Neuroscience

Articles and news from the latest research reports.

Posts tagged neuroscience

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Understanding Alzheimer’s: Study gives insights into how disease kills brain cells Exactly how Alzheimer’s disease kills brain cells is still somewhat of a mystery, but University of Michigan researchers have uncovered a clue that supports the idea that small proteins prick holes into neurons. The team also found that a certain size range of clumps of these proteins are particularly toxic to cells, while smaller and larger aggregates of the protein appear to be benign. The findings, which appear in the journal PLOS ONE, add important detail to the knowledge base regarding this disease that affects 5.4 million Americans in 2012 but remains incurable and largely untreatable. The results could potentially help pharmaceutical researchers target drugs to the right disease mechanisms. Small proteins called amyloid-beta peptides are the prime suspect for causing cell death in Alzheimer’s. They make up most of the senile plaque fibers found in the brains of autopsied patients. Researchers offer several hypotheses for how the peptides might cause the disease. They blame inflammation, oxidative stress or an imbalance of calcium ions possibly caused by holes in the cell membranes. The U-M findings strongly support the idea that amyloid peptides damage the membrane around nerve cells and lead to uncontrolled movement of calcium ions into them. Calcium signaling is an important way that cells communicate and healthy cells regulate its flow precisely. The toxic mechanism implicated in the new study could act on its own or together with the other proposed courses and ultimately lead to a loss of brain cells in patients, the researchers say.

Understanding Alzheimer’s: Study gives insights into how disease kills brain cells

Exactly how Alzheimer’s disease kills brain cells is still somewhat of a mystery, but University of Michigan researchers have uncovered a clue that supports the idea that small proteins prick holes into neurons.

The team also found that a certain size range of clumps of these proteins are particularly toxic to cells, while smaller and larger aggregates of the protein appear to be benign.

The findings, which appear in the journal PLOS ONE, add important detail to the knowledge base regarding this disease that affects 5.4 million Americans in 2012 but remains incurable and largely untreatable. The results could potentially help pharmaceutical researchers target drugs to the right disease mechanisms.

Small proteins called amyloid-beta peptides are the prime suspect for causing cell death in Alzheimer’s. They make up most of the senile plaque fibers found in the brains of autopsied patients. Researchers offer several hypotheses for how the peptides might cause the disease. They blame inflammation, oxidative stress or an imbalance of calcium ions possibly caused by holes in the cell membranes.

The U-M findings strongly support the idea that amyloid peptides damage the membrane around nerve cells and lead to uncontrolled movement of calcium ions into them. Calcium signaling is an important way that cells communicate and healthy cells regulate its flow precisely. The toxic mechanism implicated in the new study could act on its own or together with the other proposed courses and ultimately lead to a loss of brain cells in patients, the researchers say.

Filed under brain alzheimer alzheimer's disease neuron amyloid peptides neuroscience psychology science

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Calcium reveals connections between neurons A team led by MIT neuroscientists has developed a way to monitor how brain cells coordinate with each other to control specific behaviors, such as initiating movement or detecting an odor. The researchers’ new imaging technique, based on the detection of calcium ions in neurons, could help them map the brain circuits that perform such functions. It could also provide new insights into the origins of autism, obsessive-compulsive disorder and other psychiatric diseases, says Guoping Feng, senior author of a paper appearing in the Oct. 18 issue of the journal Neuron. “To understand psychiatric disorders we need to study animal models, and to find out what’s happening in the brain when the animal is behaving abnormally,” says Feng, the James W. and Patricia Poitras Professor of Neuroscience and a member of the McGovern Institute for Brain Research at MIT. “This is a very powerful tool that will really help us understand animal models of these diseases and study how the brain functions normally and in a diseased state.”

Calcium reveals connections between neurons

A team led by MIT neuroscientists has developed a way to monitor how brain cells coordinate with each other to control specific behaviors, such as initiating movement or detecting an odor.

The researchers’ new imaging technique, based on the detection of calcium ions in neurons, could help them map the brain circuits that perform such functions. It could also provide new insights into the origins of autism, obsessive-compulsive disorder and other psychiatric diseases, says Guoping Feng, senior author of a paper appearing in the Oct. 18 issue of the journal Neuron.

“To understand psychiatric disorders we need to study animal models, and to find out what’s happening in the brain when the animal is behaving abnormally,” says Feng, the James W. and Patricia Poitras Professor of Neuroscience and a member of the McGovern Institute for Brain Research at MIT. “This is a very powerful tool that will really help us understand animal models of these diseases and study how the brain functions normally and in a diseased state.”

Filed under brain brain cells neuron calcium ions neuroimaging neuroscience science

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Berkeley Lab scientists surprised to find significant adverse effects of CO2 on human decision-making performance. Overturning decades of conventional wisdom, researchers at the Department of Energy’s Lawrence Berkeley National Laboratory (Berkeley Lab) have found that moderately high indoor concentrations of carbon dioxide (CO2) can significantly impair people’s decision-making performance. The results were unexpected and may have particular implications for schools and other spaces with high occupant density. “In our field we have always had a dogma that CO2 itself, at the levels we find in buildings, is just not important and doesn’t have any direct impacts on people,” said Berkeley Lab scientist William Fisk, a co-author of the study, which was published in Environmental Health Perspectives online last month. “So these results, which were quite unambiguous, were surprising.” The study was conducted with researchers from State University of New York (SUNY) Upstate Medical University. On nine scales of decision-making performance, test subjects showed significant reductions on six of the scales at CO2 levels of 1,000 parts per million (ppm) and large reductions on seven of the scales at 2,500 ppm. The most dramatic declines in performance, in which subjects were rated as “dysfunctional,” were for taking initiative and thinking strategically. “Previous studies have looked at 10,000 ppm, 20,000 ppm; that’s the level at which scientists thought effects started,” said Berkeley Lab scientist Mark Mendell, also a co-author of the study. “That’s why these findings are so startling.” Read more: Elevated Indoor Carbon Dioxide Impairs Decision-Making Performance

Berkeley Lab scientists surprised to find significant adverse effects of CO2 on human decision-making performance.

Overturning decades of conventional wisdom, researchers at the Department of Energy’s Lawrence Berkeley National Laboratory (Berkeley Lab) have found that moderately high indoor concentrations of carbon dioxide (CO2) can significantly impair people’s decision-making performance. The results were unexpected and may have particular implications for schools and other spaces with high occupant density.

“In our field we have always had a dogma that CO2 itself, at the levels we find in buildings, is just not important and doesn’t have any direct impacts on people,” said Berkeley Lab scientist William Fisk, a co-author of the study, which was published in Environmental Health Perspectives online last month. “So these results, which were quite unambiguous, were surprising.” The study was conducted with researchers from State University of New York (SUNY) Upstate Medical University.

On nine scales of decision-making performance, test subjects showed significant reductions on six of the scales at CO2 levels of 1,000 parts per million (ppm) and large reductions on seven of the scales at 2,500 ppm. The most dramatic declines in performance, in which subjects were rated as “dysfunctional,” were for taking initiative and thinking strategically. “Previous studies have looked at 10,000 ppm, 20,000 ppm; that’s the level at which scientists thought effects started,” said Berkeley Lab scientist Mark Mendell, also a co-author of the study. “That’s why these findings are so startling.”

Read more: Elevated Indoor Carbon Dioxide Impairs Decision-Making Performance

Filed under carbon dioxide brain decision-making human performance thinking neuroscience psychology science

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Prion protein hints at role in aiding learning and memory

Research has found that prion helps our brains to absorb zinc, which is believed to be crucial to our ability to learn and the wellbeing of our memory.

The findings published in Nature Communications show that prion protein regulates the amount of zinc in the brain by helping cells absorb it through channels in the cell surface. It is already known that high levels of zinc between brain cells are linked with diseases such as Alzheimer’s and Parkinson’s.

Professor Nigel Hooper from the University’s Faculty of Biological Sciences explains: “With ageing, the level of prion protein in our brains falls and less zinc is absorbed by brain cells, which could explain why our memory and learning capabilities change as we get older. By studying both their roles in the body, we hope to uncover exactly how prion and zinc affect memory and learning. This could help us better understand how to maintain healthy brain cells and limit the effects of ageing on the brain.”

Whilst the abnormal infectious form of prion - which causes Creutzfeldt-Jakob disease (CJD) in humans and bovine spongiform encephalopathy (BSE) in cattle - has been extensively studied, the Leeds team is among the first to investigate the role of the ‘normal’ form of the protein.

Lead researcher, Dr Nicole Watts, says: “Zinc is thought to aid signalling in the brain as it’s released into the space between brain cells. However, when there’s too much zinc between the brain cells it can become toxic.  High levels of zinc in this area between the brain cells are known to be a factor in neurodegenerative diseases, so regulating the amount of absorption by the cells is crucial.”

The research, funded by the Medical Research Council, Wellcome Trust and Alzheimer’s Research UK, may have implications for how we treat - and possibly prevent - neurodegenerative diseases in the future.

Dr Simon Ridley, Head of Research at Alzheimer’s Research UK, said: “We’re pleased to have helped support this study, which has uncovered new information that could one day aid the development of new treatments for Alzheimer’s. One next step would be to understand how regulating zinc levels may affect the progress of the disease. Results like these have the potential to lead to new and effective treatments - but for that to happen, we must build on these results and continue investing in research.”

(Source: fbs.leeds.ac.uk)

Filed under zinc neurodegenerative diseases prion brain brain cells neuroscience science

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Abnormal Involuntary Eye Movements in the “Lazy Eye” Disease Amblyopia Linked to Changes in Subcortical Regions of the Brain The neural mechanism underlying amblyopia, also called “lazy eye” is still not completely clear. A new study now reports abnormal eye movements of the lazy eye, which suggests that disturbed functioning of eye movement coordination between both eyes and not primarily the dysfunction of the visual cortex may be a cause of amblyopia (Xue-feng Shi et al.). Little is known about oculomotor function in amblyopia, or “lazy eye,” despite the special role of eye movements in vision. A group of scientists has discovered that abnormal visual processing and circuitry in the brain have an impact on fixational saccades (FSs), involuntary eye movements that occur during fixation and are important for the maintenance of vision. The results, which raise the question of whether the alterations in FS are the cause or the effect of amblyopia and have implications for amblyopia treatment, are available online in advance of publication in the November issue of Restorative Neurology and Neuroscience. “Although FSs are of great functional significance in neural coding, visual perception, and visual task execution, their behavioral characteristics in visual and neurological disease have been rarely studied,” says lead investigator Xue-Feng F. Shi, MD, PhD, of the Tianjin Key Laboratory of Ophthalmology and Visual Science, Tianjin Eye Institute, College of Clinical Ophthalmology, Tianjin Medical University, and the Department of Pediatric Ophthalmology and Strabismus, Tianjin Eye Hospital, Tianjin, China. “We carried out quantitative and detailed analysis of fixational saccades in amblyopia for the first time.”

Abnormal Involuntary Eye Movements in the “Lazy Eye” Disease Amblyopia Linked to Changes in Subcortical Regions of the Brain

The neural mechanism underlying amblyopia, also called “lazy eye” is still not completely clear. A new study now reports abnormal eye movements of the lazy eye, which suggests that disturbed functioning of eye movement coordination between both eyes and not primarily the dysfunction of the visual cortex may be a cause of amblyopia (Xue-feng Shi et al.).

Little is known about oculomotor function in amblyopia, or “lazy eye,” despite the special role of eye movements in vision. A group of scientists has discovered that abnormal visual processing and circuitry in the brain have an impact on fixational saccades (FSs), involuntary eye movements that occur during fixation and are important for the maintenance of vision. The results, which raise the question of whether the alterations in FS are the cause or the effect of amblyopia and have implications for amblyopia treatment, are available online in advance of publication in the November issue of Restorative Neurology and Neuroscience.

“Although FSs are of great functional significance in neural coding, visual perception, and visual task execution, their behavioral characteristics in visual and neurological disease have been rarely studied,” says lead investigator Xue-Feng F. Shi, MD, PhD, of the Tianjin Key Laboratory of Ophthalmology and Visual Science, Tianjin Eye Institute, College of Clinical Ophthalmology, Tianjin Medical University, and the Department of Pediatric Ophthalmology and Strabismus, Tianjin Eye Hospital, Tianjin, China. “We carried out quantitative and detailed analysis of fixational saccades in amblyopia for the first time.”

Filed under brain vision amblyopia eye movements lazy eye fixational saccades neuroscience science

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New findings illuminate basis in brain for social decisions, reactions The social brain consists of the structures and circuits that help people understand others’ intentions, beliefs, and desires, and how to behave appropriately. Its smooth functioning is essential to humans’ ability to cooperate. Its dysfunction is implicated in a range of disorders, from autism, to psychopathology, to schizophrenia. New findings show that: • Primates employ three different parts of the prefrontal cortex in decisions about whether to give or keep prized treats. These findings illuminate a poorly understood brain circuit, and offer possible insights into human sharing and other social behavior (Steve Chang, PhD, abstract 129.10). • Different brain regions are engaged in altruistic behavior that is motivated by genuine caring versus altruistic behavior motivated by a concern for reputation or self-image (Cendri Hutcherson, PhD, abstract 129.06). • The experience of racial discrimination triggers activity in the same brain regions that respond to pain, social rejection, and other stressful experiences (Arpana Gupta, PhD, abstract 402.06). Another recent finding discussed shows that: • Competition against a human opponent or a computer engages the same parts of the brain, with one exception: the temporal parietal junction is used to predict only a human’s upcoming actions (Ronald Carter, PhD).

New findings illuminate basis in brain for social decisions, reactions

The social brain consists of the structures and circuits that help people understand others’ intentions, beliefs, and desires, and how to behave appropriately. Its smooth functioning is essential to humans’ ability to cooperate. Its dysfunction is implicated in a range of disorders, from autism, to psychopathology, to schizophrenia.

New findings show that:

• Primates employ three different parts of the prefrontal cortex in decisions about whether to give or keep prized treats. These findings illuminate a poorly understood brain circuit, and offer possible insights into human sharing and other social behavior (Steve Chang, PhD, abstract 129.10).
• Different brain regions are engaged in altruistic behavior that is motivated by genuine caring versus altruistic behavior motivated by a concern for reputation or self-image (Cendri Hutcherson, PhD, abstract 129.06).
• The experience of racial discrimination triggers activity in the same brain regions that respond to pain, social rejection, and other stressful experiences (Arpana Gupta, PhD, abstract 402.06).

Another recent finding discussed shows that:
• Competition against a human opponent or a computer engages the same parts of the brain, with one exception: the temporal parietal junction is used to predict only a human’s upcoming actions (Ronald Carter, PhD).

Filed under brain social brain decision making perception Neuroscience 2012 neuroscience psychology science

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Studies report early childhood trauma takes visible toll on brain; changes found in regions controlling heart and behavior Trauma in infancy and childhood shapes the brain, learning, and behavior, and fuels changes that can last a lifetime, according to new human and animal research released today. The studies delve into the effects of early physical abuse, socioeconomic status (SES), and maternal treatment. Documenting the impact of early trauma on brain circuitry and volume, the activation of genes, and working memory, researchers suggest it increases the risk of mental disorders, as well as heart disease and stress-related conditions in adulthood. Today’s findings show: • Physical abuse in early childhood may realign communication between key “body-control” brain areas, possibly predisposing adults to cardiovascular disease and mental health problems (Layla Banihashemi, PhD, abstract 691.12). • Rodent studies provide insight into brain changes that allow tolerance of pain within mother-pup attachment (Regina Sullivan, PhD, abstract 399.19). • Childhood poverty is associated with changes in working memory and attention years later in adults; yet training in childhood is associated with improved cognitive functions (Eric Pakulak, PhD, abstract 908.04). • Chronic stress experienced by infant primates leads to fearful and aggressive behaviors; these are associated with changes in stress hormone production and in the development of the amygdala (Mar Sanchez, PhD, abstract 691.10). Another recent finding discussed shows that: • Parent education and income is associated with children’s brain size, including structures important for memory and emotion (Suzanne Houston, MA).

Studies report early childhood trauma takes visible toll on brain; changes found in regions controlling heart and behavior

Trauma in infancy and childhood shapes the brain, learning, and behavior, and fuels changes that can last a lifetime, according to new human and animal research released today. The studies delve into the effects of early physical abuse, socioeconomic status (SES), and maternal treatment. Documenting the impact of early trauma on brain circuitry and volume, the activation of genes, and working memory, researchers suggest it increases the risk of mental disorders, as well as heart disease and stress-related conditions in adulthood.

Today’s findings show:

• Physical abuse in early childhood may realign communication between key “body-control” brain areas, possibly predisposing adults to cardiovascular disease and mental health problems (Layla Banihashemi, PhD, abstract 691.12).
• Rodent studies provide insight into brain changes that allow tolerance of pain within mother-pup attachment (Regina Sullivan, PhD, abstract 399.19).
• Childhood poverty is associated with changes in working memory and attention years later in adults; yet training in childhood is associated with improved cognitive functions (Eric Pakulak, PhD, abstract 908.04).
• Chronic stress experienced by infant primates leads to fearful and aggressive behaviors; these are associated with changes in stress hormone production and in the development of the amygdala (Mar Sanchez, PhD, abstract 691.10).

Another recent finding discussed shows that:
• Parent education and income is associated with children’s brain size, including structures important for memory and emotion (Suzanne Houston, MA).

Filed under brain childhood trauma working memory stress physical abuse Neuroscience 2012 neuroscience psychology science

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Findings reveal brain mechanisms at work during sleep One in five American adults show signs of chronic sleep deprivation, making the condition a widespread public health problem. Sleeplessness is related to health issues such as obesity, cardiovascular problems, and memory problems. Today’s findings show that: • Sleepiness disrupts the coordinated activity of an important network of brain regions; the impaired function of this network is also implicated in Alzheimer’s disease (Andrew Ward, abstract 909.05). • Sleeplessness plays havoc with communication between the hippocampus, which is vital for memory, and the brain’s “default mode network;” the changes may weaken event recollection (Hengyi Rao, PhD, abstract 626.08). • In a mouse model, fearful memories can be intentionally weakened during sleep, indicating new possibilities for treatment of post-traumatic stress disorder (Asya Rolls, abstract 807.06). • Loss of less than half a night’s sleep can impair memory and alter the normal behavior of brain cells (Ted Abel, PhD, abstract 807.13). Other recent findings discussed show: • How sleep enables the remodeling of memories — including the weakening of irrelevant memories — and the coherent integration of old and new information (Gina Poe, PhD). • The common logic behind seemingly contradictory theories of how sleep remodels synapses, aiding cognition and memory consolidation (Giulio Tononi, MD, PhD).

Findings reveal brain mechanisms at work during sleep

One in five American adults show signs of chronic sleep deprivation, making the condition a widespread public health problem. Sleeplessness is related to health issues such as obesity, cardiovascular problems, and memory problems.

Today’s findings show that:

• Sleepiness disrupts the coordinated activity of an important network of brain regions; the impaired function of this network is also implicated in Alzheimer’s disease (Andrew Ward, abstract 909.05).
• Sleeplessness plays havoc with communication between the hippocampus, which is vital for memory, and the brain’s “default mode network;” the changes may weaken event recollection (Hengyi Rao, PhD, abstract 626.08).
• In a mouse model, fearful memories can be intentionally weakened during sleep, indicating new possibilities for treatment of post-traumatic stress disorder (Asya Rolls, abstract 807.06).
• Loss of less than half a night’s sleep can impair memory and alter the normal behavior of brain cells (Ted Abel, PhD, abstract 807.13).

Other recent findings discussed show:
• How sleep enables the remodeling of memories — including the weakening of irrelevant memories — and the coherent integration of old and new information (Gina Poe, PhD).
• The common logic behind seemingly contradictory theories of how sleep remodels synapses, aiding cognition and memory consolidation (Giulio Tononi, MD, PhD).

Filed under sleep sleep deprivation obesity health Neuroscience 2012 neuroscience brain science

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Scientists reveal brain circuitry involved in post-traumatic stress and related disorders Post-traumatic stress disorder (PTSD) is a severe anxiety disorder that can develop after experience of a traumatic or terrifying event, such as those experienced in combat or from sexual aggression. Such events can overwhelm the individual’s ability to cope and lead to a long-lasting disorder. Symptoms include re-experiencing the original trauma through flashbacks or nightmares, often triggered by seemingly innocuous events. PTSD can harm an individual’s relationships, ability to work, to sleep, and other aspects of life. The lifetime prevalence of PTSD among adult Americans is 8 percent. Neither drug nor behavioral treatments currently available are consistently effective in treating PTSD. Therefore, scientists are studying brain changes associated with PTSD and related cognitive disorders, looking for clues to help in the development of new treatments. Today’s findings show that: A fast-acting antidepressant, ketamine, appears to aid the formation of new nerve connections in the brain, helping to extinguish fearful memories. The mouse study could possibly lead to new PTSD treatments (Neil Fournier, PhD, abstract 399.09). In a mouse model, when dopamine neurons in the brain’s reward system are turned on and off with a genetically engineered “light switch,” depressive symptoms also come and go. The research highlights the importance of this neural circuit as a potential target for new depression treatments (Dipesh Chaudhury, PhD, abstract 522.01). Brain images of adolescents taken before and after the 2011 Japanese earthquake reveal that pre-existing weakness in certain brain connections could be a risk factor for intensified anxiety and PTSD after a traumatic life experience (Atsushi Sekiguchi, MD, PhD, abstract 168.12). Rodent studies show that repeated violent, competitive encounters drive changes in brain activity that shapes the ongoing behavior of losers and winners in distinct ways, and can contribute to depression and/or anxiety (Tamara Franklin, PhD, abstract 399.10). Other recent findings discussed show: How exposure to stress causes molecular changes that weaken the ability of the prefrontal cortex to regulate behavior, thought, and emotion, while strengthening more primitive brain circuits (Amy Arnsten, PhD, abstract 310).   

Scientists reveal brain circuitry involved in post-traumatic stress and related disorders

Post-traumatic stress disorder (PTSD) is a severe anxiety disorder that can develop after experience of a traumatic or terrifying event, such as those experienced in combat or from sexual aggression. Such events can overwhelm the individual’s ability to cope and lead to a long-lasting disorder. Symptoms include re-experiencing the original trauma through flashbacks or nightmares, often triggered by seemingly innocuous events. PTSD can harm an individual’s relationships, ability to work, to sleep, and other aspects of life.

The lifetime prevalence of PTSD among adult Americans is 8 percent. Neither drug nor behavioral treatments currently available are consistently effective in treating PTSD. Therefore, scientists are studying brain changes associated with PTSD and related cognitive disorders, looking for clues to help in the development of new treatments.

Today’s findings show that:

  • A fast-acting antidepressant, ketamine, appears to aid the formation of new nerve connections in the brain, helping to extinguish fearful memories. The mouse study could possibly lead to new PTSD treatments (Neil Fournier, PhD, abstract 399.09).
  • In a mouse model, when dopamine neurons in the brain’s reward system are turned on and off with a genetically engineered “light switch,” depressive symptoms also come and go. The research highlights the importance of this neural circuit as a potential target for new depression treatments (Dipesh Chaudhury, PhD, abstract 522.01).
  • Brain images of adolescents taken before and after the 2011 Japanese earthquake reveal that pre-existing weakness in certain brain connections could be a risk factor for intensified anxiety and PTSD after a traumatic life experience (Atsushi Sekiguchi, MD, PhD, abstract 168.12).
  • Rodent studies show that repeated violent, competitive encounters drive changes in brain activity that shapes the ongoing behavior of losers and winners in distinct ways, and can contribute to depression and/or anxiety (Tamara Franklin, PhD, abstract 399.10).

Other recent findings discussed show:

  • How exposure to stress causes molecular changes that weaken the ability of the prefrontal cortex to regulate behavior, thought, and emotion, while strengthening more primitive brain circuits (Amy Arnsten, PhD, abstract 310).   

Filed under PTSD anxiety stress brain brain activity Neuroscience 2012 neuroscience science

170 notes

New research reveals more about how the brain processes facial expressions and emotions Facial mimicry—a social behavior in which the observer automatically activates the same facial muscles as the person she is imitating—plays a role in learning, understanding, and rapport. Mimicry can activate muscles that control both smiles and frowns, and evoke their corresponding emotions, positive and negative. The studies reveal new roles of facial mimicry and some of its underlying brain circuitry. New findings show that: Special brains cells dubbed “eye cells” activate in the amygdala of a monkey looking into the eyes of another monkey, even as the monkey mimics the expressions of its counterpart (Katalin Gothard, MD, PhD, abstract 402.02).  Social status and self-perceptions of power affect facial mimicry, such that powerful individuals suppress their smile mimicry towards other high-status people, while powerless individuals mimic everyone’s smile (Evan Carr, BS, abstract 402.11). Brain imaging studies in monkeys have revealed the specific roles of different regions of the brain in understanding facial identity and emotional expression, including one brain region previously identified for its role in vocal processing (Shih-pi Ku, PhD, abstract 263.22). Subconscious facial mimicry plays a strong role in interpreting the meaning of ambiguous smiles (Sebastian Korb, PhD, abstract 402.23).  Another recent finding discussed shows that: Early difficulties in interactions between parents and infants with cleft lip appear to have a neurological basis, as change in a baby’s facial structure can disrupt the way adult brains react to a child (Christine Parsons, PhD). (Image Credit: iStockphoto/Joan Vicent Cantó Roig)

New research reveals more about how the brain processes facial expressions and emotions

Facial mimicry—a social behavior in which the observer automatically activates the same facial muscles as the person she is imitating—plays a role in learning, understanding, and rapport. Mimicry can activate muscles that control both smiles and frowns, and evoke their corresponding emotions, positive and negative. The studies reveal new roles of facial mimicry and some of its underlying brain circuitry.

New findings show that:

  • Special brains cells dubbed “eye cells” activate in the amygdala of a monkey looking into the eyes of another monkey, even as the monkey mimics the expressions of its counterpart (Katalin Gothard, MD, PhD, abstract 402.02). 
  • Social status and self-perceptions of power affect facial mimicry, such that powerful individuals suppress their smile mimicry towards other high-status people, while powerless individuals mimic everyone’s smile (Evan Carr, BS, abstract 402.11).
  • Brain imaging studies in monkeys have revealed the specific roles of different regions of the brain in understanding facial identity and emotional expression, including one brain region previously identified for its role in vocal processing (Shih-pi Ku, PhD, abstract 263.22).
  • Subconscious facial mimicry plays a strong role in interpreting the meaning of ambiguous smiles (Sebastian Korb, PhD, abstract 402.23). 

Another recent finding discussed shows that:

  • Early difficulties in interactions between parents and infants with cleft lip appear to have a neurological basis, as change in a baby’s facial structure can disrupt the way adult brains react to a child (Christine Parsons, PhD).

(Image Credit: iStockphoto/Joan Vicent Cantó Roig)

Filed under Neuroscience 2012 behavior brain communication emotion facial expressions neuroscience perception science

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