Posts tagged amygdala
Articles and news from the latest research reports.
Testosterone in Healthy Men Increases Their Brains’ Response to Threat
Testosterone, a steroid hormone, is well known to contribute to aggressive behavior in males, but the neural circuits through which testosterone exerts these effects have not been clear.
Prior studies found that the administration of a single dose of testosterone influenced brain circuit function. Surprisingly, however, these studies were conducted exclusively in women.
Researchers, led by Dr. Justin Carré, sought to rectify this gap by conducting a study of the effects of testosterone on the brain’s response to threat cues in healthy men.
They focused their attention on brain structures that mediate threat processing and aggressive behavior, including the amygdala, hypothalamus, and periaqueductal gray.
The researchers recruited 16 healthy young male volunteers, who completed two test days on which they received either testosterone or placebo. On both testing days, the men first received a drug that suppressed their testosterone. This step ensured that testosterone levels were similar among all study participants. The amount of testosterone administered in this study only returned testosterone levels to the normal range. Subjects then completed a face-matching task while undergoing a functional magnetic resonance imaging scan.
Data analyses revealed that, compared with placebo, testosterone increased reactivity of the amygdala, hypothalamus and periaqueductal grey when viewing angry facial expressions.
"We were able to show for the first time that increasing levels of testosterone within the normal physiological range can have a profound effect on brain circuits that are involved in threat-processing and human aggression," said Carré, Assistant Professor at Nipissing University.
"Understanding testosterone effects on the brain activity patterns associated with threat and aggression may help us to better understand the ‘fight or flight’ response in males that may be relevant to aggression and anxiety," commented Dr. John Krystal, Editor of Biological Psychiatry.
Expanding our knowledge of exactly how testosterone affects the male brain is particularly important, as testosterone augmentation has become increasingly promoted and aggressively marketed as a solution to reduced virility in aging men. Further work is indeed continuing, Carré said. “Our current work is examining the extent to which a single administration of testosterone influences aggressive and competitive behavior in men.”
(Source: elsevier.com)
Notch Developmental Pathway Regulates Fear Memory Formation
Nature is thrifty. The same signals that embryonic cells use to decide whether to become nerves, skin or bone come into play again when adult animals are learning whether to become afraid.
Researchers at Yerkes National Primate Research Center, Emory University, have learned that the molecule Notch, critical in many processes during embryonic development, is also involved in fear memory formation. Understanding fear memory formation is critical to developing more effective treatments and preventions for anxiety disorders such as post-traumatic stress disorder (PTSD). The results are scheduled for publication online this week by the journal Neuron.
"We are finding that developmental pathways that appear to be quiescent during adulthood are transiently reactivated to allow new memory formation to occur," says Kerry Ressler, MD, PhD, professor of psychiatry and behavioral sciences at Emory University School of Medicine and Yerkes National Primate Research Center, and senior author of the paper.
The first author of the paper is postdoctoral fellow Brian Dias, PhD, and co-authors include undergraduates Jared Goodman, Ranbir Ahluwalia and Audrey Easton, and post-doctoral researcher Raul Andero, PhD.
The Notch signaling pathway, present in insects, worms and vertebrates, is involved in embryonic patterning as well as nervous system and cardiovascular development. It’s a way for cells to communicate and coordinate which cells are going to become what types of tissues.
Dias and Ressler probed the Notch pathway because they were examining many genes that are activated in the brains of mice after they learn to become afraid of a sound paired with a mild foot-shock. They were looking for changes in the amygdala, a region of the brain known to regulate fear learning.
The researchers were particularly interested in micro RNAs. MicroRNAs do not encode proteins but can inhibit other genes, often several at once in a coordinated way. Dias and Ressler found that levels of miRNA-34a are increased in the amygdala after fear learning occurs. A day after fear training, animals whose brains were injected with a virus engineered to carry a “sponge” against miRNA-34a froze less often than control animals.
The researchers found that miRNA-34a regulated several genes that encode components of the Notch pathway. They believe their study is the first to link miRNA-34a and Notch signaling to a role in memory consolidation.
Notch is under investigation as a target in the treatment of various cancers and some drugs that target Notch have been well-tolerated by humans.
"From a therapeutic perspective, our data suggest that relevant drugs that regulate Notch signaling could potentially be a starting point for preventing or treating PTSD," Dias says.
(Source: yerkes.emory.edu)
Our brains judge a face’s trustworthiness - Even when we can’t see it
Our brains are able to judge the trustworthiness of a face even when we cannot consciously see it, a team of scientists has found. Their findings, which appear in the Journal of Neuroscience, shed new light on how we form snap judgments of others.
“Our findings suggest that the brain automatically responds to a face’s trustworthiness before it is even consciously perceived,” explains Jonathan Freeman, an assistant professor in New York University’s Department of Psychology and the study’s senior author.
“The results are consistent with an extensive body of research suggesting that we form spontaneous judgments of other people that can be largely outside awareness,” adds Freeman, who conducted the study as a faculty member at Dartmouth College.
The study’s other authors included Ryan Stolier, an NYU doctoral candidate, Zachary Ingbretsen, a research scientist who previously worked with Freeman and is now at Harvard University, and Eric Hehman, a post-doctoral researcher at NYU.
The researchers focused on the workings of the brain’s amygdala, a structure that is important for humans’ social and emotional behavior. Previous studies have shown this structure to be active in judging the trustworthiness of faces. However, it had not been known if the amygdala is capable of responding to a complex social signal like a face’s trustworthiness without that signal reaching perceptual awareness.
To gauge this part of the brain’s role in making such assessments, the study’s authors conducted a pair of experiments in which they monitored the activity of subjects’ amygdala while the subjects were exposed to a series of facial images.
These images included both standardized photographs of actual strangers’ faces as well as artificially generated faces whose trustworthiness cues could be manipulated while all other facial cues were controlled. The artificially generated faces were computer synthesized based on previous research showing that cues such as higher inner eyebrows and pronounced cheekbones are seen as trustworthy and lower inner eyebrows and shallower cheekbones are seen as untrustworthy.
Prior to the start of these experiments, a separate group of subjects examined all the real and computer-generated faces and rated how trustworthy or untrustworthy they appeared. As previous studies have shown, subjects strongly agreed on the level of trustworthiness conveyed by each given face.
In the experiments, a new set of subjects viewed these same faces inside a brain scanner, but were exposed to the faces very briefly—for only a matter of milliseconds. This rapid exposure, together with another feature known as “backward masking,” prevented subjects from consciously seeing the faces. Backward masking works by presenting subjects with an irrelevant “mask” image that immediately follows an extremely brief exposure to a face, which is thought to terminate the brain’s ability to further process the face and prevent it from reaching awareness. In the first experiment, the researchers examined amygdala activity in response to three levels of a face’s trustworthiness: low, medium, and high. In the second experiment, they assessed amygdala activity in response to a fully continuous spectrum of trustworthiness.
Across the two experiments, the researchers found that specific regions inside the amygdala exhibited activity tracking how untrustworthy a face appeared, and other regions inside the amygdala exhibited activity tracking the overall strength of the trustworthiness signal (whether untrustworthy or trustworthy)—even though subjects could not consciously see any of the faces.
“These findings provide evidence that the amygdala’s processing of social cues in the absence of awareness may be more extensive than previously understood,” observes Freeman. “The amygdala is able to assess how trustworthy another person’s face appears without it being consciously perceived.”
Small DNA modifications predict brain’s threat response
The tiny addition of a chemical mark atop a gene that is well known for its involvement in clinical depression and posttraumatic stress disorder can affect the way a person’s brain responds to threats, according to a new study by Duke University researchers.
The results, which appear online August 3 in Nature Neuroscience, go beyond genetics to help explain why some individuals may be more vulnerable than others to stress and stress-related psychiatric disorders.
The study focused on the serotonin transporter, a molecule that regulates the amount of serotonin signaling between brain cells and is a major target for treatment of depression and mood disorders. In the 1990s, scientists discovered that differences in the DNA sequence of the serotonin transporter gene seemed to give some individuals exaggerated responses to stress, including the development of depression.
(Image caption: An artist’s conception shows how molecules called methyl groups attach to a specific stretch of DNA, changing expression of the serotonin transporter gene in a way that ultimately shapes individual differences in the brain’s reactivity to threat. The methyl groups in this diagram are overlaid on the amygdala of the brain, where threat perception occurs. Credit: Annchen Knodt, Duke University)
Sitting on top of the serotonin transporter’s DNA (and studding the entire genome), are chemical marks called methyl groups that help regulate where and when a gene is active, or expressed. DNA methylation is one form of epigenetic modification being studied by scientists trying to understand how the same genetic code can produce so many different cells and tissues as well as differences between individuals as closely related as twins.
In looking for methylation differences, “we decided to start with the serotonin transporter because we know a lot about it biologically, pharmacologically, behaviorally, and it’s one of the best characterized genes in neuroscience,” said senior author Ahmad Hariri, a professor of psychology and neuroscience and member of the Duke Institute for Brain Sciences.
"If we’re going to make claims about the importance of epigenetics in the human brain, we wanted to start with a gene that we have a fairly good understanding of," Hariri said.
This work is part of the ongoing Duke Neurogenetics Study (DNS), a comprehensive study linking genes, brain activity and other biological markers to risk for mental illness in young adults.
The group performed non-invasive brain imaging in the first 80 college-aged participants of the DNS, showing them pictures of angry or fearful faces and watching the responses of a deep brain region called the amygdala, which helps shape our behavioral and biological responses to threat and stress.
The team also measured the amount of methylation on serotonin transporter DNA isolated from the participants’ saliva, in collaboration with Karestan Koenen at Columbia University’s Mailman School of Public Health in New York.
The greater the methylation of an individual’s serotonin transporter gene, the greater the reactivity of the amygdala, the study found. Increased amygdala reactivity may in turn contribute to an exaggerated stress response and vulnerability to stress-related disorders.
To the group’s surprise, even small methylation variations between individuals were sufficient to create differences between individuals’ amygdala reactivity, said lead author Yuliya Nikolova, a graduate student in Hariri’s group. The amount of methylation was a better predictor of amygdala activity than DNA sequence variation, which had previously been associated with risk for depression and anxiety.
The team was excited about the discovery but also cautious, Hariri said, because there have been many findings in genetics that were never replicated.
That’s why they jumped at the chance to look for the same pattern in a different set of participants, this time in the Teen Alcohol Outcomes Study (TAOS) at the University of Texas Health Science Center at San Antonio.
Working with TAOS director, Douglas Williamson, the group again measured amygdala reactivity to angry and fearful faces as well as methylation of the serotonin transporter gene isolated from blood in 96 adolescents between 11 and 15 years old. The analyses revealed an even stronger link between methylation and amygdala reactivity.
"Now over 10 percent of the differences in amygdala function mapped onto these small differences in methylation," Hariri said. The DNS study had found just under 7 percent.
Taking the study one step further, the group also analyzed patterns of methylation in the brains of dead people in collaboration with Etienne Sibille at the University of Pittsburgh, now at the Centre for Addiction and Mental Health in Toronto.
Once again, they saw that methylation of a single spot in the serotonin transporter gene was associated with lower levels of serotonin transporter expression in the amygdala.
"That’s when we thought, ‘Alright, this is pretty awesome,’" Hariri said.
Hariri said the work reveals a compelling mechanistic link: Higher methylation is generally associated with less reading of the gene, and that’s what they saw. He said methylation dampens expression of the gene, which then affects amygdala reactivity, presumably by altering serotonin signaling.
The researchers would now like to see how methylation of this specific bit of DNA affects the brain. In particular, this region of the gene might serve as a landing place for cellular machinery that binds to the DNA and reads it, Nikolova said.
The group also plans to look at methylation patterns of other genes in the serotonin system that may contribute to the brain’s response to threatening stimuli.
The fact that serotonin transporter methylation patterns were similar in saliva, blood and brain also suggests that these patterns may be passed down through generations rather than acquired by individuals based on their own experiences.
Hariri said he hopes that other researchers looking for biomarkers of mental illness will begin to consider methylation above and beyond DNA sequence-based variation and across different tissues.
(Source: eurekalert.org)
(Image caption: Brain image showing activity in the amygdala, the area of the brain involved with emotion. The amydgala was more active during the graphic scenarios only when the harm being described was intentional. Credit: Marois Lab / Vanderbilt)
Fault trumps gruesome evidence when it comes to meting out punishment
Issues of crime and punishment, vengeance and justice date back to the dawn of human history, but it is only in the last few years that scientists have begun exploring the basic nature of the complex neural processes in the brain that underlie these fundamental behaviors.
Now a new brain imaging study – published online Aug. 3 by the journal Nature Neuroscience – has identified the brain mechanisms that underlie our judgment of how severely a person who has harmed another should be punished. Specifically, the study determined how the area of the brain that determines whether such an act was intentional or unintentional trumps the emotional urge to punish the person, however gruesome the harm may be.
“A fundamental aspect of the human experience is the desire to punish harmful acts, even when the victim is a perfect stranger. Equally important, however, is our ability to put the brakes on this impulse when we realize the harm was done unintentionally,” said Rene Marois, the Vanderbilt University professor of psychology who headed the research team. “This study helps us begin to elucidate the neural circuitry that permits this type of regulation.”
The study
In the experiment, the brains of 30 volunteers (20 male, 10 female, average age 23 years) were imaged using functional MRI (fMRI) while they read a series of brief scenarios that described how the actions of a protagonist named John brought harm to either Steve or Mary. The scenarios depicted four different levels of harm: death, maiming, physical assault and property damage. In half of them, the harm was clearly identified as intentional and in half it was clearly identified as unintentional.
Two versions of each scenario were created: one with a factual description of the harm and the other with a graphic description. For example, in a mountain climbing scenario where John cuts Steve’s rope, the factual version states, “Steve falls 100 feet to the ground below. Steve experiences significant bodily harm from the fall and he dies from his injuries shortly after impact.” And the graphic version reads, “Steve plummets to the rocks below. Nearly every bone in his body is broken upon impact. Steve’s screams are muffled by thick, foamy blood flowing from his mouth as he bleeds to death.”
After reading each scenario the participants were asked to list how much punishment John deserved on a scale from zero (no punishment) to nine (most severe punishment the subject endorsed).
Analysis of the responses
When the responses were analyzed, the researchers found that the manner in which the harmful consequences of an action are described significantly influences the level of punishment that people consider appropriate: When the harm was described in a graphic or lurid fashion then people set the punishment level higher than when it was described matter-of-factly. However, this higher punishment level only applied when the participants considered the resulting harm to be intentional. When they considered it to be unintentional, the way it was described didn’t have any effect.
“What we’ve shown is that manipulations of gruesome language leads to harsher punishment, but only in cases where the harm was intentional. Language had no effect when the harm was caused unintentionally,” summarized Michael Treadway, a post-doctoral fellow at Harvard Medical School and lead author of the study.
According to the researchers, the fact that the mere presence of graphic language could cause participants to ratchet up the severity of the punishments suggests that photographs, video and other graphic materials sampled from a crime scene is likely to have an even stronger impact on an individual’s desire to punish.
“Although the underlying scientific basis of this effect wasn’t known until now, the legal system recognized it a long time ago and made provisions to counteract it,” said Treadway. “Judges are permitted to exclude relevant evidence from a trial if they decide that its probative value is substantially outweighed by its prejudicial nature.”
Underlying neuroanatomy
The fMRI scans revealed the areas of the brain that are involved in this complex process. They found that the amygdala, an almond-shaped set of neurons that plays a key role in processing emotions, responded most strongly to the graphic language condition. Like the punishment ratings themselves, however, this effect in the amygdala was only present when harm was done intentionally. Moreover, in this situation the researchers found that the amygdala showed stronger communication with the dorsolateral prefrontal cortex (dlPFC), an area that is critical for punishment decision-making. When the harm was done unintentionally, however, a different regulatory network – one involved in decoding the mental states of other people – became more active and appeared to suppress amygdala responses to the graphic language, thereby preventing the amygdala from affecting decision-making areas in dlPFC.
“This is basically a reassuring finding,” said Marois. “It indicates that, when the harm is not intended, we don’t simply shunt aside the emotional impulse to punish. Instead, it appears that the brain down-regulates the impulse so we don’t feel it as strongly. That is preferable because the urge to punish is less likely to resurface at a future date.”
A New Brain-Based Marker of Stress Susceptibility
Some people can handle stressful situations better than others, and it’s not all in their genes: Even identical twins show differences in how they respond.
(Image: iStockphoto)
Researchers have identified a specific electrical pattern in the brains of genetically identical mice that predicts how well individual animals will fare in stressful situations.
The findings, published July 29 in Nature Communications, may eventually help researchers prevent potential consequences of chronic stress — such as post-traumatic stress disorder, depression and other psychiatric disorders — in people who are prone to these problems.
“In soldiers, we have this dramatic, major stress exposure, and in some individuals it’s leading to major issues, such as problems sleeping or being around other people,” said senior author Kafui Dzirasa, M.D., Ph.D., an assistant professor of psychiatry and behavioral sciences at Duke University Medical Center and a member of the Duke Institute for Brain Sciences. “If we can find that common trigger or common pathway and tune it, we may be able to prevent the emergence of a range of mental illnesses down the line.”
In the new study, Dzirasa’s team analyzed the interaction between two interconnected brain areas that control fear and stress responses in both mice and men: the prefrontal cortex and the amygdala. The amygdala plays a role in the ‘fight-or-flight’ response. The prefrontal cortex is involved in planning and other higher-level functions. It suppresses the amygdala’s reactivity to danger and helps people continue to function in stressful situations.
Implanting electrodes into the brains of the mice allowed the researchers to listen in on the tempo at which the prefrontal cortex and the amygdala were firing and how tightly the two areas were linked — with the ultimate goal of figuring whether the electrical pattern of cross talk could help decide how well animals would respond when faced with an acute stressor.
Indeed, in mice that had been subjected to a chronically stressful situation — daily exposure to an aggressive male mouse for about two weeks — the degree to which the prefrontal cortex seemed to control amygdala activity was related to how well the animals coped with the stress, the group found.
Next the group looked at how the brain reacted to the first instance of stress, before the mice were put in a chronically stressful situation. The mice more sensitive to chronic stress showed greater activation of their prefrontal cortex-amygdala circuit, compared with resilient mice.
“We were really both surprised and excited to find that this signature was present in the animals before they were chronically stressed,” Dzirasa said. “You can find this signature the very first time they were ever exposed to this aggressive dangerous experience.”
Dzirasa hopes to use the signatures to come up with potential treatments for stress. “If we pair the signatures and treatments together, can we prevent symptoms from emerging, even when an animal is stressed? That’s the first question,” he said.
The group also hopes to delve further into the brain, to see whether the circuit-level patterns can interact with genetic variations that confer risk for psychiatric disorders such as schizophrenia. The new study will enable Dzirasa and other basic researchers to segregate stress-susceptible and resilient animals before they are subjected to stress and look at their molecular, cellular and systemic differences.
(Source: today.duke.edu)
Learning the smell of fear: Mothers teach babies their own fears via odor
Babies can learn what to fear in the first days of life just by smelling the odor of their distressed mothers, new research suggests. And not just “natural” fears: If a mother experienced something before pregnancy that made her fear something specific, her baby will quickly learn to fear it too — through the odor she gives off when she feels fear.
In the first direct observation of this kind of fear transmission, a team of University of Michigan Medical School and New York University studied mother rats who had learned to fear the smell of peppermint – and showed how they “taught” this fear to their babies in their first days of life through their alarm odor released during distress.
In a new paper in the Proceedings of the National Academy of Sciences, the team reports how they pinpointed the specific area of the brain where this fear transmission takes root in the earliest days of life.
Their findings in animals may help explain a phenomenon that has puzzled mental health experts for generations: how a mother’s traumatic experience can affect her children in profound ways, even when it happened long before they were born.
The researchers also hope their work will lead to better understanding of why not all children of traumatized mothers, or of mothers with major phobias, other anxiety disorders or major depression, experience the same effects.
“During the early days of an infant rat’s life, they are immune to learning information about environmental dangers. But if their mother is the source of threat information, we have shown they can learn from her and produce lasting memories,” says Jacek Debiec, M.D., Ph.D., the U-M psychiatrist and neuroscientist who led the research.
“Our research demonstrates that infants can learn from maternal expression of fear, very early in life,” he adds. “Before they can even make their own experiences, they basically acquire their mothers’ experiences. Most importantly, these maternally-transmitted memories are long-lived, whereas other types of infant learning, if not repeated, rapidly perish.”
Peering inside the fearful brain
Debiec, who treats children and mothers with anxiety and other conditions in the U-M Department of Psychiatry, notes that the research on rats allows scientists to see what’s going on inside the brain during fear transmission, in ways they could never do in humans.
He began the research during his fellowship at NYU with Regina Marie Sullivan, Ph.D., senior author of the new paper, and continues it in his new lab at U-M’s Molecular and Behavioral Neuroscience Institute.
The researchers taught female rats to fear the smell of peppermint by exposing them to mild, unpleasant electric shocks while they smelled the scent, before they were pregnant. Then after they gave birth, the team exposed the mothers to just the minty smell, without the shocks, to provoke the fear response. They also used a comparison group of female rats that didn’t fear peppermint.
They exposed the pups of both groups of mothers to the peppermint smell, under many different conditions with and without their mothers present.
Using special brain imaging, and studies of genetic activity in individual brain cells and cortisol in the blood, they zeroed in on a brain structure called the lateral amygdala as the key location for learning fears. During later life, this area is key to detecting and planning response to threats – so it makes sense that it would also be the hub for learning new fears.
But the fact that these fears could be learned in a way that lasted, during a time when the baby rat’s ability to learn any fears directly was naturally suppressed, is what makes the new findings so interesting, says Debiec.
The team even showed that the newborns could learn their mothers’ fears even when the mothers weren’t present. Just the piped-in scent of their mother reacting to the peppermint odor she feared was enough to make them fear the same thing.
Even when just the odor of the frightened mother was piped in to a chamber where baby rats were exposed to peppermint smell, the babies developed a fear of the same smell, and their blood cortisol levels rose when they smelled it.
And when the researchers gave the baby rats a substance that blocked activity in the amygdala, they failed to learn the fear of peppermint smell from their mothers. This suggests, Debiec says, that there may be ways to intervene to prevent children from learning irrational or harmful fear responses from their mothers, or reduce their impact.
From animals to humans: next steps
The new research builds on what scientists have learned over time about the fear circuitry in the brain, and what can go wrong with it. That work has helped psychiatrists develop new treatments for human patients with phobias and other anxiety disorders – for instance, exposure therapy that helps them overcome fears by gradually confronting the thing or experience that causes their fear.
In much the same way, Debiec hopes that exploring the roots of fear in infancy, and how maternal trauma can affect subsequent generations, could help human patients. While it’s too soon to know if the same odor-based effect happens between human mothers and babies, the role of a mother’s scent in calming human babies has been shown.
Debiec, who hails from Poland, recalls working with the grown children of Holocaust survivors, who experienced nightmares, avoidance instincts and even flashbacks related to traumatic experiences they never had themselves. While they would have learned about the Holocaust from their parents, this deeply ingrained fear suggests something more at work, he says.
(Source: uofmhealth.org)
Brain responses to emotional images predict PTSD symptoms after Boston Marathon bombing
The area of the brain that plays a primary role in emotional learning and the acquisition of fear – the amygdala – may hold the key to who is most vulnerable to post-traumatic stress disorder.
Researchers at the University of Washington, Boston Children’s Hospital, Harvard Medical School and Boston University collaborated on a unique opportunity to study whether patterns of brain activity predict teenagers’ response to a terrorist attack.
The team had already performed brain scans on Boston-area adolescents for a study on childhood trauma. Then in April 2013 two bombs went off at the finish line of the Boston Marathon, killing three people and injuring hundreds more. Even people who were nowhere near the bombing reported distress about the attack and the days-long manhunt for the suspects.
So, one month after the attack, Katie McLaughlin, then at Boston Children’s Hospital and Harvard Medical School and now an assistant professor of psychology at the UW; co-author Margaret Sheridan, of Boston Children’s Hospital and Harvard Medical School; and their fellow researchers sent online surveys to teenagers who had previously participated in studies to assess PTSD symptoms related to the attack.
By using functional Magnetic Resonance Imaging scans from before the attack and survey data from after, the researchers found that heightened amygdala reaction to negative emotional stimuli was a risk factor for later developing symptoms of PTSD.
The research study was published July 3 in the journal Depression and Anxiety.
“The amygdala responds to both negative and positive stimuli, but it’s particularly attuned to identifying potential threats in the environment,” said McLaughlin, the study’s first author. “In the current study of adolescents the more their amygdala responded to negative images, the more likely they were to have symptoms of PTSD following the terrorist attacks.”
The brain scans were conducted during the year prior to the bombing. At that time, the teens were evaluated for their responses to emotional stimuli by viewing neutral and negative images. Neutral images included items such as a chair or button. Negative images showed people who were sad, fighting or threatening someone else. Participants rated the degree of emotion they felt while looking at each image. The MRIs measured whether blood flow increased to the amygdala and the hippocampus when viewing negative images as compared to neutral images.
In the follow-up survey the teens were asked whether they were at the finish line during the bombing, how much media exposure they had after the attack, whether they were part of the lockdown at home or school while authorities searched for the suspects, and how their parents responded to the incident. They also were asked about specific PTSD symptoms, such as how often they had trouble concentrating and whether they kept thinking about the bombing when they tried not to.
Researchers found a significant association between amygdala activation while viewing negative images and whether the teens developed PTSD symptoms after the bombing.
McLaughlin said a number of previous studies have shown that people with PTSD had heightened amygdala responses to negative emotions, but researchers didn’t know whether that came before or after the trauma.
“It’s often really difficult to collect neurobiological markers before a traumatic event has occurred,” she said. By scanning the adolescents’ brains before the bombing, she and her fellow researchers were able to show that “amygdala reactivity before a traumatic event predicts your response to that traumatic event.”
While two-thirds of Americans will be exposed to some kind of traumatic event during their lifetime, most, fortunately, will not develop PTSD.
“The more we understand the underlying neurobiological systems that shape reactions to traumatic events, the closer we move to understanding a person’s increased vulnerability to them,” McLaughlin said. “That could help us develop early interventions to help people who might develop PTSD later.”
(Source: washington.edu)
Brain activity in sex addiction mirrors that of drug addiction
Pornography triggers brain activity in people with compulsive sexual behaviour – known commonly as sex addiction – similar to that triggered by drugs in the brains of drug addicts, according to a University of Cambridge study published in the journal PLOS ONE. However, the researchers caution that this does not necessarily mean that pornography itself is addictive.
Although precise estimates are unknown, previous studies have suggested that as many as one in 25 adults is affected by compulsive sexual behaviour, an obsession with sexual thoughts, feelings or behaviour which they are unable to control. This can have an impact on a person’s personal life and work, leading to significant distress and feelings of shame. Excessive use of pornography is one of the main features identified in many people with compulsive sexual behaviour. However, there is currently no formally accepted definition of diagnosing the condition.
In a study funded by the Wellcome Trust, researchers from the Department of Psychiatry at the University of Cambridge looked at brain activity in nineteen male patients affected by compulsive sexual behaviour and compared them to the same number of healthy volunteers. The patients started watching pornography at earlier ages and in higher proportions relative to the healthy volunteers.
“The patients in our trial were all people who had substantial difficulties controlling their sexual behaviour and this was having significant consequences for them, affecting their lives and relationships,” explains Dr Valerie Voon, a Wellcome Trust Intermediate Clinical Fellow at the University of Cambridge. “In many ways, they show similarities in their behaviour to patients with drug addictions. We wanted to see if these similarities were reflected in brain activity, too.”
The study participants were shown a series of short videos featuring either sexually explicit content or sports whilst their brain activity was monitored using functional magnetic resonance imaging (fMRI), which uses a blood oxygen level dependent (BOLD) signal to measure brain activity.
The researchers found that three regions in particular were more active in the brains of the people with compulsive sexual behaviour compared with the healthy volunteers. Significantly, these regions – the ventral striatum, dorsal anterior cingulate and amygdala – were regions that are also particularly activated in drug addicts when shown drug stimuli. The ventral striatum is involved in processing reward and motivation, whilst the dorsal anterior cingulate is implicated in anticipating rewards and drug craving. The amygdala is involved in processing the significance of events and emotions.
The researchers also asked the participants to rate the level of sexual desire that they felt whilst watching the videos, and how much they liked the videos. Drug addicts are thought to be driven to seek their drug because they want – rather than enjoy – it. This abnormal process is known as incentive motivation, a compelling theory in addiction disorders.
As anticipated, patients with compulsive sexual behaviour showed higher levels of desire towards the sexually explicit videos, but did not necessarily rate them higher on liking scores. In the patients, desire was also correlated with higher interactions between regions within the network identified – with greater cross-talk between the dorsal cingulate, ventral striatum and amygdala – for explicit compared to sports videos.
Dr Voon and colleagues also found a correlation between brain activity and age – the younger the patient, the greater the level of activity in the ventral striatum in response to pornography. Importantly, this association was strongest in individuals with compulsive sexual behaviour. The frontal control regions of the brain – essentially, the ‘brakes’ on our compulsivity – continue to develop into the mid-twenties and this imbalance may account for greater impulsivity and risk taking behaviours in younger people. The age-related findings in individuals with compulsive sexual behaviours suggest that the ventral striatum may be important in developmental aspects of compulsive sexual behaviours in a similar fashion as it is in drug addictions, although direct testing of this possibility is needed.
“There are clear differences in brain activity between patients who have compulsive sexual behaviour and healthy volunteers. These differences mirror those of drug addicts,” adds Dr Voon. “Whilst these findings are interesting, it’s important to note, however, that they could not be used to diagnose the condition. Nor does our research necessarily provide evidence that these individuals are addicted to porn – or that porn is inherently addictive. Much more research is required to understand this relationship between compulsive sexual behaviour and drug addiction.”
Dr John Williams, Head of Neuroscience and Mental Health at the Wellcome Trust, says: “Compulsive behaviours, including watching porn to excess, over-eating and gambling, are increasingly common. This study takes us a step further to finding out why we carry on repeating behaviours that we know are potentially damaging to us. Whether we are tackling sex addiction, substance abuse or eating disorders, knowing how best, and when, to intervene in order to break the cycle is an important goal of this research.”
The anatomy of fear: Understanding the biological underpinnings of anxiety, phobias and PTSD
Fear in a mouse brain looks much the same as fear in a human brain.
When a frightening stimulus is encountered, the thalamus shoots a message to the amygdala — the primitive part of the brain — even before it informs the parts responsible for higher cognition. The amygdala then goes into its hard-wired fight-or-flight response, triggering a host of predictable symptoms, including racing heart, heavy breathing, startle response, and sweating.
The similarities of fear response in the brains of mice and men have allowed scientists to understand the neural circuitry and molecular processes of fear and fear behaviors perhaps better than any other response. That understanding has spurred breakthroughs in treatments for psychiatric disorders that are underpinned by fear.
Anxiety disorders are one of the most common mental illnesses in the country, with nearly one-third of Americans experiencing symptoms at least once during their lives. There are generalized anxiety disorders and fear-related disorders, which include panic disorders, phobias, and post-traumatic stress disorder (PTSD).
Emory psychiatrist and researcher Kerry Ressler is on the front lines of fear-disorder research. In his lab at Yerkes National Primate Research Center, he studies the molecular and cellular mechanisms of fear learning and extinction in mouse models. At Grady Memorial Hospital, he investigates the psychology, genetics, and biology of PTSD. And through the Grady Trauma Project, he works to draw attention to the problem of inner city intergenerational violence.
"If you look at Kerry’s work, it can seem like it’s all over the place — he’s got so many studies going on, and he collaborates with so many other scientists," says Barbara Rothbaum, associate vice chair of clinical research in psychiatry and director of the Trauma and Anxiety Recovery Program at Emory. "But they are all pieces to the same puzzle. All his work, from molecular to clinical to policy, fits together and starts telling a story." A Howard Hughes Medical Institute investigator, Ressler was recently elected to the Institute of Medicine — one of the highest honors in the fields of health and medicine. He was named a member of a new national PTSD consortium led by Draper Laboratory. And he recently appeared on the Charlie Rose show’s brain series.
Panic attacks seem to tie the fear-related disorders together, he explained on Charlie Rose. Everyone experiences fear, which evolved as a survival mechanism, but it only rises to a clinical level when people are unable to function normally in the face of it. For instance, PTSD includes not only intrusive thoughts, memories, nightmares, and startle responses, but also the concept of avoidance, which may extend to other areas of the individual’s life.
"There’s a patient I’ve seen who was attacked in a dark alley," Ressler shared on the show. "Initially it just felt dangerous to go out at night, but after a while she grew afraid of men and couldn’t go to that part of town. Then she couldn’t leave her house, and finally, her bedroom. The world got more and more dangerous."