Neuroscience

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Posts tagged anxiety

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Early stress may sensitize girls’ brains for later anxiety
High levels of family stress in infancy are linked to differences in everyday brain function and anxiety in teenage girls, according to new results of a long-running population study by University of Wisconsin-Madison scientists.
The study highlights evidence for a developmental pathway through which early life stress may drive these changes. Here, babies who lived in homes with stressed mothers were more likely to grow into preschoolers with higher levels of cortisol, a stress hormone. In addition, these girls with higher cortisol also showed less communication between brain areas associated with emotion regulation 14 years later. Last, both high cortisol and differences in brain activity predicted higher levels of adolescent anxiety at age 18.
The young men in the study did not show any of these patterns.
"We wanted to understand how stress early in life impacts patterns of brain development which might lead to anxiety and depression,” says first author Dr. Cory Burghy of the Waisman Laboratory for Brain Imaging and Behavior. "Young girls who, as preschoolers, had heightened cortisol levels, go on to show lower brain connectivity in important neural pathways for emotion regulation — and that predicts symptoms of anxiety during adolescence."
To test this, scans designed by Dr. Rasmus Birn, assistant professor of psychiatry in the UW School of Medicine and Public Health, showed that teenage girls whose mothers reported high levels of family stress when the girls were babies show reduced connections between the amygdala or threat center of the brain and the ventromedial prefrontal cortex, a part of the brain responsible for emotional regulation. Birn used a method called resting-state functional connectivity (fcMRI), which looks at the brain connections while the brain is at a resting state.
The study was published in Nature Neuroscience.

Early stress may sensitize girls’ brains for later anxiety

High levels of family stress in infancy are linked to differences in everyday brain function and anxiety in teenage girls, according to new results of a long-running population study by University of Wisconsin-Madison scientists.

The study highlights evidence for a developmental pathway through which early life stress may drive these changes. Here, babies who lived in homes with stressed mothers were more likely to grow into preschoolers with higher levels of cortisol, a stress hormone. In addition, these girls with higher cortisol also showed less communication between brain areas associated with emotion regulation 14 years later. Last, both high cortisol and differences in brain activity predicted higher levels of adolescent anxiety at age 18.

The young men in the study did not show any of these patterns.

"We wanted to understand how stress early in life impacts patterns of brain development which might lead to anxiety and depression,” says first author Dr. Cory Burghy of the Waisman Laboratory for Brain Imaging and Behavior. "Young girls who, as preschoolers, had heightened cortisol levels, go on to show lower brain connectivity in important neural pathways for emotion regulation — and that predicts symptoms of anxiety during adolescence."

To test this, scans designed by Dr. Rasmus Birn, assistant professor of psychiatry in the UW School of Medicine and Public Health, showed that teenage girls whose mothers reported high levels of family stress when the girls were babies show reduced connections between the amygdala or threat center of the brain and the ventromedial prefrontal cortex, a part of the brain responsible for emotional regulation. Birn used a method called resting-state functional connectivity (fcMRI), which looks at the brain connections while the brain is at a resting state.

The study was published in Nature Neuroscience.

Filed under brain stress anxiety adolescents stress hormones brain activity neuroscience psychology science

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The brain of OCD sufferers is more active when faced with a moral dilemma
Patients with obsessive-compulsive disorder are characterised by persistent thoughts and repetitive behaviours. A new study reveals that sufferers worry considerably more than the general population in the face of morality problems.
Along with the help of experts from the Barcelona’s Hospital del Mar and the University of Melbourne (Australia), researchers at the Hospital de Bellvitge in Barcelona have proven that patients with obsessive-compulsive disorder, known as OCD, are more morally sensitive.
"Faced with a problem of this type, people suffering from this type of anxiety disorder show that they worry considerably more," as explained to SINC by Carles Soriano, researcher at the Catalan hospital and one of the lead authors of the work published in the journal Archives of General Psychiatry.

The brain of OCD sufferers is more active when faced with a moral dilemma

Patients with obsessive-compulsive disorder are characterised by persistent thoughts and repetitive behaviours. A new study reveals that sufferers worry considerably more than the general population in the face of morality problems.

Along with the help of experts from the Barcelona’s Hospital del Mar and the University of Melbourne (Australia), researchers at the Hospital de Bellvitge in Barcelona have proven that patients with obsessive-compulsive disorder, known as OCD, are more morally sensitive.

"Faced with a problem of this type, people suffering from this type of anxiety disorder show that they worry considerably more," as explained to SINC by Carles Soriano, researcher at the Catalan hospital and one of the lead authors of the work published in the journal Archives of General Psychiatry.

Filed under brain OCD anxiety morality neuroscience psychology science

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Researchers Find Why Nicotine in Cigarettes May Relieve Anxiety in Smokers
Preclinical data suggests inactivation of a specific sub-class of nicotinic receptors may be an effective strategy to help smokers quit without feeling anxious, according to Virginia Commonwealth University researchers.
These findings could one day point researchers to the development of novel therapies to help smokers quit without feeling anxious.
Smokers use cigarettes for many reasons, but many report that they smoke to relieve anxiety, despite the health danger of cigarette smoking. Researchers are now working to understand the underlying neurochemical pathways that support smoking behavior.
In a study, published online this week in PLoS ONE, researchers observed that low doses of nicotine and a nicotinic receptor blocker had similar effects to reduce anxiety-like behavior in an animal model. They found that inactivation of beta2 subunit, a specific sub-class of nicotinic receptors that bind nicotine, appears to reduce anxiety. This is different from the mechanism that regulates nicotine reward and likely occurs in a separate brain area.
“This work is unique because it suggests that nicotine may be acting through inactivation, rather than activation, of the high affinity nicotinic receptors,” said Darlene Brunzell, Ph.D., assistant professor in the Department of Pharmacology and Toxicology in the VCU School of Medicine.
“Nicotine acts like a key that unlocks nicotine receptors in the brain. Usually that key opens the receptor, but at other times nicotine is like a key that has gotten broken inside of the lock. Our findings suggest that low-dose nicotine may block a specific subtype of receptor from opening that is important for regulating anxiety behavior,” she said, adding that anxiety is a major reason why people relapse to smoking.

Researchers Find Why Nicotine in Cigarettes May Relieve Anxiety in Smokers

Preclinical data suggests inactivation of a specific sub-class of nicotinic receptors may be an effective strategy to help smokers quit without feeling anxious, according to Virginia Commonwealth University researchers.

These findings could one day point researchers to the development of novel therapies to help smokers quit without feeling anxious.

Smokers use cigarettes for many reasons, but many report that they smoke to relieve anxiety, despite the health danger of cigarette smoking. Researchers are now working to understand the underlying neurochemical pathways that support smoking behavior.

In a study, published online this week in PLoS ONE, researchers observed that low doses of nicotine and a nicotinic receptor blocker had similar effects to reduce anxiety-like behavior in an animal model. They found that inactivation of beta2 subunit, a specific sub-class of nicotinic receptors that bind nicotine, appears to reduce anxiety. This is different from the mechanism that regulates nicotine reward and likely occurs in a separate brain area.

“This work is unique because it suggests that nicotine may be acting through inactivation, rather than activation, of the high affinity nicotinic receptors,” said Darlene Brunzell, Ph.D., assistant professor in the Department of Pharmacology and Toxicology in the VCU School of Medicine.

“Nicotine acts like a key that unlocks nicotine receptors in the brain. Usually that key opens the receptor, but at other times nicotine is like a key that has gotten broken inside of the lock. Our findings suggest that low-dose nicotine may block a specific subtype of receptor from opening that is important for regulating anxiety behavior,” she said, adding that anxiety is a major reason why people relapse to smoking.

Filed under brain nicotine anxiety nicotinic receptors smoking neuroscience psychology science

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PTSD linked to smaller brain area regulating fear response
Recent combat veterans who are diagnosed with post traumatic stress disorder have significantly smaller volume in an area of the brain critical for regulating fear and anxiety responses, according to research led by scientists at Duke University and the Durham VA Medical Center.
The finding, published Nov. 5, 2012, in the journal Archives of General Psychiatry, for the first time provides clear evidence that smaller amygdala volume is associated with PTSD, regardless of the severity of trauma. But it’s not clear whether the physiological difference was caused by a traumatic event, or whether PTSD develops more readily in people who naturally have smaller amygdalas.
“Researchers found 20 years ago that there were changes in volume of the hippocampus associated with PTSD, but the amygdala is more relevant to the disorder,” said Rajendra A. Morey, M.D., M.S., assistant professor at Duke and lead author of the study. Morey said studies in animals have established the amygdala’s role in regulating fear, anxiety and stress responses, but its effect on human behavior is less well known.
“It’s associated with how fear is processed, especially abnormal fear processing.” Morey said. “So it makes sense to look at the structure of the amygdala.”

(Photo: U.S. Army)

PTSD linked to smaller brain area regulating fear response

Recent combat veterans who are diagnosed with post traumatic stress disorder have significantly smaller volume in an area of the brain critical for regulating fear and anxiety responses, according to research led by scientists at Duke University and the Durham VA Medical Center.

The finding, published Nov. 5, 2012, in the journal Archives of General Psychiatry, for the first time provides clear evidence that smaller amygdala volume is associated with PTSD, regardless of the severity of trauma. But it’s not clear whether the physiological difference was caused by a traumatic event, or whether PTSD develops more readily in people who naturally have smaller amygdalas.

“Researchers found 20 years ago that there were changes in volume of the hippocampus associated with PTSD, but the amygdala is more relevant to the disorder,” said Rajendra A. Morey, M.D., M.S., assistant professor at Duke and lead author of the study. Morey said studies in animals have established the amygdala’s role in regulating fear, anxiety and stress responses, but its effect on human behavior is less well known.

“It’s associated with how fear is processed, especially abnormal fear processing.” Morey said. “So it makes sense to look at the structure of the amygdala.”

(Photo: U.S. Army)

Filed under brain PTSD stress fear anxiety amygdala neuroscience psychology science

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Decreased Gene Activity Is Likely Involved in Childhood Risk for Anxiety and Depression

Decreased activity of a group of genes may explain why in young children the “fear center” of the anxious brain can’t learn to distinguish real threats from the imaginary, according to a new University of Wisconsin study.

The study, published this week in the Proceedings of the National Academy of Sciences (PNAS), lays out evidence that young primates with highly anxious temperaments have decreased activity of specific genes within the amygdala, the brain’s fear center.

The authors hypothesize that this may result in over activity of the brain circuit that leads to higher risk for developing disabling anxiety and depression.

This may be particularly important since the genes involved play a major role in forming the brain connections needed for learning about fears. While all children have fears and anxieties, the authors suggest that children with low levels of activity of these genes develop anxious dispositions because they fail to learn to cope by overcoming their early childhood fears.

“Working with my close collaborator and graduate student, Drew Fox, we focused on understanding the function of genes that promote learning and plasticity in the amygdala,” says Dr. Ned H. Kalin, chair of psychiatry at the University of Wisconsin School of Medicine and Public Health, who led the research. “We found reduced activity in key genes that could impair the ability to sculpt the brain, resulting in a failure to develop the capacity to discriminate between real and imaginary fears.”

Kalin says the study helps support the need for early intervention in children identified as excessively shy and anxious. It may also point a way to better treatments aimed at decreasing the likelihood of children developing more severe psychiatric problems. Anxiety in children is quite common and can lead to anxiety and depression in adolescence and often precedes anxiety disorders, depression and substance abuse in adults.

Most small children go through a phase when they’re frightened of many things, including monsters or new social situations, Kalin says, but their maturing brains soon learn to distinguish real threats from the imaginary. But some children do not adapt, generalize their fears to numerous situations, and may later develop serious anxiety and mood disorders. These children tend to be more sensitive to stress, produce more stress hormones and have heightened nervous-system activity.

Kalin, Fox and co-authors wondered whether some differences in the developing amygdala prevent it from learning how to regulate and adapt to anxiety. Kalin’s earlier work identified a subset of young monkeys, similar to extremely shy children, with an inherited anxious disposition. Using brain imaging, the authors showed that high levels of amygdala activity predicted trait-like anxiety in anxious young primates. Like their stable and enduring anxious dispositions, these individuals also had chronically elevated levels of amygdala activity.

“We believe that this pinpoints a critical region in the brain that determines an individual’s level of trait anxiety,’’ Kalin explains.

In examining a specific part of the amygdala, the central nucleus, the researchers analyzed gene expression, which reflects both environmental and inherited influences. Within the central nucleus of the amygdala the authors found that anxious individuals tended to have decreased expression of a gene called neurotrophic tyrosine kinase, receptor, type 3 (NTRK3). Low levels of this gene that encodes for a brain cell surface receptor may be why the amygdala of an anxious monkey or child is chronically overactive and unable to overcome anxiety and fears.

“This is the first demonstration that the early risk to develop anxiety and depression may be related to the underactivity of particular genes in the developing primate amygdala,’’ Kalin says. “These findings have provided the basis for our hypothesis that can explain the early childhood risk to develop anxiety and depression. It also suggests some creative ways to help children with extreme anxiety by developing new treatments focused on increasing the activity of specific genes involved in facilitating the brain development that underlies fear learning and coping.”

(Source: newswise.com)

Filed under brain brain connections anxiety depression fear genes childhood neuroscience psychology 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

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UMD Study Shows Exercise May Protect Against Future Emotional Stress

Moderate exercise may help people cope with anxiety and stress for an extended period of time post-workout, according to a study by kinesiology researchers in the University of Maryland School of Public Health published in the journal Medicine and Science in Sports and Exercise.

"While it is well-known that exercise improves mood, among other benefits, not as much is known about the potency of exercise’s impact on emotional state and whether these positive effects endure when we’re faced with everyday stressors once we leave the gym," explains J. Carson Smith, assistant professor in the Department of Kinesiology. "We found that exercise helps to buffer the effects of emotional exposure. If you exercise, you’ll not only reduce your anxiety, but you’ll be better able to maintain that reduced anxiety when confronted with emotional events."

Smith, whose research explores how exercise and physical activity affect brain function, aging and mental health, compared how moderate intensity cycling versus a period of quiet rest (both for 30 minutes) affected anxiety levels in a group of healthy college students. He assessed their anxiety state before the period of activity (or rest), shortly afterward (15 minutes after) and finally after exposing them to a variety of highly arousing pleasant and unpleasant photographs, as well as neutral images. At each point, study participants answered 20 questions from the State-Trait Anxiety inventory, which is designed to assess different symptoms of anxiety. All participants were put through both the exercise and the rest states (on different days) and tested for anxiety levels pre-exercise, post-exercise, and post-picture viewing.

Smith found that exercise and quiet rest were equally effective at reducing anxiety levels initially. However, once they were emotionally stimulated (by being shown 90 photographs from the International Affective Picture System, a database of photographs used in emotion research) for ~20 minutes, the anxiety levels of those who had simply rested went back up to their initial levels, whereas those who had exercised maintained their reduced anxiety levels.

"The set of photographic stimuli we used from the IAPS database was designed to simulate the range of emotional events you might experience in daily life," Smith explains. "They represent pleasant emotional events, neutral events and unpleasant events or stimuli. These vary from pictures of babies, families, puppies and appetizing food items, to very neutral things like plates, cups, furniture and city landscapes, to very unpleasant images of violence, mutilations and other gruesome things."

The study findings suggest that exercise may play an important role in helping people to better endure life’s daily anxieties and stressors.

Smith plans to explore if exercise could have the same persistent beneficial effect in patients who regularly experience anxiety and depression symptoms. In collaboration with the new Maryland Neuroimaging Center, he is also exploring the addition of functional magnetic resonance imaging, or fMRI, to measure brain activity during the period of exposure to emotionally stimulating images to see how exercise may alter the brain’s emotion-related neural networks.

Smith also investigates the role of exercise in preventing cognitive decline in older adults. His research has shown that physical activity promotes changes in the brain that may protect those at high risk for Alzheimer’s disease.

(Source: newsdesk.umd.edu)

Filed under exercise physical activity stress anxiety brain neuroscience psychology emotion science

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Reduced Brain Connections Seen in People With Generalized Anxiety Disorder

A new University of Wisconsin-Madison imaging study shows the brains of people with generalized anxiety disorder (GAD) have weaker connections between a brain structure that controls emotional response and the amygdala, which suggests the brain’s “panic button” may stay on due to lack of regulation.

Anxiety disorders are the most common class of mental disorders and GAD, which is characterized by excessive, uncontrollable worry, affects nearly 6 percent of the population.

Lead author Dr. Jack Nitschke, associate professor of psychiatry in the UW School of Medicine and Public Health, says the findings support the theory that reduced communications between parts of the brain explains the intense anxiety felt by people with GAD.

In this case, two types of scans showed the amygdala, which alerts us to threat in our surroundings and initiates the “fight-or-flight” response, seems to have weaker “white matter” connections to the prefrontal and anterior cingulate cortex (ACC), the center of emotional regulation.

The researchers did two types of imaging - diffusion tensor imaging (DTI) and functional magnetic resonance (fMRI) - on the brains of 49 GAD patients and 39 healthy volunteers. Compared with the healthy volunteers, the imaging showed the brains of people with GAD had reduced connections between the prefrontal and anterior cingulate cortex and the amygdala via the uncinate fasciculus, a primary “white matter” tract that connects these brain regions. This reduced connectivity was not found in other white matter tracts elsewhere in their brains.

"We know that in the brain, if you use a circuit you build it up, the way you build muscle by exercise,” says Nitschke, a clinical psychologist who treats patients with anxiety disorders and does research at the UW-Madison’s Waisman Center.

Nitschke says that researchers wonder if this weak connection results in the intense anticipatory anxiety and worry that is the hallmark of GAD, because the ACC is unable to tell the amygdala to “chill out.” It also suggests that behavioral therapy that teaches patients to consciously exercise this emotional regulation works to reduce anxiety by strengthening the connection.

"It’s possible that this is exactly what we’re doing when we teach patients to regulate their reactions to the negative events that come up in everyone’s lives,” Nitschke says. "We can help build people’s tolerance to uncontrollable future events by teaching them to regulate their emotions to the uncertainty that surrounds those events.

(Source: news.wisc.edu)

Filed under GAD anxiety anxiety disorder brain neuroscience psychology science neuroimaging

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