Neuroscience

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Autism as a disorder of prediction Autism is characterized by many different symptoms: difficulty interacting with others, repetitive behaviors, and hypersensitivity to sound and other stimuli. MIT neuroscientists have put forth a new hypothesis that accounts for these behaviors and may provide a neurological foundation for many of the disparate features of the disorder. The researchers suggest that autism may be rooted in an impaired ability to predict events and other people’s actions. From the perspective of the autistic child, the world appears to be a “magical” rather than an orderly place, because events seem to occur randomly and unpredictably. In this view, autism symptoms such as repetitive behavior, and an insistence on a highly structured environment, are coping strategies to help deal with this unpredictable world. The researchers hope that this unifying theory, if validated, could offer new strategies for treating autism. “At the moment, the treatments that have been developed are driven by the end symptoms. We’re suggesting that the deeper problem is a predictive impairment problem, so we should directly address that ability,” says Pawan Sinha, an MIT professor of brain and cognitive sciences and the lead author of a paper describing the hypothesis in the Proceedings of the National Academy of Sciences this week. “I don’t know what techniques would be most effective for improving predictive skills, but it would at least argue for the target of a therapy being predictive skills rather than other manifestations of autism,” he adds. The paper’s senior author is Richard Held, a professor emeritus in the Department of Brain and Cognitive Sciences. Other authors are research affiliates Margaret Kjelgaard and Sidney Diamond, postdoc Tapan Gandhi, technical associates Kleovoulos Tsourides and Annie Cardinaux, and research scientist Dimitrios Pantazis. Dealing with an unpredictable world Sinha and his colleagues first began thinking about prediction skills as a possible underpinning for autism based on reports from parents that their autistic children insist on a very controlled, predictable environment. “The need for sameness is one of the most uniform characteristics of autism,” Sinha says. “It’s a short step away from that description to think that the need for sameness is another way of saying that the child with autism needs a very predictable setting.” Most people can routinely estimate the probabilities of certain events, such as other people’s likely behavior, or the trajectory of a ball in flight. The MIT team began to think that autistic children may not have the same computational abilities when it comes to prediction. This hypothesized deficit could produce several of the most common autism symptoms. For example, repetitive behaviors and insistence on rigid structure have been shown to soothe anxiety produced by unpredictability, even in individuals without autism. “These may be proactive attempts on the part of the person to try to impose some structure on an environment that otherwise seems chaotic,” Sinha says. Impaired prediction skills would also help to explain why autistic children are often hypersensitive to sensory stimuli. Most people are able to become used to ongoing sensory stimuli such as background noises, because they can predict that the noise or other stimulus will probably continue, but autistic children have much more trouble habituating. “If we were unable to habituate to stimuli, then the world would become overwhelming very quickly. It’s like you can’t escape this cacophony that’s falling on your ears or that you’re observing,” Sinha says. Autistic children also often have a reduced ability to understand another person’s thoughts, feelings, and motivations — a skill known as “theory of mind.” The MIT team believes this could result from an inability to predict another person’s behavior based on past interactions. People with autism have difficulty using this type of context, and tend to interpret behavior based only on what is happening in that very moment.  Leonard Rappaport, chief of the division of developmental medicine at Boston Children’s Hospital, says he believes the new theory is “a uniting concept that could lead us to new approaches to understanding the etiology and perhaps lead to completely new treatment paradigms for this complex disorder.” “This is not the first theory to explain the complex of symptoms we see every day in our clinical programs, but it seems to explain more of what we see than other theories that explain individual symptoms,” says Rappaport, who was not involved in the research. Timing is everything The researchers believe that different children may show different symptoms of autism based on the timing of the predictive impairment. “In the millisecond range, you would expect to have more of an impairment in language,” Sinha says. “In the tens of milliseconds range, it might be more of a motor impairment, and in the range of seconds, you would expect to see more of a social and planning impairment.” The hypothesis also predicts that some cognitive skills — those based more on rules than on prediction — should remain unharmed, or even be enhanced, in autistic individuals. This includes tasks such as math, drawing, and music, which are often strengths for autistic children. A few previous studies have tried to pinpoint which parts of the brain are involved in making predictions. So far, the strongest candidates are the basal ganglia, the nucleus accumbens, and the cerebellum — structures that are often structurally abnormal in autistic patients. “It’s a very tentative connection at the moment, but I think this is a fruitful line of inquiry for the future,” Sinha says. Sinha’s team has already begun testing some elements of the prediction-deficit hypothesis. Initial results of one study suggest that autistic children do have an impairment in habituation to sensory stimuli; in another set of experiments, the researchers are testing autistic children’s ability to track moving objects, such as a ball. “The hypothesis is guiding us toward very concrete studies,” Sinha says. “We hope to enlist the participation of families and children touched by autism to help put the theory through its paces.”

Autism as a disorder of prediction

Autism is characterized by many different symptoms: difficulty interacting with others, repetitive behaviors, and hypersensitivity to sound and other stimuli. MIT neuroscientists have put forth a new hypothesis that accounts for these behaviors and may provide a neurological foundation for many of the disparate features of the disorder.

The researchers suggest that autism may be rooted in an impaired ability to predict events and other people’s actions. From the perspective of the autistic child, the world appears to be a “magical” rather than an orderly place, because events seem to occur randomly and unpredictably. In this view, autism symptoms such as repetitive behavior, and an insistence on a highly structured environment, are coping strategies to help deal with this unpredictable world.

The researchers hope that this unifying theory, if validated, could offer new strategies for treating autism.

“At the moment, the treatments that have been developed are driven by the end symptoms. We’re suggesting that the deeper problem is a predictive impairment problem, so we should directly address that ability,” says Pawan Sinha, an MIT professor of brain and cognitive sciences and the lead author of a paper describing the hypothesis in the Proceedings of the National Academy of Sciences this week.

“I don’t know what techniques would be most effective for improving predictive skills, but it would at least argue for the target of a therapy being predictive skills rather than other manifestations of autism,” he adds.

The paper’s senior author is Richard Held, a professor emeritus in the Department of Brain and Cognitive Sciences. Other authors are research affiliates Margaret Kjelgaard and Sidney Diamond, postdoc Tapan Gandhi, technical associates Kleovoulos Tsourides and Annie Cardinaux, and research scientist Dimitrios Pantazis.

Dealing with an unpredictable world

Sinha and his colleagues first began thinking about prediction skills as a possible underpinning for autism based on reports from parents that their autistic children insist on a very controlled, predictable environment.

“The need for sameness is one of the most uniform characteristics of autism,” Sinha says. “It’s a short step away from that description to think that the need for sameness is another way of saying that the child with autism needs a very predictable setting.”

Most people can routinely estimate the probabilities of certain events, such as other people’s likely behavior, or the trajectory of a ball in flight. The MIT team began to think that autistic children may not have the same computational abilities when it comes to prediction.

This hypothesized deficit could produce several of the most common autism symptoms. For example, repetitive behaviors and insistence on rigid structure have been shown to soothe anxiety produced by unpredictability, even in individuals without autism.

“These may be proactive attempts on the part of the person to try to impose some structure on an environment that otherwise seems chaotic,” Sinha says.

Impaired prediction skills would also help to explain why autistic children are often hypersensitive to sensory stimuli. Most people are able to become used to ongoing sensory stimuli such as background noises, because they can predict that the noise or other stimulus will probably continue, but autistic children have much more trouble habituating.

“If we were unable to habituate to stimuli, then the world would become overwhelming very quickly. It’s like you can’t escape this cacophony that’s falling on your ears or that you’re observing,” Sinha says.

Autistic children also often have a reduced ability to understand another person’s thoughts, feelings, and motivations — a skill known as “theory of mind.” The MIT team believes this could result from an inability to predict another person’s behavior based on past interactions. People with autism have difficulty using this type of context, and tend to interpret behavior based only on what is happening in that very moment. 

Leonard Rappaport, chief of the division of developmental medicine at Boston Children’s Hospital, says he believes the new theory is “a uniting concept that could lead us to new approaches to understanding the etiology and perhaps lead to completely new treatment paradigms for this complex disorder.”

“This is not the first theory to explain the complex of symptoms we see every day in our clinical programs, but it seems to explain more of what we see than other theories that explain individual symptoms,” says Rappaport, who was not involved in the research.

Timing is everything

The researchers believe that different children may show different symptoms of autism based on the timing of the predictive impairment.

“In the millisecond range, you would expect to have more of an impairment in language,” Sinha says. “In the tens of milliseconds range, it might be more of a motor impairment, and in the range of seconds, you would expect to see more of a social and planning impairment.”

The hypothesis also predicts that some cognitive skills — those based more on rules than on prediction — should remain unharmed, or even be enhanced, in autistic individuals. This includes tasks such as math, drawing, and music, which are often strengths for autistic children.

A few previous studies have tried to pinpoint which parts of the brain are involved in making predictions. So far, the strongest candidates are the basal ganglia, the nucleus accumbens, and the cerebellum — structures that are often structurally abnormal in autistic patients. “It’s a very tentative connection at the moment, but I think this is a fruitful line of inquiry for the future,” Sinha says.

Sinha’s team has already begun testing some elements of the prediction-deficit hypothesis. Initial results of one study suggest that autistic children do have an impairment in habituation to sensory stimuli; in another set of experiments, the researchers are testing autistic children’s ability to track moving objects, such as a ball. “The hypothesis is guiding us toward very concrete studies,” Sinha says. “We hope to enlist the participation of families and children touched by autism to help put the theory through its paces.”

Filed under autism anxiety cerebellum nucleus accumbens basal ganglia neuroscience science

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How curiosity changes the brain to enhance learning The more curious we are about a topic, the easier it is to learn information about that topic. New research publishing online October 2 in the Cell Press journal Neuron provides insights into what happens in our brains when curiosity is piqued. The findings could help scientists find ways to enhance overall learning and memory in both healthy individuals and those with neurological conditions. "Our findings potentially have far-reaching implications for the public because they reveal insights into how a form of intrinsic motivation—curiosity—affects memory. These findings suggest ways to enhance learning in the classroom and other settings," says lead author Dr. Matthias Gruber, of University of California at Davis. For the study, participants rated their curiosity to learn the answers to a series of trivia questions. When they were later presented with a selected trivia question, there was a 14 second delay before the answer was provided, during which time the participants were shown a picture of a neutral, unrelated face. Afterwards, participants performed a surprise recognition memory test for the faces that were presented, followed by a memory test for the answers to the trivia questions. During certain parts of the study, participants had their brains scanned via functional magnetic resonance imaging. The study revealed three major findings. First, as expected, when people were highly curious to find out the answer to a question, they were better at learning that information. More surprising, however, was that once their curiosity was aroused, they showed better learning of entirely unrelated information (face recognition) that they encountered but were not necessarily curious about. People were also better able to retain the information learned during a curious state across a 24-hour delay. “Curiosity may put the brain in a state that allows it to learn and retain any kind of information, like a vortex that sucks in what you are motivated to learn, and also everything around it,” explains Dr. Gruber. Second, the investigators found that when curiosity is stimulated, there is increased activity in the brain circuit related to reward. “We showed that intrinsic motivation actually recruits the very same brain areas that are heavily involved in tangible, extrinsic motivation,” says Dr. Gruber. This reward circuit relies on dopamine, a chemical messenger that relays messages between neurons. Third, the team discovered that when curiosity motivated learning, there was increased activity in the hippocampus, a brain region that is important for forming new memories, as well as increased interactions between the hippocampus and the reward circuit. “So curiosity recruits the reward system, and interactions between the reward system and the hippocampus seem to put the brain in a state in which you are more likely to learn and retain information, even if that information is not of particular interest or importance,” explains principal investigator Dr. Charan Ranganath, also of UC Davis. The findings could have implications for medicine and beyond. For example, the brain circuits that rely on dopamine tend to decline in function as people get older, or sooner in people with neurological conditions. Understanding the relationship between motivation and memory could therefore stimulate new efforts to improve memory in the healthy elderly and to develop new approaches for treating patients with disorders that affect memory. And in the classroom or workplace, learning what might be considered boring material could be enhanced if teachers or managers are able to harness the power of students’ and workers’ curiosity about something they are naturally motivated to learn.

How curiosity changes the brain to enhance learning

The more curious we are about a topic, the easier it is to learn information about that topic. New research publishing online October 2 in the Cell Press journal Neuron provides insights into what happens in our brains when curiosity is piqued. The findings could help scientists find ways to enhance overall learning and memory in both healthy individuals and those with neurological conditions.

"Our findings potentially have far-reaching implications for the public because they reveal insights into how a form of intrinsic motivation—curiosity—affects memory. These findings suggest ways to enhance learning in the classroom and other settings," says lead author Dr. Matthias Gruber, of University of California at Davis.

For the study, participants rated their curiosity to learn the answers to a series of trivia questions. When they were later presented with a selected trivia question, there was a 14 second delay before the answer was provided, during which time the participants were shown a picture of a neutral, unrelated face. Afterwards, participants performed a surprise recognition memory test for the faces that were presented, followed by a memory test for the answers to the trivia questions. During certain parts of the study, participants had their brains scanned via functional magnetic resonance imaging.

The study revealed three major findings. First, as expected, when people were highly curious to find out the answer to a question, they were better at learning that information. More surprising, however, was that once their curiosity was aroused, they showed better learning of entirely unrelated information (face recognition) that they encountered but were not necessarily curious about. People were also better able to retain the information learned during a curious state across a 24-hour delay. “Curiosity may put the brain in a state that allows it to learn and retain any kind of information, like a vortex that sucks in what you are motivated to learn, and also everything around it,” explains Dr. Gruber.

Second, the investigators found that when curiosity is stimulated, there is increased activity in the brain circuit related to reward. “We showed that intrinsic motivation actually recruits the very same brain areas that are heavily involved in tangible, extrinsic motivation,” says Dr. Gruber. This reward circuit relies on dopamine, a chemical messenger that relays messages between neurons.

Third, the team discovered that when curiosity motivated learning, there was increased activity in the hippocampus, a brain region that is important for forming new memories, as well as increased interactions between the hippocampus and the reward circuit. “So curiosity recruits the reward system, and interactions between the reward system and the hippocampus seem to put the brain in a state in which you are more likely to learn and retain information, even if that information is not of particular interest or importance,” explains principal investigator Dr. Charan Ranganath, also of UC Davis.

The findings could have implications for medicine and beyond. For example, the brain circuits that rely on dopamine tend to decline in function as people get older, or sooner in people with neurological conditions. Understanding the relationship between motivation and memory could therefore stimulate new efforts to improve memory in the healthy elderly and to develop new approaches for treating patients with disorders that affect memory. And in the classroom or workplace, learning what might be considered boring material could be enhanced if teachers or managers are able to harness the power of students’ and workers’ curiosity about something they are naturally motivated to learn.

Filed under curiosity hippocampus memory learning nucleus accumbens midbrain neuroscience science

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Researchers Identify Brain Areas Activated by Itch-Relieving Drug

Areas of the brain that respond to reward and pleasure are linked to the ability of a drug known as butorphanol to relieve itch, according to new research led by Gil Yosipovitch, MD, Professor and Chair of the Department of Dermatology at Temple University School of Medicine (TUSM), and Director of the Temple Itch Center. The findings point to the involvement of the brain’s opioid receptors—widely known for their roles in pain, reward, and addiction—in itch relief, potentially opening up new avenues to the development of treatments for chronic itch.

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The article, published online September 11, in the Journal of Investigative Dermatology, is the first to show precisely where in the brain butorphanol works to relieve itch. In identifying those areas, the study helps to explain why butorphanol works better for chronic itching mediated by histamine, a small molecule involved in allergic reactions, than for nonhistamine-related types of itch.

"The research allows us to assess butorphanol’s effects," Dr. Yosipovitch said. "We can now identify better targets in the brain that drugs can work on to relieve itch."

The research marks an important step toward the development of itch-specific agents. As Dr. Yosipovitch explained, chronic itching, which affects roughly 12 percent of the population, comprises not just one disease, but many—ranging from atopic eczema and psoriasis to systemic diseases such as lymphoma and chronic liver failure. Biochemically, each of those diseases induces itching via one of two main pathways: one that is mediated by histamine and one that is not. Most pathological itching originates along nonhistaminergic pathways.

Working with Alexandru D. P. Papoiu, MD, PhD, at Wake Forest University School of Medicine, Dr. Yosipovitch experimentally induced itch in human volunteers using either histamine or cowhage, which incites nonhistaminergic itching. Study volunteers were then treated with either butorphanol or a placebo and subjected to functional magnetic resonance imaging (fMRI) to analyze brain activity and assess the effects of butorphanol (or placebo). When volunteers returned seven days later, they received the other treatment and again underwent fMRI.

Butorphanol suppressed histamine itching in all cases and reduced cowhage itching in 35 percent of subjects. The drug’s suppression of histamine itching was associated specifically with the activation of brain areas known as the nucleus accumbens and septal nuclei—areas located deep at the base of the forebrain. The regions are notably rich in so-called kappa (κ)-opioid receptors, on which butorphanol acts. By contrast, the relief of cowhage itch by butorphanol was linked to effects in other brain areas.

The findings suggest that butorphanol works primarily on κ-opioid receptors to suppress the itch sensation induced by histamine. But the drug also has important effects on an itch pathway that does not involve histamine, where the demand for new treatments is greatest.

How nonhistaminergic itching is reduced through the involvement of opioid receptors remains unclear. Opioid receptors modulate the transmission of information about itch in the brain and occur in high levels in the areas of the brain that house neural pathways associated with reward. Reward pathways are known particularly for their response to pleasurable stimuli. Dr. Yosipovitch and Dr. Papoiu have shown in previous work that the activation of reward circuits is correlated with pleasurability and the degree of itch relief derived from self-scratching.

The new study, which Yosipovitch carried out at Wake Forest University prior to joining the TUSM faculty in 2013, further illustrates the power of applying imaging technologies to basic questions in itch research. At Temple’s Itch Center, Yosipovitch is continuing to explore those applications.

"We are in a position now to better understand the itch-scratch cycle," he said. "To break the cycle from the top down, knowing where to target receptors in the brain, would be a major achievement."

(Source: temple.edu)

Filed under nucleus accumbens opioid receptors butorphanol itching histamine neuroscience science

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Evidence Supports Deep Brain Stimulation for Obsessive-Compulsive Disorder

Available research evidence supports the use of deep brain stimulation (DBS) for patients with obsessive-compulsive disorder (OCD) who don’t respond to other treatments, concludes a review in the October issue of Neurosurgery, official journal of the Congress of Neurological Surgeons (CNS). The journal is published by Lippincott Williams & Wilkins, a part of Wolters Kluwer Health.

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Based on evidence, two specific bilateral DBS techniques are recommended for treatment of carefully selected patients with OCD, according to a new clinical practice guideline endorsed by the CNS and the American Association of Neurological Surgeons. While calling for further research in key areas, Dr. Clement Hamani of Toronto Western Hospital and coauthors emphasize that patients with OCD symptoms that don’t respond to other treatments should continue to have access to DBS.

Deep Brain Stimulation for OCD—What’s the Evidence?

Dr. Hamani led a multispecialty expert group in performing a systematic review of research on the effectiveness of DBS for OCD. Deep brain stimulation—placement of electrodes in specific areas of the brain, followed by electrical stimulation of those areas—has become an important treatment for patients with Parkinson’s disease and other movement disorders.

Although many patients with OCD respond well to medications and/or psychotherapy, 40 to 60 percent continue to experience symptoms despite treatment. Over the past decade, a growing number of reports have suggested that DBS may be an effective alternative in these “medically refractory” cases.

Dr. Hamani and colleagues were tasked with analyzing the supporting evidence and developing an initial clinical practice guideline for the use of DBS for patients with OCD. The review and guideline development process was sponsored by the American Society of Stereotactic and Functional Neurosurgery and the CNS. Out of more than 350 papers, the reviewers identified seven high-quality studies evaluating DBS for OCD.

Based on that evidence, they conclude that bilateral stimulation (on both sides of the brain) of two brain “targets”—areas called the subthalamic nucleus and the nucleus accumbens—can be regarded as effective treatments for OCD. In controlled clinical trials, both techniques improved OCD symptoms by around 30 percent on a standard rating scale.

While Research Proceeds, well-selected treatment-resistant severe OCD Patients Should Have Access to DBS

That evidence forms the basis for a clinical guideline stating that bilateral DBS is a “reasonable therapeutic option” for patients with severe OCD that does not respond to other treatments. The guideline also notes that there is “insufficient evidence” supporting the use of any type of unilateral DBS target (one side of the brain) for OCD.

The review highlights the difficulties of studying the effectiveness of DBS for OCD—because most patients respond to medical treatment, studies of this highly specialized treatment typically include only small numbers of patients. Dr. Hamani and coauthors identify some priorities for future research: particularly to identify the most effective brain targets and the subgroups of patients most likely to benefit.

Despite the limited evidence base, DBS therapy for OCD has been approved by the Food and Drug Administration under a humanitarian device exemption. Dr. Hamani and coauthors note that various safeguards are in place to ensure appropriate use, and prevent overuse, of DBS for OCD.

While research continues, they believe that functional neurosurgeons should continue to work with other specialists to ensure that patients with severe, medically refractory OCD continue to have access to potentially beneficial DBS therapy.

(Source: wolterskluwerhealth.com)

Filed under OCD deep brain stimulation nucleus accumbens DBS neuroscience science

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The Yin and Yang of Overcoming Cocaine Addiction Yaoying Ma says that biology, by nature, has a yin and a yang—a push and a pull. Addiction, particularly relapse, she finds, is no exception. Ma is a research associate in the lab of Yan Dong, assistant professor of neuroscience in the University of Pittsburgh’s Kenneth P. Dietrich School of Arts and Sciences. She is the lead author of a paper published online today in the journal Neuron that posits that it may be possible to ramp up an intrinsic anti-addiction response as a means to fight cocaine relapse and keep the wolves of relapse at bay. This paper is the first to establish the existence of a brain circuitry that resists a relapse of cocaine use through a naturally occurring neural remodeling with “silent synapses.” The work is a follow-up on a recent study conducted by Dong and his colleagues, which was published in Nature Neuroscience last November. The team used rat models to examine the effects of cocaine self-administration and withdrawal on nerve cells in the nucleus accumbens, a small region in the brain that is commonly associated with reward, emotion, motivation, and addiction. Specifically, they investigated the roles of synapses—the structures at the ends of nerve cells that relay signals. The team reported in its Nature Neuroscience study that when a rat uses cocaine, some immature synapses are generated, which are called “silent synapses” because they are semifunctional and send few signals under normal physiological conditions. After that rat stops using cocaine, these “silent synapses” go through a maturation phase and acquire their full function to send signals. Once they can send signals, the synapses will send craving signals for cocaine if the rat is exposed to cues previously associated with the drug. The current Neuron paper shows that there’s another side of “silent synapse” remodeling. Silent synapses that are generated in a specific cortical projection to the nucleus accumbens by cocaine exposure become “unsilenced” after cocaine withdrawal, resulting in a profound remodeling of this cortical projection. Additional experiments show that silent synapse-based remodeling of this cortical projection decreases cocaine craving. Importantly, this anti-relapse circuitry remodeling is induced by cocaine exposure itself, suggesting that our body has its own way to fight addiction. Dong, the paper’s senior author, says that the pro-relapse response is predominant after cocaine exposure. But since the anti-relapse response exists inside the brain, it could possibly be clinically tweaked to achieve therapeutic benefits. Ma notes that this finding “may provide insight into ways to manipulate this yin-yang balance and hopefully provide new neurobiological targets for interventions designed to decrease relapse.” “The story won’t stop here,” Ma adds. “Our ongoing study is exploring some unusual but simple ways to beef up the endogenous anti-relapse mechanism.” (Image: PA)

The Yin and Yang of Overcoming Cocaine Addiction

Yaoying Ma says that biology, by nature, has a yin and a yang—a push and a pull.

Addiction, particularly relapse, she finds, is no exception.

Ma is a research associate in the lab of Yan Dong, assistant professor of neuroscience in the University of Pittsburgh’s Kenneth P. Dietrich School of Arts and Sciences. She is the lead author of a paper published online today in the journal Neuron that posits that it may be possible to ramp up an intrinsic anti-addiction response as a means to fight cocaine relapse and keep the wolves of relapse at bay.

This paper is the first to establish the existence of a brain circuitry that resists a relapse of cocaine use through a naturally occurring neural remodeling with “silent synapses.”

The work is a follow-up on a recent study conducted by Dong and his colleagues, which was published in Nature Neuroscience last November. The team used rat models to examine the effects of cocaine self-administration and withdrawal on nerve cells in the nucleus accumbens, a small region in the brain that is commonly associated with reward, emotion, motivation, and addiction. Specifically, they investigated the roles of synapses—the structures at the ends of nerve cells that relay signals.

The team reported in its Nature Neuroscience study that when a rat uses cocaine, some immature synapses are generated, which are called “silent synapses” because they are semifunctional and send few signals under normal physiological conditions. After that rat stops using cocaine, these “silent synapses” go through a maturation phase and acquire their full function to send signals. Once they can send signals, the synapses will send craving signals for cocaine if the rat is exposed to cues previously associated with the drug.

The current Neuron paper shows that there’s another side of “silent synapse” remodeling. Silent synapses that are generated in a specific cortical projection to the nucleus accumbens by cocaine exposure become “unsilenced” after cocaine withdrawal, resulting in a profound remodeling of this cortical projection. Additional experiments show that silent synapse-based remodeling of this cortical projection decreases cocaine craving. Importantly, this anti-relapse circuitry remodeling is induced by cocaine exposure itself, suggesting that our body has its own way to fight addiction.

Dong, the paper’s senior author, says that the pro-relapse response is predominant after cocaine exposure. But since the anti-relapse response exists inside the brain, it could possibly be clinically tweaked to achieve therapeutic benefits.

Ma notes that this finding “may provide insight into ways to manipulate this yin-yang balance and hopefully provide new neurobiological targets for interventions designed to decrease relapse.”

“The story won’t stop here,” Ma adds. “Our ongoing study is exploring some unusual but simple ways to beef up the endogenous anti-relapse mechanism.”

(Image: PA)

Filed under cocaine cocaine addiction nucleus accumbens synapses neurons neuroscience science

103 notes

Brain imaging shows brain differences in risk-taking teens

According to the CDC, unintentional injuries are the leading cause of death for adolescents. Compared to the two leading causes of death for all Americans, heart disease and cancer, a pattern of questionable decision-making in dire situations comes to light in teen mortality. New research from the Center for BrainHealth at The University of Texas at Dallas investigating brain differences associated with risk-taking teens found that connections between certain brain regions are amplified in teens more prone to risk.

“Our brains have an emotional-regulation network that exists to govern emotions and influence decision-making,” explained the study’s lead author, Sam Dewitt. “Antisocial or risk-seeking behavior may be associated with an imbalance in this network.”

The study, published June 30 in Psychiatry Research: Neuroimaging, looked at 36 adolescents ages 12-17; eighteen risk-taking teens were age- and sex-matched to a group of 18 non-risk-taking teens. Participants were screened for risk-taking behaviors, such as drug and alcohol use, sexual promiscuity, and physical violence and underwent functional MRI (fMRI) scans to examine communication between brain regions associated with the emotional-regulation network. Interestingly, the risk-taking group showed significantly lower income compared to the non-risk taking group.

“Most fMRI scans used to be done in conjunction with a particular visual task. In the past several years, however, it has been shown that performing an fMRI scan of the brain during a ‘mind-wandering’ state is just as valuable,”said Sina Aslan, Ph.D., President of Advance MRI and Adjunct Assistant Professor at the Center for BrainHealth at The University of Texas at Dallas.“In this case, brain regions associated with emotion and reward centers show increased connection even when they are not explicitly engaged.”

The study, conducted by Francesca Filbey, Ph.D., Director of Cognitive Neuroscience Research of Addictive Behaviors at the Center for BrainHealth and her colleagues, shows that risk-taking teens exhibit hyperconnectivity between the amygdala, a center responsible for emotional reactivity, and specific areas of the prefrontal cortex associated with emotion regulation and critical thinking skills. The researchers also found increased activity between areas of the prefrontal cortex and the nucleus accumbens, a center for reward sensitivity that is often implicated in addiction research.

“Our findings are crucial in that they help identify potential brain biomarkers that, when taken into context with behavioral differences, may help identify which adolescents are at risk for dangerous and pathological behaviors in the future,” Dewitt explained.

He also points out that even though the risk-taking group did partake in risky behavior, none met clinical criteria for behavioral or substance use disorders.

By identifying these factors early on, the research team hopes to have a better chance of providing effective cognitive strategies to help risk-seeking adolescents regulate their emotions and avoid risk-taking behavior and substance abuse.

(Source: brainhealth.utdallas.edu)

Filed under risk-taking prefrontal cortex amygdala nucleus accumbens neuroimaging neuroscience science

313 notes

Study reveals brain mechanism behind chronic pain’s sapping of motivation

Chronic pain is among the most abundant of all medical afflictions in the developed world. It differs from a short-term episode of pain not only in its duration, but also in triggering in its sufferers a psychic exhaustion best described by the question, “Why bother?”

A new study in mice, conducted by investigators at the Stanford University School of Medicine, has identified a set of changes in key parts of the brain that may explain chronic pain’s capacity to stifle motivation. The discovery could lead to entirely new classes of treatment for this damaging psychological consequence of chronic pain.

Many tens of millions of people in the United States suffer persistent pain due to diverse problems including migraines, arthritis, lower back pain, sports injuries, irritable bowel syndrome and shingles. For many of these conditions, there are no good treatments, and a crippling loss of mojo can result.

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“With chronic pain, your whole life changes in a way that doesn’t happen with acute pain,” said Robert Malenka, MD, PhD, the Nancy Friend Pritzker Professor in Psychiatry and Behavioral Sciences and the study’s senior author. “Yet this absence of motivation caused by chronic pain, which can continue even when the pain is transiently relieved, has been largely ignored by medical science.”

A series of experiments in mice by Malenka and his colleagues, described in a study published Aug. 1 in Science, showed that persistent pain causes changes in a set of nerve cells in a deep-brain structure known to be important in reward-seeking behavior: the pursuit of goals likely to yield pleasurable results. Malenka’s lab has been studying this brain structure, the nucleus accumbens, for two decades.

“We showed that those brain changes don’t go away when you transiently relieve the mice’s pain,” Malenka said. The experiments also indicated that the mice’s diminished motivation to perform reward-generating tasks didn’t stem from their pain’s rendering them incapable of experiencing pleasure or from any accompanying physical impairment, he said.

How pain and reward interact

“This study is important — to my knowledge, the first to explain how pain and reward interact. It begins to get to an understanding of why it’s such a struggle for people undergoing chronic pain to get through the day,” said Howard Fields, MD, PhD, a professor of neurology at the University of California-San Francisco and founder of that school’s pain management center.

Fields, who did not participate in the Malenka group’s study but wrote an accompanying perspective piece published simultaneously in Science, described the psychological effect of chronic pain as “the clouding of the future. There’s no escape from it. You want it to end, but it doesn’t.” As a result, people become pessimistic and irritable, he said. “People come to expect the next day is going to wind up being painful. It just takes the edge off of life’s little pleasures — and big pleasures, for that matter.”

The experiments were spearheaded by the study’s first author, Neil Schwartz, PhD, a postdoctoral scholar in Malenka’s lab. “You can’t just ask a hungry mouse how motivated it is to pursue its heart’s desire,” Malenka said. “But there are ways of asking that mouse, ‘How hard are you willing to work for food?’”

Schwartz, Malenka and their associates looked at lab mice enduring chronic paw pain due either to persistent inflammation or to nerve damage. The mice also happened to be hungry. The scientists trained the mice to poke their noses into a hole to get a food pellet. At first, a single nose poke earned a pellet. But over time, the number of nose pokes required for a reward was increased. In essence, the researchers were asking these mice: How hard are you willing to work for food? Will you poke your nose into that hole once to satisfy your hunger? Ten times? Even 150 times?

Fading motivation

Within a week after the onset of chronic pain, the animals grew increasingly less likely to work hard for food than pain-free control animals were. The researchers next explored three possible explanations: Were the mice unable to work because their pain was too severe? Did something about being in pain cause them to not value the food reward as much? Or was their failure to seek food due simply to a lack of motivation? Additional tests showed that the mice had no movement problems. “Like other research groups, we found that they can scamper around just fine,” said Malenka. Also, when the mice were given free access to food, they ate just as much as the animals who weren’t in pain — so they still valued the food. But they were less willing to put in an effort to obtain food than mice who’d suffered no pain.

Moreover, the difference didn’t disappear even when the scientists relieved the mice’s pain with analgesics. “They were in demonstrably less pain, but they were still less willing to work,” Malenka said.

The Stanford scientists then focused on the nucleus accumbens, a brain structure known to be involved in computing the behavioral strategies that prompt us to seek or avoid things that can affect our survival. They found that chronic pain permanently changed certain connections to the nucleus accumbens, causing an enduring downshift in the excitation transmitted by them. Importantly, Malenka’s group showed that a particular brain chemical called galanin plays a critical role in this enduring suppression of nucleus accumbens excitability.

Galanin is a short signaling-protein snippet secreted by certain cells in various places in the brain. While its presence in the brain has been known for a good 60 years or so, galanin’s role is not well-defined and probably differs widely in different brain structures. There have been hints, though, that galanin activity might play a role in pain. For example, it’s been previously shown in animal models that galanin levels in the brain increase with the persistence of pain.

Possible therapies?

Schwartz, Malenka and their peers identified receptors for galanin on a set of nerve cells in the nucleus accumbens and demonstrated that disabling galanin’s signaling via this receptor prevented the long-term suppression of motivation seen in mice — and people — with chronic pain. This suggests that therapeutic compounds with similar effects could someday be developed, although they would have to be carefully targeted so as to not disrupt galanin signaling in other important brain circuits.

“There’s no reason to think this finding won’t generalize to people,” said Fields of UCSF. “Our brains have galanin, and a nucleus accumbens, just as mouse brains do. However, before jumping from mice to humans it would be wise to test other animal species. If the same things happen in a non-rodent species that happen in mice, then it’s probable they happen in humans, too.”

(Source: med.stanford.edu)

Filed under pain chronic pain motivation reward nucleus accumbens neuroscience science

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(Image caption: Whole brain functional connectivity between the nucleus accumbens (NAc) and other brain areas in response to cannabis cues (vs. neutral cues) in all participants) Dependence Alters the Brain’s Response to Pot Paraphernalia New research from The University of Texas at Dallas demonstrates that drug paraphernalia triggers the reward areas of the brain differently in dependent and non-dependent marijuana users. The study, published July 1 in Drug and Alcohol Dependence, demonstrated that different areas of the brain activated when dependent and non-dependent users were exposed to drug-related cues. The 2012 National Survey on Drug Use and Health shows marijuana is the most widely used illicit drug in the United States. According to a 2013 survey from the Pew Research Center, 48 percent of Americans ages 18 and older have tried marijuana. The National Institute on Drug Abuse says that 9 percent of daily users will become dependent on marijuana. “We know that people have a hard time staying abstinent because seeing cues for the drug use triggers this intense desire to seek out the drugs,” said Dr. Francesca Filbey, lead author of the study and professor at the Center for BrainHealth in the School of Behavioral and Brain Sciences. “That’s a clinically validated phenomenon and behavioral studies have also shown this to be the case. What we didn’t know was what was driving those effects in the brain.” To find this effect, Filbey and colleagues conducted brain-imaging scans, called functional magnetic resonance imaging (fMRI), on 71 participants who regularly used marijuana. Just more than half of those were classified as dependent users. While being scanned, the participants were given either a used marijuana pipe or a pencil of approximately the same size that they could see and feel. A comparison of the images revealed that the nucleus accumbens, the reward region in the brain, was activated in all users in response to the pipe. However, the strengths of the connections with other areas differed between dependent and non-dependent users. “We found that the reward network is actually being driven by other areas unrelated to reward, like the areas in memory and attention or emotion,” Filbey said. Non-dependent users showed greater activations in the orbital frontal cortex and hippocampus, suggesting that memory and attention were connected to the activation of the reward network. Dependent users had greater activations in the amygdala and anterior cingulate gyrus, suggesting a more emotional connection. Additionally, the areas of the brain activated resemble areas activated for other addictions, such as nicotine or cocaine, lending greater support to the addictiveness of marijuana. These findings suggest that marijuana abuse intervention needs to cater more specifically to a user’s level of addiction. "Clinicians treating people with problems with marijuana dependence should consider the different processes that trigger the reward response when determining possible pharmacological or behavioral interventions,” Filbey said.

(Image caption: Whole brain functional connectivity between the nucleus accumbens (NAc) and other brain areas in response to cannabis cues (vs. neutral cues) in all participants)

Dependence Alters the Brain’s Response to Pot Paraphernalia

New research from The University of Texas at Dallas demonstrates that drug paraphernalia triggers the reward areas of the brain differently in dependent and non-dependent marijuana users.

The study, published July 1 in Drug and Alcohol Dependence, demonstrated that different areas of the brain activated when dependent and non-dependent users were exposed to drug-related cues.

The 2012 National Survey on Drug Use and Health shows marijuana is the most widely used illicit drug in the United States. According to a 2013 survey from the Pew Research Center, 48 percent of Americans ages 18 and older have tried marijuana. The National Institute on Drug Abuse says that 9 percent of daily users will become dependent on marijuana.

“We know that people have a hard time staying abstinent because seeing cues for the drug use triggers this intense desire to seek out the drugs,” said Dr. Francesca Filbey, lead author of the study and professor at the Center for BrainHealth in the School of Behavioral and Brain Sciences. “That’s a clinically validated phenomenon and behavioral studies have also shown this to be the case. What we didn’t know was what was driving those effects in the brain.”

To find this effect, Filbey and colleagues conducted brain-imaging scans, called functional magnetic resonance imaging (fMRI), on 71 participants who regularly used marijuana. Just more than half of those were classified as dependent users. While being scanned, the participants were given either a used marijuana pipe or a pencil of approximately the same size that they could see and feel.

A comparison of the images revealed that the nucleus accumbens, the reward region in the brain, was activated in all users in response to the pipe. However, the strengths of the connections with other areas differed between dependent and non-dependent users.

“We found that the reward network is actually being driven by other areas unrelated to reward, like the areas in memory and attention or emotion,” Filbey said.

Non-dependent users showed greater activations in the orbital frontal cortex and hippocampus, suggesting that memory and attention were connected to the activation of the reward network. Dependent users had greater activations in the amygdala and anterior cingulate gyrus, suggesting a more emotional connection.

Additionally, the areas of the brain activated resemble areas activated for other addictions, such as nicotine or cocaine, lending greater support to the addictiveness of marijuana.

These findings suggest that marijuana abuse intervention needs to cater more specifically to a user’s level of addiction.

"Clinicians treating people with problems with marijuana dependence should consider the different processes that trigger the reward response when determining possible pharmacological or behavioral interventions,” Filbey said.

Filed under paraphernalia marijuana reward system neuroimaging nucleus accumbens brain activity neuroscience science

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Bad learning University of Iowa researchers have discovered a new form of neurotransmission that influences the long-lasting memory created by addictive drugs, like cocaine and opioids, and the subsequent craving for these drugs of abuse. Loss of this type of neurotransmission creates changes in brains cells that resemble the changes caused by drug addiction. The findings, published June 22 in the journal Nature Neuroscience, suggest that targeting this type of neurotransmission might lead to new therapies for treating drug addiction. “Molecular therapies for drug addiction are pretty much non-existent,” says Collin Kreple, UI graduate student and co-first author of the study. “I think this finding at least provides the possibility of a new molecular target.” The new form of neurotransmission involves proteins called acid-sensing ion channels (ASICs), which have previously been shown to promote learning and memory, and which are abundant in a part of the brain that is involved in drug addiction. The researchers, led by John Wemmie, professor of psychiatry in the UI Carver College of Medicine, reasoned that disrupting ASIC activity in this brain region (the nucleus accumbens) should reduce learned addiction-related behaviors. However, their experiments showed that loss of ASIC signaling actually increases learned drug-seeking in mice. When mice learned to associate one side of a chamber with receiving cocaine, animals that lacked the ASIC protein developed an even stronger preference for the “cocaine side” than control mice, suggesting that loss of ASIC had increased addiction behavior. The same result was seen for morphine, another drug of abuse, which has a different mechanism of action than cocaine. "Always before, the data suggested that when you get rid of ASICs, learning and memory are impaired," Wemmie says. "So we expected the same trend when we studied reward-related learning and behavior and we were surprised to find the opposite." In a second experiment, rats learned to press a lever to self-administer cocaine. Blocking or removing ASIC in the rat brains caused the animals to self-administer more cocaine than control animals. Conversely, increasing the amount of ASIC by over-expressing the protein seemed to decrease the animals’ craving for cocaine. "There are many forms of addiction," says Wemmie, who also holds appointments in the UI Departments of Molecular Physiology and Biophysics and Neurosurgery, and with the Iowa City VA Medical Center. "We’d like to see if these mechanisms also apply to other addictions besides cocaine and morphine. And, we want to move forward to see if this pathway can be used to target addiction." Novel neurotransmission As the name suggests, acid-sensing ion channels are activated by acid, in the form of protons. This research and a second UI study recently published in PNAS show that protons and ASICs form a previously unrecognized neurotransmitter pair that helps neurons communicate in a novel way; and appear to influence several forms of learning and memory, including fear, as well as addiction. Manipulating the activity of ASICs or the level of protons (acidity) may provide a new way to treat addiction. "We are still a long way from using these findings to create a therapy," notes Yuan Lu, co-first author and UI postdoctoral scholar. "The key significance of this study is that we have found new, different targets [that might allow us to inhibit the addiction behavior].” Drugs change the brain Previous research has shown that drug abuse and addiction physically alter the connections between neurons (synapses) that are important for the creation and storage of memories. Although normal learning requires synapses to be dynamic and plastic, exposure to addictive drugs abnormally increases synaptic plasticity in a way that is thought to underlie drug-related learning and addiction behaviors. The UI study found that absence of ASIC-proton mediated neurotransmission also increased synaptic plasticity in a way that resembled the changes created by addiction and drug withdrawal. "It seemed like everything we looked at (physiology and structural changes) really paralleled what you would see in an animal undergoing drug withdrawal, even though these animals missing ASIC had never been exposed to drugs," Kreple says. Overall the study findings suggest that ASIC-related neurotransmission in the nucleus accumbens may play a role in reducing synaptic plasticity and appropriately stabilizing synapses.

Bad learning

University of Iowa researchers have discovered a new form of neurotransmission that influences the long-lasting memory created by addictive drugs, like cocaine and opioids, and the subsequent craving for these drugs of abuse. Loss of this type of neurotransmission creates changes in brains cells that resemble the changes caused by drug addiction.

The findings, published June 22 in the journal Nature Neuroscience, suggest that targeting this type of neurotransmission might lead to new therapies for treating drug addiction.

“Molecular therapies for drug addiction are pretty much non-existent,” says Collin Kreple, UI graduate student and co-first author of the study. “I think this finding at least provides the possibility of a new molecular target.”

The new form of neurotransmission involves proteins called acid-sensing ion channels (ASICs), which have previously been shown to promote learning and memory, and which are abundant in a part of the brain that is involved in drug addiction. The researchers, led by John Wemmie, professor of psychiatry in the UI Carver College of Medicine, reasoned that disrupting ASIC activity in this brain region (the nucleus accumbens) should reduce learned addiction-related behaviors. However, their experiments showed that loss of ASIC signaling actually increases learned drug-seeking in mice.

When mice learned to associate one side of a chamber with receiving cocaine, animals that lacked the ASIC protein developed an even stronger preference for the “cocaine side” than control mice, suggesting that loss of ASIC had increased addiction behavior. The same result was seen for morphine, another drug of abuse, which has a different mechanism of action than cocaine.

"Always before, the data suggested that when you get rid of ASICs, learning and memory are impaired," Wemmie says. "So we expected the same trend when we studied reward-related learning and behavior and we were surprised to find the opposite."

In a second experiment, rats learned to press a lever to self-administer cocaine. Blocking or removing ASIC in the rat brains caused the animals to self-administer more cocaine than control animals. Conversely, increasing the amount of ASIC by over-expressing the protein seemed to decrease the animals’ craving for cocaine.

"There are many forms of addiction," says Wemmie, who also holds appointments in the UI Departments of Molecular Physiology and Biophysics and Neurosurgery, and with the Iowa City VA Medical Center. "We’d like to see if these mechanisms also apply to other addictions besides cocaine and morphine. And, we want to move forward to see if this pathway can be used to target addiction."

Novel neurotransmission

As the name suggests, acid-sensing ion channels are activated by acid, in the form of protons. This research and a second UI study recently published in PNAS show that protons and ASICs form a previously unrecognized neurotransmitter pair that helps neurons communicate in a novel way; and appear to influence several forms of learning and memory, including fear, as well as addiction.

Manipulating the activity of ASICs or the level of protons (acidity) may provide a new way to treat addiction.

"We are still a long way from using these findings to create a therapy," notes Yuan Lu, co-first author and UI postdoctoral scholar. "The key significance of this study is that we have found new, different targets [that might allow us to inhibit the addiction behavior].”

Drugs change the brain

Previous research has shown that drug abuse and addiction physically alter the connections between neurons (synapses) that are important for the creation and storage of memories. Although normal learning requires synapses to be dynamic and plastic, exposure to addictive drugs abnormally increases synaptic plasticity in a way that is thought to underlie drug-related learning and addiction behaviors. The UI study found that absence of ASIC-proton mediated neurotransmission also increased synaptic plasticity in a way that resembled the changes created by addiction and drug withdrawal.

"It seemed like everything we looked at (physiology and structural changes) really paralleled what you would see in an animal undergoing drug withdrawal, even though these animals missing ASIC had never been exposed to drugs," Kreple says.

Overall the study findings suggest that ASIC-related neurotransmission in the nucleus accumbens may play a role in reducing synaptic plasticity and appropriately stabilizing synapses.

Filed under drug addiction neurotransmission nucleus accumbens ion channels cocaine synaptic plasticity neuroscience science

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Individual Brain Activity Predicts Tendency to Succumb to Daily Temptations

Activity in areas of the brain related to reward and self-control may offer neural markers that predict whether people are likely to resist or give in to temptations, like food, in daily life, according to research in Psychological Science, a journal of the Association for Psychological Science.

image

“Most people have difficulty resisting temptation at least occasionally, even if what tempts them differs,” say psychological scientists Rich Lopez and Todd Heatherton of Dartmouth College, authors on the study. “The overarching motivation of our work is to understand why some people are more likely to experience this self-regulation failure than others.”

The research findings reveal that activity in reward areas of the brain in response to pictures of appetizing food predicts whether people tend to give in to food cravings and desires in real life, whereas activity in prefrontal areas during taxing self-control tasks predicts their ability to resist tempting food.

Lopez and colleagues used functional MRI (fMRI) to explore the interplay between activity in prefrontal brain regions associated with self-control (e.g., inferior frontal gyrus) and subcortical areas involved in affect and reward (e.g., nucleus accumbens), and to see whether the interplay between these regions predicts how successful (or unsuccessful) people are in controlling their desires to eat on a daily basis.

The researchers recruited 31 female participants to take part in an initial fMRI scanning session that included two important tasks.

For the first task, the participants were presented with various images, including some of high-calorie foods, like dessert items, fast-food items, and snacks. The participants were simply asked to indicate whether each image was set indoors or outdoors — the researchers were specifically interested in measuring activity in the nucleus accumbens in response to the food-related images.

For the second task, the participants were asked to press or not press a button based on the specific cues provided with each image, a task designed to gauge self-control ability. During this task, the researchers measured activity in the inferior frontal gyrus (IFG).

The fMRI scanning session was followed by 1 week of so-called “experience sampling,” in which participants were signaled several times a day on a smartphone and asked to report their food desires and eating behaviors. Any time participants reported a food desire, they were then asked about the strength of the desire and their resistance to it. If they ultimately gave in to the craving, they were asked to say how much they had eaten.

As expected, participants who had relatively higher activity in the nucleus accumbens in response to the food images tended to experience more intense food desires. More importantly, they were also more likely to give in to their food cravings and eat the desired food.

The researchers were surprised by how robust this association was:

“Reward-related brain activity, which can be considered an implicit measure, predicted who gave in to temptations to eat, as well as who ate more, above and beyond the desire strength reported by participants in the moment,” say Lopez and Heatherton. “This could help to explain a previous finding from our lab that people who show this kind of brain activity the most are also the most likely to gain weight over six months.”

But brain activity also predicted who was more likely to be able to resist temptation: Participants who showed relatively higher IFG activity on the self-control task acted on their cravings less often.

When the researchers grouped the participants according to their IFG activity, the data revealed that participants who had high IFG activity were more successful at controlling how much they ate in particularly tempting situations than those who had low IFG activity. In fact, participants with low IFG activity were about 8.2 times more likely to give in to a food desire than those who had high IFG activity.

“Taken together, the results from the present study provide initial evidence for neural markers of everyday eating behaviors that can identify individuals who are more likely than others to give in to temptations to eat,” the researchers write.

Lopez, Heatherton, and colleagues are currently conducting studies focused on groups of people who are especially prone to self-regulation failure: chronic dieters.

They’re investigating, for example, how dieters’ brains respond to food cues after they’ve exhausted their self-control resources. The researchers hypothesize that depleting self-control may heighten reward-related brain activity, effectively “turning up the volume on temptations,” and predicting behaviors like overeating in daily life.

“Failures of self-control contribute to nearly half of all death in the United States each year,” the researchers note. “Our findings and future research may ultimately help people learn ways to resist their temptations.”

Filed under brain activity self-control nucleus accumbens neuroimaging psychology neuroscience science

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