Posts tagged reward system
Articles and news from the latest research reports.
New insights could boost treatment for P addiction
A Kiwi researcher’s discovery of new ways methamphetamine can alter the brain could help the development of new drug-based therapies for addiction treatment.
In 2009, New Zealand had one of the highest rates of P users in the world, and today, more than 25,000 Kiwis were estimated to still be using the drug.
Now, new research by a Victoria of University of Wellington graduate has provided valuable insights into how the brain’s natural reward pathways are strongly stimulated following exposure to methamphetamine.
Music can be soothing or stirring, it can make us dance or make us sad. Blood pressure, heartbeat, respiration and even body temperature – music affects the body in a variety of ways. It triggers especially powerful physical reactions in pregnant women. Scientists at the Max Planck Institute for Human Cognitive and Brain Sciences in Leipzig have discovered that pregnant women compared to their non-pregnant counterparts rate music as more intensely pleasant and unpleasant, associated with greater changes in blood pressure. Music appears to have an especially strong influence on pregnant women, a fact that may relate to a prenatal conditioning of the fetus to music.
For their study, the Max Planck researchers played short musical sequences of 10 or 30 seconds’ duration to female volunteers. They changed the passages and played them backwards or incorporated dissonances. By doing so, they distorted the originally lively instrumental pieces and made listening to them less pleasant.
The pregnant women rated the pieces of music slightly differently, they perceived the pleasant music as more pleasant and the unpleasant as more unpleasant. The blood pressure response to music was much stronger in the pregnant group. Forward-dissonant music produced a particularly pronounced fall in blood pressure, whereas backwards-dissonant music led to a higher blood pressure after 10 seconds and a lower one after 30 seconds. “Thus, unpleasant music does not cause an across-the-board increase in blood pressure, unlike some other stress factors”, says Tom Fritz of the Max Planck Institute in Leipzig. “Instead, the body’s response is just as dynamic as the music itself.”
According to the results, music is a very special stimulus for pregnant women, to which they react strongly. “Every acoustic manipulation of music affects blood pressure in pregnant women far more intensely than in non-pregnant women”, says Fritz. Why music has such a strong physiological influence on pregnant woman is still unknown. Originally, the scientists suspected the hormone oestrogen to play a mayor part in this process, because it has an influence on the brain’s reward system, which is responsible for the pleasant sensations experienced while listening to music. However, non-pregnant women showed constant physiological responses throughout the contraceptive cycle, which made them subject to fluctuations in oestrogen levels. “Either oestrogen levels are generally too low in non-pregnant women, or other physiological changes during pregnancy are responsible for this effect”, explains Fritz.
The researchers suspect that foetuses are conditioned to music perception while still in the womb by the observed intense physiological music responses of the mothers. From 28 weeks, i.e. at the start of the third trimester of pregnancy, the heart rate of the foetus already changes when it hears a familiar song. From 35 weeks, there is even a change in its movement patterns.
(Image caption: A cross-section of mouse brain in the nucleus accumbens, a region of the brain known to be involved in reward and motivation, taken by a fluorescence microscope. Blue corresponds to cell nuclei, and green to fluorescence emitted by a green-fluorescent protein (NdT: the original incorrectly states “green fluorescente protein”) that identifies neurons having received the virus that can genetically abolish the expression of lipoprotein lipase protein. Credit: ©Serge Luquet, CNRS/Université Paris Diderot)
Obesity: are lipids hard drugs for the brain?
Why can we get up for a piece of chocolate, but never because we fancy a carrot? Serge Luquet’s team at the “Biologie Fonctionnelle et Adaptative” laboratory (CNRS/Université Paris Diderot) has demonstrated part of the answer: triglycerides, fatty substances from food, may act in our brains directly on the reward circuit, the same circuit that is involved in drug addiction. These results, published on April 15, 2014 in Molecular Psychiatry, show a strong link in mice between fluctuations in triglyceride concentration and brain reward development. Identifying the action of nutritional lipids on motivation and the search for pleasure in dietary intake will help us better understand the causes of some compulsive behaviors and obesity.
Though the act of eating responds to a biological need, it is also an essential cultural and social function in our modern societies. Meals are generally associated with a strong notion of pleasure, a feeling that pushes us towards food. Sometimes this is dangerous: 2.8 million people worldwide die from the consequences of obesity each year. Fundamentally, obesity is caused by imbalance between calories consumed and expended. A sedentary life combined with an abundance of sugary, fatty foods provides fertile ground for this disease.
The body uses sugars and fats as energy sources. The brain only consumes glucose. So why do we find an enzyme that can decompose triglycerides, lipids that come in particular from food, at its core, at the heart of the reward mechanism? A team at the “Biologie Fonctionnelle et Adaptative” laboratory (CNRS/Université Paris Diderot) led by Serge Luquet, a CNRS researcher, has tackled this fundamental question.
If they have the choice, normal behavior in mice is to prefer a high-fat diet to simpler foods. To simulate the action of a good meal, researchers have developed an approach that allows small quantities of lipids to be injected directly into the brains of mice. They observed that an infusion of triglycerides in the brain reduces the animal’s motivation to press a lever to obtain a food reward. It also reduces physical activity by half. What is more, an “infused” mouse balances its diet between the two food sources offered (high-fat foods and simpler foods).
To ensure that it is indeed the lipids injected that change the mice’s behavior, these Parisian scientists made sure that the lipids could not be detected by the animal’s brain any longer. They managed to remove the specific enzyme for triglycerides by silencing its coding gene, but only at the heart of the reward mechanism. The animal then shows increased motivation to obtain a reward, and if given the choice, consumes much richer food than average. This work echoes the previous work by their colleagues: reducing this enzyme in the hippocampus causes obesity.
Paradoxically, with obesity, blood (and therefore brain) triglyceride levels are higher than average. So obesity is often associated with overconsumption of sugary, fatty foods. The researchers explain this: with long-lasting high exposure to triglycerides, mice always display lower locomotor activity. By contrast, food rewards are still attractive! The ideal conditions for weight gain are therefore in place. At high triglyceride contents, the brain adapts to obtain its reward, similar to the mechanisms observed when people consume drugs.
This work, financed in particular by CNRS and ANR, indicate for the first time that triglycerides from food may act as hard drugs in the brain, on the reward system, controlling the motivational and pleasureseeking component of food intake.
The Social Circuits that Track How We Like People and Ideas
Whether at the office, dorm, PTA meeting, or any other social setting, we all know intuitively who the popular people are – who is most liked – even if we can’t always put our finger on why. That information is often critical to professional or social success as you navigate your social networks. Yet until now, scientists have not understood how our brains recognize these popular people. In new work, researchers say that we track people’s popularity largely through the brain region involved in anticipating rewards.
“Being able to track other people’s status in your group is incredibly important in survival terms,” says Kevin Ochsner of Columbia University. “Knowing who is popular or likeable is critically important in times of need or distress, when you seek an alliance, or need help – whether physical or political – etc.” While sociologists, psychologists, and anthropologists have long studied these group dynamics, neuroscientists have only begun to scratch the surface of how we think about people’s social status.
That is all changing, though, Ochsner says with many areas of work bringing together social psychology and sociology with cognitive neuroscience to better understand how individual brain processes connect to group membership. As will be presented today at the annual meeting of the Cognitive Neuroscience Society (CNS) in Boston, researchers are now studying at the neural level everything from social popularity to how ideas successfully spread in groups.
(Source: cogneurosociety.org)
Meditation helps pinpoint neurological differences between two types of love
These findings won’t appear on any Hallmark card, but romantic love tends to activate the same reward areas of the brain as cocaine, research has shown.
Now Yale School of Medicine researchers studying meditators have found that a more selfless variety of love — a deep and genuine wish for the happiness of others without expectation of reward — actually turns off the same reward areas that light up when lovers see each other.
“When we truly, selflessly wish for the well-being of others, we’re not getting that same rush of excitement that comes with, say, a tweet from our romantic love interest, because it’s not about us at all,” said Judson Brewer, adjunct professor of psychiatry at Yale now at the University of Massachusetts.
Brewer and Kathleen Garrison, postdoctoral researcher in Yale’s Department of Psychiatry, report their findings in a paper scheduled to be published online Feb. 12 in the journal Brain and Behavior.
The neurological boundaries between these two types of love become clear in fMRI scans of experienced meditators. The reward centers of the brain that are strongly activated by a lover’s face (or a picture of cocaine) are almost completely turned off when a meditator is instructed to silently repeat sayings such as “May all beings be happy.”
Such mindfulness meditations are a staple of Buddhism and are now commonly practiced in Western stress reduction programs, Brewer notes. The tranquility of this selfless love for others — exemplified in such religious figures such as Mother Theresa or the Dalai Llama — is diametrically opposed to the anxiety caused by a lovers’ quarrel or extended separation. And it carries its own rewards.
“The intent of this practice is to specifically foster selfless love — just putting it out there and not looking for or wanting anything in return,” Brewer said. “If you’re wondering where the reward is in being selfless, just reflect on how it feels when you see people out there helping others, or even when you hold the door for somebody the next time you are at Starbucks.”
Happiness lowers blood pressure
A synthetic gene module controlled by the happiness hormone dopamine produces an agent that lowers blood pressure. This opens up new avenues for therapies that are remote-controlled via the subsconscious.
The endogenous hormone dopamine triggers feelings of happiness. While its release is induced, among other things, by the “feel-good” classics sex, drugs or food, the brain does not content itself with a kick; it remembers the state of happiness and keeps wanting to achieve it again. Dopamine enables us to make the “right” decisions in order to experience even more moments of happiness.
Biological components reconnected
Now a team of researchers headed by ETH-Zurich professor Martin Fussenegger from the Department of Biosystems Science and Engineering (D-BSSE) in Basel has discovered a way to use the body’s dopamine system therapeutically. The researchers have created a new genetic module that can be controlled via dopamine. The feel-good messenger molecule activates the module depending on the dosage. In response to an increase in the dopamine level in the blood, the module produces the desired active agent.
The module consists of several biological components of the human organism, which are interconnected to form a synthetic signalling cascade. Dopamine receptors are found at the beginning of the cascade as sensors. A particular agent is produced as an end product: either a model protein called SEAP or ANP, a powerful vasodilator lowering blood pressure. The researchers placed these signal cascades in human cells, so-called HEK cells, around 100,000 of which were in turn inserted into capsules. These were then implanted in the abdomens of mice.
Contact with females activates module
These animals were subsequently exposed to situations that corresponded to their central reward system, such as sexual arousal, which a female mouse triggered in males, the injection of the drug methamphetamine or the drinking of golden syrup. In each case, the mouse brain responded with a “state of happiness”, the formation of dopamine and its release into the blood via the peripheral nervous system. In mice which received different concentrations of golden syrup, the “state of happiness” varied: the more the sugar was diluted, the smaller the amount of dopamine and thus the active agent that circulated in the blood. “This shows that dopamine does not merely switch our module on and off, but also that it responds based on the concentration of the happiness hormone,” says Fussenegger.
In another step, the scientists linked the dopamine sensor module to the production of the antihypertensive agent ANP and implanted the customised cells in the abdomens of hypertensive male mice. Contact with a female mouse triggered such feelings of happiness in the males that the dopamine-induced ANP production corrected the hypertension and the blood pressure even reached a normal level.
Serum dopamine linked to brain
Based on their experiments, the researchers were also able to demonstrate that dopamine is not only formed in the brain in corresponding feel-good situations, but also in nerves in the vegetative system, the so-called sympathetic nervous system, which are closely knit around blood vessels. The brain is interlinked with the rest of the body via the sympathetic nervous system, despite the fact that the brain is unable to release “its” dopamine directly into the circulation due to the blood-brain barrier. Dopamine receptors have also been known to exist in body tissue such as the kidneys, adrenalin glands or on blood vessels, as well as in the brain.
Dopamine, which circulates in the blood serum, regulates the breathing and the blood sugar balance. For a long time, it was thus assumed that the activities of brain and serum dopamine were connected. The fact that the ETH-Zurich researchers in Basel have now managed to demonstrate this connection deepens our understanding of the body’s reward system.
Eating as therapeutic input
Martin Fussenegger says that eating, for instance, can be seen as therapeutic input thanks to this module. “Using the gene network, we link up with the normal reward system,” he explains. Good food triggers feelings of happiness, which activate the module and intervene in a process that is normally only controlled by the subconscious. As a result, daily activities could be used for therapeutic interventions.
For the time being, however, the dopamine hypertension model is only a prototype. With their work, the scientists have proved that they can intervene in the body’s reward system as a result. Nonetheless, it is more than merely an idea or experiment in living cells. “It works in a mouse model that simulates a human disease and the components we used to produce the module also came from humans.” When and whether a treatment based on the happiness hormone will hit the market, however, remains uncertain. The development of prototypes into a marketable product takes years or even decades.
Further reading
Rössger K, Charpin-El-Hamri G & Fussenegger M. Reward-based hypertension control by a synthetic brain-dopamine interface. PNAS Early Edition, online 14th Oct. 2013.
Addiction: Can You Ever Really Completely Leave It Behind?
A new study in Biological Psychiatry suggests the answer is no
It is often said that once people develop an addiction, they can never completely eliminate their attraction to the abused substance. New findings provide further support for this notion by suggesting that even long-term abstinence from cocaine does not result in a complete normalization of brain circuitry.
Scientists are currently trying to answer some of the ‘chicken and egg’ questions surrounding the abuse of drugs. In particular, one of those questions is whether individuals who abuse psychostimulants like cocaine are more impulsive and show alterations in brain reward circuits as a consequence of using the drug, or whether such abnormalities existed prior to their drug use. In the former case, one might expect brain alterations to normalize following prolonged drug abstinence.
To address these questions, Krishna Patel at Institute of Living/Hartford Hospital and colleagues compared neural responses between three groups of people who were asked to complete a task that resembles bidding on eBay items. The 3 groups consisted of 47 healthy controls, 42 currently drug-abusing cocaine users, and 35 former cocaine users who had been abstinent an average of 4 years. They also compared all three groups on their levels of impulsivity and reward responding.
They found that active users showed abnormal activation in multiple brain regions involved with reward processing, and that the abstinent individuals who were previously cocaine dependent manifested differences in a subset of those regions. Both current and former cocaine users displayed similarly elevated impulsivity measures compared to healthy controls, which may indicate that these individuals had a pre-existing risk for addiction. Indeed, the degree of impulsivity correlated with several of the brain activation abnormalities.
These findings suggest that prolonged abstinence from cocaine may normalize only a subset of the brain abnormalities associated with active drug use.
"The knowledge that some neural changes associated with addiction persist despite long periods of abstinence is important because it supports clinical wisdom that recovery from addiction is a lifelong process," says Dr. John Krystal, Editor of Biological Psychiatry. "Further, it is the start of a deeper question: How do these persisting changes develop and how can they be reversed?"
The authors agree that further studies will be needed to investigate such questions, including the continued attempt to determine the extent to which differences in former cocaine users reflect aspects of pre-existing features, exposure to cocaine, or recovery.
(Image: Shutterstock)
'Love hormone' may play wider role in social interaction than previously thought
Researchers at the Stanford University School of Medicine have shown that oxytocin — often referred to as “the love hormone” because of its importance in the formation and maintenance of strong mother-child and sexual attachments — is involved in a broader range of social interactions than previously understood.
The discovery may have implications for neurological disorders such as autism, as well as for scientific conceptions of our evolutionary heritage.
Scientists estimate that the advent of social living preceded the emergence of pair living by 35 million years. The new study suggests that oxytocin’s role in one-on-one bonding probably evolved from an existing, broader affinity for group living.
Oxytocin is the focus of intense scrutiny for its apparent roles in establishing trust between people, and has been administered to children with autism spectrum disorders in clinical trials. The new study, published Sept. 12 in Nature, pinpoints a unique way in which oxytocin alters activity in a part of the brain that is crucial to experiencing the pleasant sensation neuroscientists call “reward.” The findings not only provide validity for ongoing trials of oxytocin in autistic patients, but also suggest possible new treatments for neuropsychiatric conditions in which social activity is impaired.
"People with autism-spectrum disorders may not experience the normal reward the rest of us all get from being with our friends," said Robert Malenka, MD, PhD, the study’s senior author. "For them, social interactions can be downright painful. So we asked, what in the brain makes you enjoy hanging out with your buddies?"
Some genetic evidence suggests the awkward social interaction that is a hallmark of autism-spectrum disorders may be at least in part oxytocin-related. Certain variations in the gene that encodes the oxytocin receptor — a cell-surface protein that senses the substance’s presence — are associated with increased autism risk.
Malenka, the Nancy Friend Pritzker Professor in Psychiatry and Behavioral Sciences, has spent the better part of two decades studying the reward system — a network of interconnected brain regions responsible for our sensation of pleasure in response to a variety of activities such as finding or eating food when we’re hungry, sleeping when we’re tired, having sex or acquiring a mate, or, in a pathological twist, taking addictive drugs. The reward system has evolved to reinforce behaviors that promote our survival, he said.
For this study, Malenka and lead author Gül Dölen, MD, PhD, a postdoctoral scholar in his group with over 10 years of autism-research expertise, teamed up to untangle the complicated neurophysiological underpinnings of oxytocin’s role in social interactions. They focused on biochemical events taking place in a brain region called the nucleus accumbens, known for its centrality to the reward system.
In the 1970s, biologists learned that in prairie voles, which mate for life, the nucleus accumbens is replete with oxytocin receptors. Disrupting the binding of oxytocin to these receptors impaired prairie voles’ monogamous behavior. In many other species that are not monogamous by nature, such as mountain voles and common mice, the nucleus accumbens appeared to lack those receptors.
"From this observation sprang a dogma that pair bonding is a special type of social behavior tied to the presence of oxytocin receptors in the nucleus accumbens. But what’s driving the more common group behaviors that all mammals engage in — cooperation, altruism or just playing around — remained mysterious, since these oxytocin receptors were supposedly absent in the nucleus accumbens of most social animals," said Dölen.
The new discovery shows that mice do indeed have oxytocin receptors at a key location in the nucleus accumbens and, importantly, that blocking oxytocin’s activity there significantly diminishes these animals’ appetite for socializing. Dölen, Malenka and their Stanford colleagues also identified, for the first time, the nerve tract that secretes oxytocin in the region, and they pinpointed the effects of oxytocin release on other nerve tracts projecting to this area.
Mice can squeak, but they can’t talk, Malenka noted. “You can’t ask a mouse, ‘Hey, did hanging out with your buddies a while ago make you happier?’” So, to explore the social-interaction effects of oxytocin activity in the nucleus accumbens, the investigators used a standard measure called the conditioned place preference test.
"It’s very simple," Malenka said. "You like to hang out in places where you had fun, and avoid places where you didn’t. We give the mice a ‘house’ made of two rooms separated by a door they can walk through at any time. But first, we let them spend 24 hours in one room with their littermates, followed by 24 hours in the other room all by themselves. On the third day we put the two rooms together to make the house, give them complete freedom to go back and forth through the door and log the amount of time they spend in each room."
Mice normally prefer to spend time in the room that reminds them of the good times they enjoyed in the company of their buddies. But that preference vanished when oxytocin activity in their nucleus accumbens was blocked. Interestingly, only social activity appeared to be affected. There was no difference, for example, in the mice’s general propensity to move around. And when the researchers trained the mice to prefer one room over the other by giving them cocaine (which mice love) only when they went into one room, blocking oxytocin activity didn’t stop the mice from picking the cocaine den.
In an extensive series of sophisticated, highly technical experiments, Dölen, Malenka and their teammates located the oxytocin receptors in the murine nucleus accumbens. These receptors lie not on nucleus accumbens nerve cells that carry signals forward to numerous other reward-system nodes but, instead, at the tips of nerve cells forming a tract from a brain region called the dorsal Raphe, which projects to the nucleus accumbens. The dorsal Raphe secretes another important substance, serotonin, triggering changes in nucleus accumbens activity. In fact, popular antidepressants such as Prozac, Paxil and Zoloft belong to a class of drugs called serotonin-reuptake inhibitors that increase available amounts of serotonin in brain regions, including the nucleus accumbens.
As the Stanford team found, oxytocin acting at the nucleus accumbens wasn’t simply squirted into general circulation, as hormones typically are, but was secreted at this spot by another nerve tract originating in the hypothalamus, a multifunction midbrain structure. Oxytocin released by this tract binds to receptors on the dorsal Raphe projections to the nucleus accumbens, in turn liberating serotonin in this key node of the brain’s reward circuitry. The serotonin causes changes in the activity of yet other nerve tracts terminating at the nucleus accumbens, ultimately resulting in altered nucleus accumbens activity — and a happy feeling.
"There are at least 14 different subtypes of serotonin receptor," said Dölen. "We’ve identified one in particular as being important for social reward. Drugs that selectively act on this receptor aren’t clinically available yet, but our study may encourage researchers to start looking at drugs that target it for the treatment of diseases such as autism, where social interactions are impaired."
Malenka and Dölen said they think their findings in mice are highly likely to generalize to humans because the brain’s reward circuitry has been so carefully conserved over the course of hundreds of millions of years of evolution. This extensive cross-species similarity probably stems from pleasure’s absolutely essential role in reinforcing behavior likely to boost an individual’s chance of survival and procreation.
(Source: med.stanford.edu)
Alcoholism Could Be Linked to a Hyper-Active Brain Dopamine System
Those vulnerable to alcoholism may experience an unusually large response in the brain’s reward-seeking pathway when they take a drink
Research from McGill University suggests that people who are vulnerable to developing alcoholism exhibit a distinctive brain response when drinking alcohol, according to a new study by Prof. Marco Leyton, of McGill University’s Department of Psychiatry. Compared to people at low risk for alcohol-use problems, those at high risk showed a greater dopamine response in a brain pathway that increases desire for rewards. These findings, published in the journal Alcoholism: Clinical & Experimental Research, could help shed light on why some people are more at risk of suffering from alcoholism and could mark an important step toward the development of treatment options.
“There is accumulating evidence that there are multiple pathways to alcoholism, each associated with a distinct set of personality traits and neurobiological features”, said Prof. Leyton, a researcher in the Mental Illness and Addiction axis at the Research Institute of the McGill University Health Centre (RI-MUHC). “These individual differences likely influence a wide range of behaviors, both positive and problematic. Our study suggests that a tendency to experience a large dopamine response when drinking alcohol might contribute to one (or more) of these pathways.”
For the study, researchers recruited 26 healthy social drinkers (18 men, 8 women), 18 to 30 years of age, from the Montreal area. The higher-risk subjects were then identified based on personality traits and having a lower intoxication response to alcohol (they did not feel as drunk despite having drunk the same amount). Finally, each participant underwent two positron emission tomography (PET) brain scan exams after drinking either juice or alcohol (about 3 drinks in 15 minutes).
“We found that people vulnerable to developing alcoholism experienced an unusually large brain dopamine response when they took a drink,” said Leyton. “This large response might energize reward-seeking behaviors and counteract the sedative effects of alcohol. Conversely, people who experience minimal dopamine release when they drink might find the sedative effects of alcohol especially pronounced.”
“Although preliminary, the results are compelling,” said Dr. Leyton. “A much larger body of research has identified a role for dopamine in reward-seeking behaviors in general. For example, in both laboratory animals and people, increased dopamine transmission seems to enhance the attractiveness of reward-related stimuli. This effect likely contributes to why having one drink increases the probability of getting a second one – the alcohol-induced dopamine response makes the second drink look all the more desirable. If some people are experiencing unusually large dopamine responses to alcohol, this might put them at risk.”
“People with loved ones struggling with alcoholism often want to know two things: How did they develop this problem? And what can be done to help? Our study helps us answer the first question by furthering our understanding of the causes of addictions. This is an important step toward developing treatments and preventing the disorder in others.”
(Source: newswise.com)
Extroverts have more sensitive brain-reward system
Extroverts may be more outgoing and cheerful in part because of their brain chemistry, reports a study by Cornell neuroscientists.
People’s brains respond differently to rewards, say the neuroscientists. Some people’s brains release more of the neurotransmitter dopamine, which ultimately gives them more reasons to be excited and engaged with the world, says Richard Depue, professor of human development in the College of Human Ecology, who co-authored the study with graduate student Yu Fu.
Their study, published in Frontiers in Human Neuroscience in June, sheds new light on how differences in the way the brain responds to reward translate into extraverted behavior, the authors say.
“Rewards like food, sex and social interactions as well as more abstract goals such as money or getting a degree trigger the release of dopamine in the brain, producing positive emotions and feelings of desire that motivate us to work toward obtaining those goals. In extroverts, this dopamine response to rewards is more robust so they experience more frequent activation of strong positive emotions,” Depue says.
“Dopamine also facilitates memory for circumstances that are associated with the reward. Our findings suggest this plays a significant role in sustaining extroverted behavior,” Depue adds. “The extroverts in our study showed greater association of context with reward than introverts, which means that over time, extroverts will acquire a more extensive network of reward-context memories that activate their brain’s reward system.”
Over a week, the researchers engaged 70 young adult males – a mix of introverts and extroverts according to a standard personality test – in a set of laboratory tasks that included viewing brief video clips of several aspects of the lab environment. On the first four days, some participants received a low dose of the stimulant methylphenidate (MP), also known as Ritalin, which triggers the release of dopamine in the brain; the others received either a placebo or MP in a different lab location. The team tested how strongly participants associated contextual cues in the lab (presented in video clips) with reward (the dopamine rush induced by MP) by assessing changes in their working memory, motor speed at a finger-tapping task and positive emotions (all known to be influenced by dopamine).
Participants who had unconsciously associated contextual cues in the lab with the reward were expected to have greater dopamine release/reward system activation on day 4 compared with day 1 when shown the same video clips. This so-called “associative conditioning” response is exactly what the team found in the extroverts. The extroverts strongly associated the lab context with reward feelings, whereas the introverts showed little to no evidence of associative conditioning.
“At a broader level, the study begins to illuminate how individual differences in brain functioning interact with environmental influences to create behavioral variation. This knowledge may someday help us to understand how such interactions create more extreme forms of emotional behavior, such as personality disorders,” says Depue.