearful), relative to diastole. Thus our hearts can also affect what we see and what we don’t see – and can guide whether we see fear.

“Lastly, we have demonstrated that the degree to which our hearts can change the way we see and process fear is influenced by how anxious we are. The anxiety level of our individual subjects altered the extent their hearts could change the way they perceived emotional faces and also altered neural circuitry underlying heart modulation of emotion.”

Dr Garfinkel says that her findings might have the potential to help people who suffer from anxiety or other conditions such as post traumatic stress disorder (PTSD).

“We have identified an important mechanism by which the heart and brain ‘speak’ to each other to change our emotions and reduce fear. We hope to explore the therapeutic implications in people with high anxiety. Anxiety disorders can be debilitating and are very prevalent in the UK and elsewhere. We hope that by increasing our understanding about how fear is processed and ways that it could be reduced, we may be able to develop more successful treatments for these people, and also for those, such as war veterans, who may be suffering from PTSD.

“In addition, there is a growing appreciation about how different forms of meditation can have therapeutic consequences. Work that integrates body, brain and mind to understand changes in emotion can help us understand how meditation and mindfulness practices can have calming effects.”

In a second presentation, Dr Alejandra Sel, a postdoctoral researcher in the Department of Psychology at City University (London, UK), investigated a part of the brain called the somatosensory cortex – the area that perceives bodily sensations, such as touch, pain, body temperature and the perception of the body’s place in space, and which is activated when we observe emotional expressions in the faces of other people.

“In order to understand other’s people emotions we need to experience the same observed emotions in our body. Specifically, observing an emotional face, as opposed to a neutral face, is associated with an increased activity in the somatosensory cortex as if we were expressing and experiencing our own emotions. It is also known that people with damage to the somatosensory cortex find it difficult to recognise emotion in other people’s faces,” Dr Sel told the news briefing.

However, until now, it has not been clear whether activity in the somatosensory cortex was simply a by-product of the way we process visual information, or whether it reacts independently to emotions expressed in other people’s faces, actively contributing to how we perceive emotions in others.

In order to discover whether the somatosensory cortex contributes to the processing of emotion independently of any visual processes, Dr Sel and her colleagues tested two situations on volunteers. Using electroencephalography (EEG) to measure the brain response to images, they showed participants either a face showing fear (emotional) or a neutral face. Secondly, they combined the showing of the face with a small tap to an index finger or the left cheek immediately afterwards.

Dr Sel said: “By tapping someone’s cheek or finger you can modify the ‘resting state’ of the somatosensory cortex inducing changes in brain electrical activity in this area. These changes are measureable and observable with EEG and this enables us to pinpoint the brain activity that is specifically related to the somatosensory cortex and its reaction to external stimuli.

“If the ‘resting state’ of the somatosensory cortex when a fearful face is shown has greater electrical activity than when a neutral face is shown, the changes in the activity of the somatosensory cortex induced by the taps and measured by EEG also will be greater when observing fearful as opposed to neutral faces.

“We subtracted results of the first situation (face only) from the second situation (face and tap), and compared changes in the activity related with the tap in the somatosensory cortex when seeing emotional faces versus neutral faces. This way, we could observe responses of the somatosensory cortex to emotional faces independently of visual processes,” she explained.

The researchers found that there was enhanced activity in the somatosensory cortex in response to fearful faces in comparison to neutral faces, independent of any visual processes. Importantly, this activity was focused in the primary and secondary somatosensory areas; the primary area receives sensory information directly from the body, while the secondary area combines sensory information from the body with information related to body movement and other information, such as memories of previous, sensitive experiences.

“Our experimental approach allows us to isolate and show for the first time (as far as we are aware) changes in somatosensory activity when seeing emotional faces after taking away all visual information in the brain. We have shown the crucial role of the somatosensory cortex in the way our minds and bodies perceive human emotions. These findings can serve as starting point for developing interventions tailored for people with problems in recognising other’s emotions, such as autistic children,” said Dr Sel.

The researchers now plan to investigate whether they get similar results when people are shown faces with other expressions such as happy or angry, and whether the timing of the physical stimulus, the tap to the finger or cheek, makes any difference. In this experiment, the tap occurred 105 milliseconds after a face was shown, and Dr Sel wonders about the effect of a longer time interval.

(Image: Shutterstock)