#nucleusaccumbens — Public Fediverse posts
Live and recent posts from across the Fediverse tagged #nucleusaccumbens, aggregated by home.social.
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DATE: September 30, 2026 at 09:00AM
SOURCE: PSYPOST.ORG** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
-------------------------------------------------TITLE: Weight-loss drug semaglutide alters reward-seeking behavior in healthy mice
URL: https://www.psypost.org/weight-loss-drug-semaglutide-alters-reward-seeking-behavior-in-healthy-mice/
A new small study in healthy mice reveals that the popular weight-loss drug semaglutide alters behavior and brain activity related to reward and stress. Researchers found that daily doses of the drug changed how animals pursued natural rewards and reacted to stressful situations, while also shifting electrical patterns in a central reward circuit. The findings were published in the journal Molecular Brain.
Semaglutide is a medication widely used to treat diabetes and obesity. The medication is frequently recognized by brand names such as Ozempic and Wegovy. It mimics a naturally occurring hormone called GLP-1, which regulates appetite and blood sugar. Recently, scientists have begun exploring whether the drug might also treat addiction by dampening the brain’s response to cravings.
Most prior research has focused on animal models with obesity or diabetes. To understand the drug’s baseline effects on a typical nervous system, researchers Alejo Mosqueira, Sanaz Ansarifar, and their colleagues at Aarhus University investigated how semaglutide impacts the behavior and brain waves of healthy mice. The research team specifically looked at the nucleus accumbens, a region deep in the brain that plays a primary role in processing motivation, pleasure, and reward.
The researchers first designed a behavioral experiment using healthy adult male mice. They divided the animals into two main treatment groups to test different dosing schedules. One group received a weekly injection of semaglutide for eight weeks, which mirrors how the drug is prescribed to human patients. The second group received daily injections to account for the faster metabolism of mice and to observe any short-term behavioral changes.
Following the injection periods, the researchers ran the mice through a battery of tests designed to measure movement, anxiety, and reward-seeking habits. They monitored the animals’ food intake, water consumption, and body weight throughout the process to track general physiological health. Both the daily and weekly groups experienced substantial weight loss, alongside noticeable reductions in eating and drinking. The researchers ran statistical analyses to confirm that the weight loss itself was not responsible for the altered behavior.
When assessing behavior, the researchers found changes exclusively in the daily injection group. In an open field test used to measure general movement and anxiety, the daily-dosed mice displayed an increase in jumping against the walls of the testing box. The researchers interpret this as an increased attempt to escape the enclosure. In a separate marble burying test used to measure repetitive actions, the differences between the treated and untreated mice were not statistically significant.
The team also used a nestlet shredding test, providing the mice with a cotton nesting material to see how much they would tear it apart. Mice given daily semaglutide shredded far less of the material than the control group. This reduction suggests a shift in how the animals explore their environment or a potential increase in underlying anxiety.
To evaluate reward-seeking behavior without relying on food, the researchers used a scent-based test. Healthy male mice naturally seek out the smell of female mouse urine, which acts as a rewarding social cue. The semaglutide-treated mice spent much less time sniffing the female urine than the untreated mice. This drop in interest indicates a suppression of natural reward-seeking drives.
Finally, the researchers placed the mice in small containers of water for a forced swimming test, which is commonly used to measure stress coping and depressive-like states. Mice treated with daily semaglutide spent less time floating motionless and more time actively swimming compared to the control group. This behavior often suggests improved stress resilience or an antidepressant-like effect.
In a separate experiment, Mosqueira and Ansarifar’s team examined how a single dose of semaglutide affects neural activity. They anesthetized a small group of healthy mice and inserted microscopic electrodes into the nucleus accumbens. The researchers recorded the animals’ baseline brain waves for 30 minutes, injected the drug, and then recorded for another hour.
The researchers focused on local field potentials, which are the collective electrical signals generated by large groups of neurons firing together. They analyzed different speeds of brain waves, breaking the signals down into slower rhythms known as delta, theta, and alpha waves. These specific wave patterns are heavily involved in how the brain anticipates and responds to rewards, making them a useful target for understanding motivation.
Following the semaglutide injection, the rhythmic electrical activity in the nucleus accumbens shifted. The dominant frequencies of the delta, theta, and alpha waves became slightly faster. At the same time, the physical strength or amplitude of these slow waves decreased. The researchers note that a reduction in delta and theta wave strength aligns with a dampened reward anticipation system.
The study relies on a relatively small number of animals, and the behavioral changes only appeared under the daily dosing schedule. The weekly injection group lost weight but did not exhibit the same behavioral shifts. This discrepancy suggests that the frequency of the dose heavily influences the behavioral outcomes in healthy animals.
The brain wave recordings took place while the mice were under anesthesia, which fundamentally alters normal electrical activity in the brain. The behavioral tests, conversely, involved awake animals taking the drug over multiple days. Because of these differing conditions, the electrical changes cannot be directly linked to the behavioral shifts.
Future research will need to record brain activity in awake, freely moving animals over longer periods. Measuring these electrical signals while mice are actively making choices could clarify exactly how semaglutide changes motivation. Testing different dosages may also help determine whether these effects apply broadly across different treatment regimens.
The study, “Semaglutide alters behaviour and nucleus accumbens oscillatory activity in healthy mice,” was authored by Alejo Mosqueira, Sanaz Ansarifar, Sadegh Nabavi, and Andrea Moreno.
URL: https://www.psypost.org/weight-loss-drug-semaglutide-alters-reward-seeking-behavior-in-healthy-mice/
-------------------------------------------------
Private, vetted email list for mental health professionals: https://www.clinicians-exchange.org
Unofficial Psychology Today Xitter to toot feed at Psych Today Unofficial Bot @PTUnofficialBot
-------------------------------------------------
#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #Semaglutide #WeightLossDrug #NucleusAccumbens #RewardSeeking #BrainOscillations #GLP1 #MiceStudy # addons: Avoid "add-ons" — just hashtags. #OpenFieldTest #StressResilience #Dopamine #BehavioralScience #Nutrition #ObesityTreatment #Ozempic Wegovy
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DATE: September 30, 2026 at 09:00AM
SOURCE: PSYPOST.ORG** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
-------------------------------------------------TITLE: Weight-loss drug semaglutide alters reward-seeking behavior in healthy mice
URL: https://www.psypost.org/weight-loss-drug-semaglutide-alters-reward-seeking-behavior-in-healthy-mice/
A new small study in healthy mice reveals that the popular weight-loss drug semaglutide alters behavior and brain activity related to reward and stress. Researchers found that daily doses of the drug changed how animals pursued natural rewards and reacted to stressful situations, while also shifting electrical patterns in a central reward circuit. The findings were published in the journal Molecular Brain.
Semaglutide is a medication widely used to treat diabetes and obesity. The medication is frequently recognized by brand names such as Ozempic and Wegovy. It mimics a naturally occurring hormone called GLP-1, which regulates appetite and blood sugar. Recently, scientists have begun exploring whether the drug might also treat addiction by dampening the brain’s response to cravings.
Most prior research has focused on animal models with obesity or diabetes. To understand the drug’s baseline effects on a typical nervous system, researchers Alejo Mosqueira, Sanaz Ansarifar, and their colleagues at Aarhus University investigated how semaglutide impacts the behavior and brain waves of healthy mice. The research team specifically looked at the nucleus accumbens, a region deep in the brain that plays a primary role in processing motivation, pleasure, and reward.
The researchers first designed a behavioral experiment using healthy adult male mice. They divided the animals into two main treatment groups to test different dosing schedules. One group received a weekly injection of semaglutide for eight weeks, which mirrors how the drug is prescribed to human patients. The second group received daily injections to account for the faster metabolism of mice and to observe any short-term behavioral changes.
Following the injection periods, the researchers ran the mice through a battery of tests designed to measure movement, anxiety, and reward-seeking habits. They monitored the animals’ food intake, water consumption, and body weight throughout the process to track general physiological health. Both the daily and weekly groups experienced substantial weight loss, alongside noticeable reductions in eating and drinking. The researchers ran statistical analyses to confirm that the weight loss itself was not responsible for the altered behavior.
When assessing behavior, the researchers found changes exclusively in the daily injection group. In an open field test used to measure general movement and anxiety, the daily-dosed mice displayed an increase in jumping against the walls of the testing box. The researchers interpret this as an increased attempt to escape the enclosure. In a separate marble burying test used to measure repetitive actions, the differences between the treated and untreated mice were not statistically significant.
The team also used a nestlet shredding test, providing the mice with a cotton nesting material to see how much they would tear it apart. Mice given daily semaglutide shredded far less of the material than the control group. This reduction suggests a shift in how the animals explore their environment or a potential increase in underlying anxiety.
To evaluate reward-seeking behavior without relying on food, the researchers used a scent-based test. Healthy male mice naturally seek out the smell of female mouse urine, which acts as a rewarding social cue. The semaglutide-treated mice spent much less time sniffing the female urine than the untreated mice. This drop in interest indicates a suppression of natural reward-seeking drives.
Finally, the researchers placed the mice in small containers of water for a forced swimming test, which is commonly used to measure stress coping and depressive-like states. Mice treated with daily semaglutide spent less time floating motionless and more time actively swimming compared to the control group. This behavior often suggests improved stress resilience or an antidepressant-like effect.
In a separate experiment, Mosqueira and Ansarifar’s team examined how a single dose of semaglutide affects neural activity. They anesthetized a small group of healthy mice and inserted microscopic electrodes into the nucleus accumbens. The researchers recorded the animals’ baseline brain waves for 30 minutes, injected the drug, and then recorded for another hour.
The researchers focused on local field potentials, which are the collective electrical signals generated by large groups of neurons firing together. They analyzed different speeds of brain waves, breaking the signals down into slower rhythms known as delta, theta, and alpha waves. These specific wave patterns are heavily involved in how the brain anticipates and responds to rewards, making them a useful target for understanding motivation.
Following the semaglutide injection, the rhythmic electrical activity in the nucleus accumbens shifted. The dominant frequencies of the delta, theta, and alpha waves became slightly faster. At the same time, the physical strength or amplitude of these slow waves decreased. The researchers note that a reduction in delta and theta wave strength aligns with a dampened reward anticipation system.
The study relies on a relatively small number of animals, and the behavioral changes only appeared under the daily dosing schedule. The weekly injection group lost weight but did not exhibit the same behavioral shifts. This discrepancy suggests that the frequency of the dose heavily influences the behavioral outcomes in healthy animals.
The brain wave recordings took place while the mice were under anesthesia, which fundamentally alters normal electrical activity in the brain. The behavioral tests, conversely, involved awake animals taking the drug over multiple days. Because of these differing conditions, the electrical changes cannot be directly linked to the behavioral shifts.
Future research will need to record brain activity in awake, freely moving animals over longer periods. Measuring these electrical signals while mice are actively making choices could clarify exactly how semaglutide changes motivation. Testing different dosages may also help determine whether these effects apply broadly across different treatment regimens.
The study, “Semaglutide alters behaviour and nucleus accumbens oscillatory activity in healthy mice,” was authored by Alejo Mosqueira, Sanaz Ansarifar, Sadegh Nabavi, and Andrea Moreno.
URL: https://www.psypost.org/weight-loss-drug-semaglutide-alters-reward-seeking-behavior-in-healthy-mice/
-------------------------------------------------
Private, vetted email list for mental health professionals: https://www.clinicians-exchange.org
Unofficial Psychology Today Xitter to toot feed at Psych Today Unofficial Bot @PTUnofficialBot
-------------------------------------------------
#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #Semaglutide #WeightLossDrug #NucleusAccumbens #RewardSeeking #BrainOscillations #GLP1 #MiceStudy # addons: Avoid "add-ons" — just hashtags. #OpenFieldTest #StressResilience #Dopamine #BehavioralScience #Nutrition #ObesityTreatment #Ozempic Wegovy
-
DATE: September 30, 2026 at 09:00AM
SOURCE: PSYPOST.ORG** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
-------------------------------------------------TITLE: Weight-loss drug semaglutide alters reward-seeking behavior in healthy mice
URL: https://www.psypost.org/weight-loss-drug-semaglutide-alters-reward-seeking-behavior-in-healthy-mice/
A new small study in healthy mice reveals that the popular weight-loss drug semaglutide alters behavior and brain activity related to reward and stress. Researchers found that daily doses of the drug changed how animals pursued natural rewards and reacted to stressful situations, while also shifting electrical patterns in a central reward circuit. The findings were published in the journal Molecular Brain.
Semaglutide is a medication widely used to treat diabetes and obesity. The medication is frequently recognized by brand names such as Ozempic and Wegovy. It mimics a naturally occurring hormone called GLP-1, which regulates appetite and blood sugar. Recently, scientists have begun exploring whether the drug might also treat addiction by dampening the brain’s response to cravings.
Most prior research has focused on animal models with obesity or diabetes. To understand the drug’s baseline effects on a typical nervous system, researchers Alejo Mosqueira, Sanaz Ansarifar, and their colleagues at Aarhus University investigated how semaglutide impacts the behavior and brain waves of healthy mice. The research team specifically looked at the nucleus accumbens, a region deep in the brain that plays a primary role in processing motivation, pleasure, and reward.
The researchers first designed a behavioral experiment using healthy adult male mice. They divided the animals into two main treatment groups to test different dosing schedules. One group received a weekly injection of semaglutide for eight weeks, which mirrors how the drug is prescribed to human patients. The second group received daily injections to account for the faster metabolism of mice and to observe any short-term behavioral changes.
Following the injection periods, the researchers ran the mice through a battery of tests designed to measure movement, anxiety, and reward-seeking habits. They monitored the animals’ food intake, water consumption, and body weight throughout the process to track general physiological health. Both the daily and weekly groups experienced substantial weight loss, alongside noticeable reductions in eating and drinking. The researchers ran statistical analyses to confirm that the weight loss itself was not responsible for the altered behavior.
When assessing behavior, the researchers found changes exclusively in the daily injection group. In an open field test used to measure general movement and anxiety, the daily-dosed mice displayed an increase in jumping against the walls of the testing box. The researchers interpret this as an increased attempt to escape the enclosure. In a separate marble burying test used to measure repetitive actions, the differences between the treated and untreated mice were not statistically significant.
The team also used a nestlet shredding test, providing the mice with a cotton nesting material to see how much they would tear it apart. Mice given daily semaglutide shredded far less of the material than the control group. This reduction suggests a shift in how the animals explore their environment or a potential increase in underlying anxiety.
To evaluate reward-seeking behavior without relying on food, the researchers used a scent-based test. Healthy male mice naturally seek out the smell of female mouse urine, which acts as a rewarding social cue. The semaglutide-treated mice spent much less time sniffing the female urine than the untreated mice. This drop in interest indicates a suppression of natural reward-seeking drives.
Finally, the researchers placed the mice in small containers of water for a forced swimming test, which is commonly used to measure stress coping and depressive-like states. Mice treated with daily semaglutide spent less time floating motionless and more time actively swimming compared to the control group. This behavior often suggests improved stress resilience or an antidepressant-like effect.
In a separate experiment, Mosqueira and Ansarifar’s team examined how a single dose of semaglutide affects neural activity. They anesthetized a small group of healthy mice and inserted microscopic electrodes into the nucleus accumbens. The researchers recorded the animals’ baseline brain waves for 30 minutes, injected the drug, and then recorded for another hour.
The researchers focused on local field potentials, which are the collective electrical signals generated by large groups of neurons firing together. They analyzed different speeds of brain waves, breaking the signals down into slower rhythms known as delta, theta, and alpha waves. These specific wave patterns are heavily involved in how the brain anticipates and responds to rewards, making them a useful target for understanding motivation.
Following the semaglutide injection, the rhythmic electrical activity in the nucleus accumbens shifted. The dominant frequencies of the delta, theta, and alpha waves became slightly faster. At the same time, the physical strength or amplitude of these slow waves decreased. The researchers note that a reduction in delta and theta wave strength aligns with a dampened reward anticipation system.
The study relies on a relatively small number of animals, and the behavioral changes only appeared under the daily dosing schedule. The weekly injection group lost weight but did not exhibit the same behavioral shifts. This discrepancy suggests that the frequency of the dose heavily influences the behavioral outcomes in healthy animals.
The brain wave recordings took place while the mice were under anesthesia, which fundamentally alters normal electrical activity in the brain. The behavioral tests, conversely, involved awake animals taking the drug over multiple days. Because of these differing conditions, the electrical changes cannot be directly linked to the behavioral shifts.
Future research will need to record brain activity in awake, freely moving animals over longer periods. Measuring these electrical signals while mice are actively making choices could clarify exactly how semaglutide changes motivation. Testing different dosages may also help determine whether these effects apply broadly across different treatment regimens.
The study, “Semaglutide alters behaviour and nucleus accumbens oscillatory activity in healthy mice,” was authored by Alejo Mosqueira, Sanaz Ansarifar, Sadegh Nabavi, and Andrea Moreno.
URL: https://www.psypost.org/weight-loss-drug-semaglutide-alters-reward-seeking-behavior-in-healthy-mice/
-------------------------------------------------
Private, vetted email list for mental health professionals: https://www.clinicians-exchange.org
Unofficial Psychology Today Xitter to toot feed at Psych Today Unofficial Bot @PTUnofficialBot
-------------------------------------------------
#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #Semaglutide #WeightLossDrug #NucleusAccumbens #RewardSeeking #BrainOscillations #GLP1 #MiceStudy # addons: Avoid "add-ons" — just hashtags. #OpenFieldTest #StressResilience #Dopamine #BehavioralScience #Nutrition #ObesityTreatment #Ozempic Wegovy
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DATE: September 24, 2026 at 02:00PM
SOURCE: PSYPOST.ORG** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
-------------------------------------------------TITLE: New study reveals that fluctuating—not just intense—brain signals play a hidden role in overeating
URL: https://www.psypost.org/fluctuating-brain-signals-linked-to-higher-body-weight-and-erratic-eating/
A recent study found that people with higher body mass index and tendencies toward disinhibited eating experience more fluctuating brain responses to food rewards. The findings, published in Translational Psychiatry, suggest that inconsistent reward signals in the brain may play a role in overweight and overeating. Meanwhile, individuals with binge eating disorder showed specific inconsistencies in how much they consciously desired food from moment to moment.
Binge eating disorder involves recurrent episodes of eating large quantities of food while experiencing a loss of control. People with this condition frequently experience high rates of overweight and obesity. Previous research into eating disorders has primarily focused on the average strength of brain signals when people encounter food cues.
One major psychological theory suggests that repeated exposure to highly rewarding foods sensitizes the brain’s motivational pathways. Over time, this sensitization could cause food cues to trigger heightened arousal and cravings. However, hunger and satiety naturally fluctuate.
If eating for pleasure repeatedly overrides the body’s natural fullness signals, a person’s response to food might become highly variable rather than uniformly strong. Instead of just looking at average brain activity, researchers suspected that fluctuations in these signals from moment to moment might better explain erratic eating patterns. To test this idea, cognitive neuroscientist Nils B. Kroemer, psychology researcher Mechteld M. van den Hoek Ostende, and their colleagues at the University of Tübingen in Germany investigated whether variability in reward processing is higher in people with binge eating disorder.
The researchers focused on the nucleus accumbens, a region deep in the brain that plays a central role in processing rewards, anticipating pleasure, and driving motivation. They also looked at the dorsolateral prefrontal cortex, a brain area involved in cognitive control, impulse regulation, and weighing the costs and benefits of a potential action.
The researchers recruited 79 women for the study. The sample included 35 participants diagnosed with binge eating disorder, 21 with subsyndromal binge eating disorder who experienced less frequent episodes, and 23 control participants with no history of binge eating. The groups were matched so that their average body mass index was similar, allowing the researchers to separate the effects of the eating disorder from the effects of body weight.
During the first session, participants completed a behavioral experiment called a grip force effort allocation task. They were asked to squeeze a specialized handgrip device to earn either monetary rewards or small snack foods. The researchers calibrated the task to each person’s maximum grip strength.
This calibration ensured that the relative effort required was identical for everyone, regardless of their baseline physical fitness. In some trials, the required effort was explicitly shown on a screen, making the physical cost obvious. In other trials, the difficulty was hidden to create uncertainty.
After each round, participants rated how much they subjectively wanted the reward and how much effort they felt they had exerted. The points earned during the task were later exchanged for actual cash or snack calories. This allowed the researchers to quantify the physical effort participants would exert for a specific prize.
The researchers found that participants with binge eating disorder showed higher variability in their trial-by-trial ratings of wanting food. Their conscious desire for the food fluctuated widely from one moment to the next, especially during the uncertain trials. This high variability in subjective desire was not seen when they played for money.
However, their actual physical effort to obtain the rewards did not vary in the same way. The researchers noted that this disconnect might mean people with binge eating disorder rely more on external cues or habitual responses to decide how much effort to expend. This could cause their physical behavior to remain steady even while their internal feelings of desire fluctuate.
For the second phase of the study, 59 of the women returned to the laboratory after an overnight fast. They completed a similar version of the handgrip task while lying inside a functional magnetic resonance imaging scanner. This machine tracks blood flow in the brain, providing an indirect measure of neural activity in real time.
The researchers specifically measured the brain’s activity during the anticipation phase, which occurred exactly when the participants first saw the reward cue but before they started squeezing the handgrip. They calculated how much the neural signals in the nucleus accumbens and the dorsolateral prefrontal cortex fluctuated across the trials.
Trial-by-trial fluctuations in the nucleus accumbens were positively associated with a higher body mass index. Across all groups, participants with higher body weight exhibited more variable reward signals in this brain region. Participants who reported higher levels of disinhibited eating on a standard eating behavior questionnaire also displayed greater variability in the nucleus accumbens.
The researchers found a similar pattern in the dorsolateral prefrontal cortex. A higher body mass index was linked to more fluctuating activity in this cognitive control region. To ensure these fluctuations were not just random brain noise, the researchers checked control regions in the temporal lobe that are not involved in reward processing.
Those control regions did not show the same variability, indicating the effect was specific to the reward and control centers. The results for binge eating disorder specifically were less definitive. While participants with the disorder showed slightly elevated variability in the nucleus accumbens compared to the control group, the evidence was not statistically significant.
The highly variable brain responses were more closely tied to overall body weight and a general tendency to eat without restraint, rather than a clinical diagnosis of the eating disorder. The study’s design includes several limitations that affect how the results can be applied. The research only included female participants, meaning the observed patterns might not generalize to men.
Sex hormones can influence eating behaviors and reward processing, which the study could not account for. The laboratory setting also tightly controlled when participants ate and minimized changes in their mood. Real-world binge eating episodes are often triggered by shifting emotional states and metabolic changes, which the sterile experimental environment was designed to eliminate.
Additionally, the researchers did not measure actual food consumption during the experiment. The study measured the willingness to work for food and the brain’s anticipation of it, rather than how much participants actually ate. Future studies tracking daily food intake would be needed to link these fluctuating brain signals directly to binge eating episodes.
Finally, slight head movements inside a brain scanner can sometimes look like variable neural activity. People with higher body weight sometimes move slightly more in scanners. While the researchers used mathematical models to correct for head movement, imaging experts often view residual motion artifacts as a potential complication in imaging research.
The study, “Obesity is associated with greater variability of reward signals in the nucleus accumbens,” was authored by Mechteld M. van den Hoek Ostende, Anne Kühnel, Monja P. Neuser, Thomas Dresler, Jennifer Svaldi, and Nils B. Kroemer.
URL: https://www.psypost.org/fluctuating-brain-signals-linked-to-higher-body-weight-and-erratic-eating/
-------------------------------------------------
Private, vetted email list for mental health professionals: https://www.clinicians-exchange.org
Unofficial Psychology Today Xitter to toot feed at Psych Today Unofficial Bot @PTUnofficialBot
-------------------------------------------------
#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #Overeating #BingeEatingDisorder #RewardSignals #NucleusAccumbens #DLPFC #BrainVariability #FoodCues #ObesityResearch #EatingBehavior #TranslationalPsychiatry
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DATE: September 24, 2026 at 02:00PM
SOURCE: PSYPOST.ORG** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
-------------------------------------------------TITLE: New study reveals that fluctuating—not just intense—brain signals play a hidden role in overeating
URL: https://www.psypost.org/fluctuating-brain-signals-linked-to-higher-body-weight-and-erratic-eating/
A recent study found that people with higher body mass index and tendencies toward disinhibited eating experience more fluctuating brain responses to food rewards. The findings, published in Translational Psychiatry, suggest that inconsistent reward signals in the brain may play a role in overweight and overeating. Meanwhile, individuals with binge eating disorder showed specific inconsistencies in how much they consciously desired food from moment to moment.
Binge eating disorder involves recurrent episodes of eating large quantities of food while experiencing a loss of control. People with this condition frequently experience high rates of overweight and obesity. Previous research into eating disorders has primarily focused on the average strength of brain signals when people encounter food cues.
One major psychological theory suggests that repeated exposure to highly rewarding foods sensitizes the brain’s motivational pathways. Over time, this sensitization could cause food cues to trigger heightened arousal and cravings. However, hunger and satiety naturally fluctuate.
If eating for pleasure repeatedly overrides the body’s natural fullness signals, a person’s response to food might become highly variable rather than uniformly strong. Instead of just looking at average brain activity, researchers suspected that fluctuations in these signals from moment to moment might better explain erratic eating patterns. To test this idea, cognitive neuroscientist Nils B. Kroemer, psychology researcher Mechteld M. van den Hoek Ostende, and their colleagues at the University of Tübingen in Germany investigated whether variability in reward processing is higher in people with binge eating disorder.
The researchers focused on the nucleus accumbens, a region deep in the brain that plays a central role in processing rewards, anticipating pleasure, and driving motivation. They also looked at the dorsolateral prefrontal cortex, a brain area involved in cognitive control, impulse regulation, and weighing the costs and benefits of a potential action.
The researchers recruited 79 women for the study. The sample included 35 participants diagnosed with binge eating disorder, 21 with subsyndromal binge eating disorder who experienced less frequent episodes, and 23 control participants with no history of binge eating. The groups were matched so that their average body mass index was similar, allowing the researchers to separate the effects of the eating disorder from the effects of body weight.
During the first session, participants completed a behavioral experiment called a grip force effort allocation task. They were asked to squeeze a specialized handgrip device to earn either monetary rewards or small snack foods. The researchers calibrated the task to each person’s maximum grip strength.
This calibration ensured that the relative effort required was identical for everyone, regardless of their baseline physical fitness. In some trials, the required effort was explicitly shown on a screen, making the physical cost obvious. In other trials, the difficulty was hidden to create uncertainty.
After each round, participants rated how much they subjectively wanted the reward and how much effort they felt they had exerted. The points earned during the task were later exchanged for actual cash or snack calories. This allowed the researchers to quantify the physical effort participants would exert for a specific prize.
The researchers found that participants with binge eating disorder showed higher variability in their trial-by-trial ratings of wanting food. Their conscious desire for the food fluctuated widely from one moment to the next, especially during the uncertain trials. This high variability in subjective desire was not seen when they played for money.
However, their actual physical effort to obtain the rewards did not vary in the same way. The researchers noted that this disconnect might mean people with binge eating disorder rely more on external cues or habitual responses to decide how much effort to expend. This could cause their physical behavior to remain steady even while their internal feelings of desire fluctuate.
For the second phase of the study, 59 of the women returned to the laboratory after an overnight fast. They completed a similar version of the handgrip task while lying inside a functional magnetic resonance imaging scanner. This machine tracks blood flow in the brain, providing an indirect measure of neural activity in real time.
The researchers specifically measured the brain’s activity during the anticipation phase, which occurred exactly when the participants first saw the reward cue but before they started squeezing the handgrip. They calculated how much the neural signals in the nucleus accumbens and the dorsolateral prefrontal cortex fluctuated across the trials.
Trial-by-trial fluctuations in the nucleus accumbens were positively associated with a higher body mass index. Across all groups, participants with higher body weight exhibited more variable reward signals in this brain region. Participants who reported higher levels of disinhibited eating on a standard eating behavior questionnaire also displayed greater variability in the nucleus accumbens.
The researchers found a similar pattern in the dorsolateral prefrontal cortex. A higher body mass index was linked to more fluctuating activity in this cognitive control region. To ensure these fluctuations were not just random brain noise, the researchers checked control regions in the temporal lobe that are not involved in reward processing.
Those control regions did not show the same variability, indicating the effect was specific to the reward and control centers. The results for binge eating disorder specifically were less definitive. While participants with the disorder showed slightly elevated variability in the nucleus accumbens compared to the control group, the evidence was not statistically significant.
The highly variable brain responses were more closely tied to overall body weight and a general tendency to eat without restraint, rather than a clinical diagnosis of the eating disorder. The study’s design includes several limitations that affect how the results can be applied. The research only included female participants, meaning the observed patterns might not generalize to men.
Sex hormones can influence eating behaviors and reward processing, which the study could not account for. The laboratory setting also tightly controlled when participants ate and minimized changes in their mood. Real-world binge eating episodes are often triggered by shifting emotional states and metabolic changes, which the sterile experimental environment was designed to eliminate.
Additionally, the researchers did not measure actual food consumption during the experiment. The study measured the willingness to work for food and the brain’s anticipation of it, rather than how much participants actually ate. Future studies tracking daily food intake would be needed to link these fluctuating brain signals directly to binge eating episodes.
Finally, slight head movements inside a brain scanner can sometimes look like variable neural activity. People with higher body weight sometimes move slightly more in scanners. While the researchers used mathematical models to correct for head movement, imaging experts often view residual motion artifacts as a potential complication in imaging research.
The study, “Obesity is associated with greater variability of reward signals in the nucleus accumbens,” was authored by Mechteld M. van den Hoek Ostende, Anne Kühnel, Monja P. Neuser, Thomas Dresler, Jennifer Svaldi, and Nils B. Kroemer.
URL: https://www.psypost.org/fluctuating-brain-signals-linked-to-higher-body-weight-and-erratic-eating/
-------------------------------------------------
Private, vetted email list for mental health professionals: https://www.clinicians-exchange.org
Unofficial Psychology Today Xitter to toot feed at Psych Today Unofficial Bot @PTUnofficialBot
-------------------------------------------------
#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #Overeating #BingeEatingDisorder #RewardSignals #NucleusAccumbens #DLPFC #BrainVariability #FoodCues #ObesityResearch #EatingBehavior #TranslationalPsychiatry
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DATE: September 24, 2026 at 02:00PM
SOURCE: PSYPOST.ORG** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
-------------------------------------------------TITLE: New study reveals that fluctuating—not just intense—brain signals play a hidden role in overeating
URL: https://www.psypost.org/fluctuating-brain-signals-linked-to-higher-body-weight-and-erratic-eating/
A recent study found that people with higher body mass index and tendencies toward disinhibited eating experience more fluctuating brain responses to food rewards. The findings, published in Translational Psychiatry, suggest that inconsistent reward signals in the brain may play a role in overweight and overeating. Meanwhile, individuals with binge eating disorder showed specific inconsistencies in how much they consciously desired food from moment to moment.
Binge eating disorder involves recurrent episodes of eating large quantities of food while experiencing a loss of control. People with this condition frequently experience high rates of overweight and obesity. Previous research into eating disorders has primarily focused on the average strength of brain signals when people encounter food cues.
One major psychological theory suggests that repeated exposure to highly rewarding foods sensitizes the brain’s motivational pathways. Over time, this sensitization could cause food cues to trigger heightened arousal and cravings. However, hunger and satiety naturally fluctuate.
If eating for pleasure repeatedly overrides the body’s natural fullness signals, a person’s response to food might become highly variable rather than uniformly strong. Instead of just looking at average brain activity, researchers suspected that fluctuations in these signals from moment to moment might better explain erratic eating patterns. To test this idea, cognitive neuroscientist Nils B. Kroemer, psychology researcher Mechteld M. van den Hoek Ostende, and their colleagues at the University of Tübingen in Germany investigated whether variability in reward processing is higher in people with binge eating disorder.
The researchers focused on the nucleus accumbens, a region deep in the brain that plays a central role in processing rewards, anticipating pleasure, and driving motivation. They also looked at the dorsolateral prefrontal cortex, a brain area involved in cognitive control, impulse regulation, and weighing the costs and benefits of a potential action.
The researchers recruited 79 women for the study. The sample included 35 participants diagnosed with binge eating disorder, 21 with subsyndromal binge eating disorder who experienced less frequent episodes, and 23 control participants with no history of binge eating. The groups were matched so that their average body mass index was similar, allowing the researchers to separate the effects of the eating disorder from the effects of body weight.
During the first session, participants completed a behavioral experiment called a grip force effort allocation task. They were asked to squeeze a specialized handgrip device to earn either monetary rewards or small snack foods. The researchers calibrated the task to each person’s maximum grip strength.
This calibration ensured that the relative effort required was identical for everyone, regardless of their baseline physical fitness. In some trials, the required effort was explicitly shown on a screen, making the physical cost obvious. In other trials, the difficulty was hidden to create uncertainty.
After each round, participants rated how much they subjectively wanted the reward and how much effort they felt they had exerted. The points earned during the task were later exchanged for actual cash or snack calories. This allowed the researchers to quantify the physical effort participants would exert for a specific prize.
The researchers found that participants with binge eating disorder showed higher variability in their trial-by-trial ratings of wanting food. Their conscious desire for the food fluctuated widely from one moment to the next, especially during the uncertain trials. This high variability in subjective desire was not seen when they played for money.
However, their actual physical effort to obtain the rewards did not vary in the same way. The researchers noted that this disconnect might mean people with binge eating disorder rely more on external cues or habitual responses to decide how much effort to expend. This could cause their physical behavior to remain steady even while their internal feelings of desire fluctuate.
For the second phase of the study, 59 of the women returned to the laboratory after an overnight fast. They completed a similar version of the handgrip task while lying inside a functional magnetic resonance imaging scanner. This machine tracks blood flow in the brain, providing an indirect measure of neural activity in real time.
The researchers specifically measured the brain’s activity during the anticipation phase, which occurred exactly when the participants first saw the reward cue but before they started squeezing the handgrip. They calculated how much the neural signals in the nucleus accumbens and the dorsolateral prefrontal cortex fluctuated across the trials.
Trial-by-trial fluctuations in the nucleus accumbens were positively associated with a higher body mass index. Across all groups, participants with higher body weight exhibited more variable reward signals in this brain region. Participants who reported higher levels of disinhibited eating on a standard eating behavior questionnaire also displayed greater variability in the nucleus accumbens.
The researchers found a similar pattern in the dorsolateral prefrontal cortex. A higher body mass index was linked to more fluctuating activity in this cognitive control region. To ensure these fluctuations were not just random brain noise, the researchers checked control regions in the temporal lobe that are not involved in reward processing.
Those control regions did not show the same variability, indicating the effect was specific to the reward and control centers. The results for binge eating disorder specifically were less definitive. While participants with the disorder showed slightly elevated variability in the nucleus accumbens compared to the control group, the evidence was not statistically significant.
The highly variable brain responses were more closely tied to overall body weight and a general tendency to eat without restraint, rather than a clinical diagnosis of the eating disorder. The study’s design includes several limitations that affect how the results can be applied. The research only included female participants, meaning the observed patterns might not generalize to men.
Sex hormones can influence eating behaviors and reward processing, which the study could not account for. The laboratory setting also tightly controlled when participants ate and minimized changes in their mood. Real-world binge eating episodes are often triggered by shifting emotional states and metabolic changes, which the sterile experimental environment was designed to eliminate.
Additionally, the researchers did not measure actual food consumption during the experiment. The study measured the willingness to work for food and the brain’s anticipation of it, rather than how much participants actually ate. Future studies tracking daily food intake would be needed to link these fluctuating brain signals directly to binge eating episodes.
Finally, slight head movements inside a brain scanner can sometimes look like variable neural activity. People with higher body weight sometimes move slightly more in scanners. While the researchers used mathematical models to correct for head movement, imaging experts often view residual motion artifacts as a potential complication in imaging research.
The study, “Obesity is associated with greater variability of reward signals in the nucleus accumbens,” was authored by Mechteld M. van den Hoek Ostende, Anne Kühnel, Monja P. Neuser, Thomas Dresler, Jennifer Svaldi, and Nils B. Kroemer.
URL: https://www.psypost.org/fluctuating-brain-signals-linked-to-higher-body-weight-and-erratic-eating/
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#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #Overeating #BingeEatingDisorder #RewardSignals #NucleusAccumbens #DLPFC #BrainVariability #FoodCues #ObesityResearch #EatingBehavior #TranslationalPsychiatry
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🔥🔥🔥 PREPRINT ALERT 🔥🔥🔥
https://doi.org/10.1101/2023.03.09.531869
We used dual-colour in vivo #twophoton #imaging and #optogenetics to learn what information the #brain ’s dorsal #hippocampus sends to #NucleusAccumbens while mice navigated to a learned #reward site. What did we learn…?While we often like to think of memories as abstract mental states, they actually serve a key role for our survival and that of our ancient ancestors: Remember where there’s a dangerous place and you can avoid it; remember where there’s food and you won’t go hungry.
But how do we go from the memory of a food location to actually approaching it when we’re hungry? We know that dorsal hippocampus (dHPC) is one of the main “memory storage” sites in the brain and important for navigation, but who sits on the receiving end of this information?
Many great colleagues (like @[email protected], @marisosa @[email protected],…) have highlighted the role of projections into the nucleus accumbens (NAc), part of the basal ganglia (BG). The BG’s role revolves around action selection, while the NAc largely deals w/ reward processing.
So we know that this dHPC>NAc pathway is needed for linking rewards with locations, but what does the HPC actually tell the NAc? What would we see if we could listen in on their private conversations? As it turns out, this is technically quite challenging because we need to combine cell identity (NAc-projecting or not) with cell activity. To achieve this, we turned to dual-colour two-photon calcium imaging. We labelled NAc-projecting neurons in red and used a pan-neuronal green calcium indicator to see live neural activity in dHPC.
We trained mice to lick in a reward zone on a cued linear treadmill to receive condensed milk which they absolutely love. After 5 days, they expertly slowed down and licked ahead of this reward zone, showing us they learned this space~reward association.
So what happens inside dHPC while mice navigate to this reward location? We hypothesised that either dHPC>NAc cells would be mostly active at the reward zone, or that they would show no spatial bias. As it turned out, neither were true…
Instead, we found that dHPC>NAc neurons showed stronger spatial tuning compared to those dHPC neurons projecting elsewhere (dHPC-). They were also more strongly modulated by the texture cues we provided, suggesting privileged spatial information routing to the NAc.
What about the reward zone though? Many previous studies found place cells clustering near reward zones. When we first looked at the data, we saw little evidence of this (sad emoji), but we noticed some mice performed better than others. When we separated high- from low-success trials, we could see the reward zone being overrepresented by place cells – this effect was particularly pronounced for dHPC>NAc neurons. We could also show that these projection neurons are better at decoding the spatial location ahead of the reward zone.
This suggests that it may be less the sensory environment that determines neural coding but the behaviour with which the mouse engages with it. This is a realisation that has swept across the neurosciences: neural activity in most brain regions seems modulated by behaviour.
Better performance usually goes in hand with deceleration as mice approach the reward zone. So do neurons “care” about speed? We found neurons that were either positively (acceleration) or negatively (deceleration) modulated by speed, as others before us. Interestingly, negatively speed-modulated neurons were overrepresented in the dHPC>NAc population, suggestive of a role in reward approach. To actually obtain the reward, mice not only needed to remember the reward zone but also needed to lick there. Strikingly, we saw that dHPC>NAc neurons became very active around the time of appetitive (but not consummatory) licking. Also, if we zoom in on the activity of individual neurons, we saw a larger proportion of dHPC>NAc neurons tuned to appetitive licking.
Does this mean that dHPC>NAc projections could “guide” the mouse’s lick activity, or do they simply receive a motor signal from elsewhere? To test this, we optogenetically activated excitatory dHPC axons in NAc after mice learned to lick for rewards.
We found that upon stimulation of this projection, mice actually started to engage in appetitive licking. This suggests that dHPC>NAc projections seem to indeed be in the driver’s seat for reward-seeking behaviours.
How can we reconcile this with our previous findings of enhanced spatial and (negative) velocity tuning? Are there separate populations for each of these aspects or do we have “multi-tasker” neurons that can do it all?
Answering this question is not trivial because, as mice approached the reward zone (space), they tended to slow down (speed) and start licking, resulting in a lot of “collinearity” in the behavioural data. To tackle this, we built computational models (GLMs) to predict neural activity based on space, speed, and lick data. We then randomly shuffled each behavioural variable to see if our models got worse. With this approach, we found that indeed dHPC>NAc neurons were more heavily tuned to space, speed, and licking, but we also found many neurons that encoded multiple behavioural features. Indeed, among the dHPC>NAc population, this seemed to be the norm rather than the exception. We tend to cherish those one-on-one relationships like position~activity (place cells) or speed~activity (speed cells), but computationally, such mixed selectivity or conjunctive coding has been suggested to help downstream brain regions to decode action-relevant stimuli. We show that the dHPC routes a strongly conjunctive code to the action-selection relevant basal ganglia (specifically, NAc).
Indeed, we find that conjunctive coding neurons improve the performance of a linear decoder tasked with identifying the reward zone. This raises the possibility that the dHPC routes enhanced conjunctive information to action-specific brain regions such as the NAc.
Overall, we show that dHPC routes an enhanced conjunctive code of space, speed, and lick information to NAc, and that this code can guide goal-directed appetitive behaviour such as licking.
I was fortunate to be joined in this work by @petra_moce and for the unwavering support from @[email protected] and @dzne @[email protected], and @[email protected], as well as funding from @ERC_Research @dfg_public and #sfb_1089. Feel free to send comments and questions! 25/25
Also, if you're coming to NWG in Göttingen next week, please feel free to hit me up at poster ***T25-19A*** Wednesday 1-1:45pm (or write me to meet up).
-
🔥🔥🔥 PREPRINT ALERT 🔥🔥🔥
https://doi.org/10.1101/2023.03.09.531869
We used dual-colour in vivo #twophoton #imaging and #optogenetics to learn what information the #brain ’s dorsal #hippocampus sends to #NucleusAccumbens while mice navigated to a learned #reward site. What did we learn…?While we often like to think of memories as abstract mental states, they actually serve a key role for our survival and that of our ancient ancestors: Remember where there’s a dangerous place and you can avoid it; remember where there’s food and you won’t go hungry.
But how do we go from the memory of a food location to actually approaching it when we’re hungry? We know that dorsal hippocampus (dHPC) is one of the main “memory storage” sites in the brain and important for navigation, but who sits on the receiving end of this information?
Many great colleagues (like @[email protected], @marisosa @[email protected],…) have highlighted the role of projections into the nucleus accumbens (NAc), part of the basal ganglia (BG). The BG’s role revolves around action selection, while the NAc largely deals w/ reward processing.
So we know that this dHPC>NAc pathway is needed for linking rewards with locations, but what does the HPC actually tell the NAc? What would we see if we could listen in on their private conversations? As it turns out, this is technically quite challenging because we need to combine cell identity (NAc-projecting or not) with cell activity. To achieve this, we turned to dual-colour two-photon calcium imaging. We labelled NAc-projecting neurons in red and used a pan-neuronal green calcium indicator to see live neural activity in dHPC.
We trained mice to lick in a reward zone on a cued linear treadmill to receive condensed milk which they absolutely love. After 5 days, they expertly slowed down and licked ahead of this reward zone, showing us they learned this space~reward association.
So what happens inside dHPC while mice navigate to this reward location? We hypothesised that either dHPC>NAc cells would be mostly active at the reward zone, or that they would show no spatial bias. As it turned out, neither were true…
Instead, we found that dHPC>NAc neurons showed stronger spatial tuning compared to those dHPC neurons projecting elsewhere (dHPC-). They were also more strongly modulated by the texture cues we provided, suggesting privileged spatial information routing to the NAc.
What about the reward zone though? Many previous studies found place cells clustering near reward zones. When we first looked at the data, we saw little evidence of this (sad emoji), but we noticed some mice performed better than others. When we separated high- from low-success trials, we could see the reward zone being overrepresented by place cells – this effect was particularly pronounced for dHPC>NAc neurons. We could also show that these projection neurons are better at decoding the spatial location ahead of the reward zone.
This suggests that it may be less the sensory environment that determines neural coding but the behaviour with which the mouse engages with it. This is a realisation that has swept across the neurosciences: neural activity in most brain regions seems modulated by behaviour.
Better performance usually goes in hand with deceleration as mice approach the reward zone. So do neurons “care” about speed? We found neurons that were either positively (acceleration) or negatively (deceleration) modulated by speed, as others before us. Interestingly, negatively speed-modulated neurons were overrepresented in the dHPC>NAc population, suggestive of a role in reward approach. To actually obtain the reward, mice not only needed to remember the reward zone but also needed to lick there. Strikingly, we saw that dHPC>NAc neurons became very active around the time of appetitive (but not consummatory) licking. Also, if we zoom in on the activity of individual neurons, we saw a larger proportion of dHPC>NAc neurons tuned to appetitive licking.
Does this mean that dHPC>NAc projections could “guide” the mouse’s lick activity, or do they simply receive a motor signal from elsewhere? To test this, we optogenetically activated excitatory dHPC axons in NAc after mice learned to lick for rewards.
We found that upon stimulation of this projection, mice actually started to engage in appetitive licking. This suggests that dHPC>NAc projections seem to indeed be in the driver’s seat for reward-seeking behaviours.
How can we reconcile this with our previous findings of enhanced spatial and (negative) velocity tuning? Are there separate populations for each of these aspects or do we have “multi-tasker” neurons that can do it all?
Answering this question is not trivial because, as mice approached the reward zone (space), they tended to slow down (speed) and start licking, resulting in a lot of “collinearity” in the behavioural data. To tackle this, we built computational models (GLMs) to predict neural activity based on space, speed, and lick data. We then randomly shuffled each behavioural variable to see if our models got worse. With this approach, we found that indeed dHPC>NAc neurons were more heavily tuned to space, speed, and licking, but we also found many neurons that encoded multiple behavioural features. Indeed, among the dHPC>NAc population, this seemed to be the norm rather than the exception. We tend to cherish those one-on-one relationships like position~activity (place cells) or speed~activity (speed cells), but computationally, such mixed selectivity or conjunctive coding has been suggested to help downstream brain regions to decode action-relevant stimuli. We show that the dHPC routes a strongly conjunctive code to the action-selection relevant basal ganglia (specifically, NAc).
Indeed, we find that conjunctive coding neurons improve the performance of a linear decoder tasked with identifying the reward zone. This raises the possibility that the dHPC routes enhanced conjunctive information to action-specific brain regions such as the NAc.
Overall, we show that dHPC routes an enhanced conjunctive code of space, speed, and lick information to NAc, and that this code can guide goal-directed appetitive behaviour such as licking.
I was fortunate to be joined in this work by @petra_moce and for the unwavering support from @[email protected] and @dzne @[email protected], and @[email protected], as well as funding from @ERC_Research @dfg_public and #sfb_1089. Feel free to send comments and questions! 25/25
Also, if you're coming to NWG in Göttingen next week, please feel free to hit me up at poster ***T25-19A*** Wednesday 1-1:45pm (or write me to meet up).
-
🔥🔥🔥 PREPRINT ALERT 🔥🔥🔥
https://doi.org/10.1101/2023.03.09.531869
We used dual-colour in vivo #twophoton #imaging and #optogenetics to learn what information the #brain ’s dorsal #hippocampus sends to #NucleusAccumbens while mice navigated to a learned #reward site. What did we learn…?While we often like to think of memories as abstract mental states, they actually serve a key role for our survival and that of our ancient ancestors: Remember where there’s a dangerous place and you can avoid it; remember where there’s food and you won’t go hungry.
But how do we go from the memory of a food location to actually approaching it when we’re hungry? We know that dorsal hippocampus (dHPC) is one of the main “memory storage” sites in the brain and important for navigation, but who sits on the receiving end of this information?
Many great colleagues (like @[email protected], @marisosa @[email protected],…) have highlighted the role of projections into the nucleus accumbens (NAc), part of the basal ganglia (BG). The BG’s role revolves around action selection, while the NAc largely deals w/ reward processing.
So we know that this dHPC>NAc pathway is needed for linking rewards with locations, but what does the HPC actually tell the NAc? What would we see if we could listen in on their private conversations? As it turns out, this is technically quite challenging because we need to combine cell identity (NAc-projecting or not) with cell activity. To achieve this, we turned to dual-colour two-photon calcium imaging. We labelled NAc-projecting neurons in red and used a pan-neuronal green calcium indicator to see live neural activity in dHPC.
We trained mice to lick in a reward zone on a cued linear treadmill to receive condensed milk which they absolutely love. After 5 days, they expertly slowed down and licked ahead of this reward zone, showing us they learned this space~reward association.
So what happens inside dHPC while mice navigate to this reward location? We hypothesised that either dHPC>NAc cells would be mostly active at the reward zone, or that they would show no spatial bias. As it turned out, neither were true…
Instead, we found that dHPC>NAc neurons showed stronger spatial tuning compared to those dHPC neurons projecting elsewhere (dHPC-). They were also more strongly modulated by the texture cues we provided, suggesting privileged spatial information routing to the NAc.
What about the reward zone though? Many previous studies found place cells clustering near reward zones. When we first looked at the data, we saw little evidence of this (sad emoji), but we noticed some mice performed better than others. When we separated high- from low-success trials, we could see the reward zone being overrepresented by place cells – this effect was particularly pronounced for dHPC>NAc neurons. We could also show that these projection neurons are better at decoding the spatial location ahead of the reward zone.
This suggests that it may be less the sensory environment that determines neural coding but the behaviour with which the mouse engages with it. This is a realisation that has swept across the neurosciences: neural activity in most brain regions seems modulated by behaviour.
Better performance usually goes in hand with deceleration as mice approach the reward zone. So do neurons “care” about speed? We found neurons that were either positively (acceleration) or negatively (deceleration) modulated by speed, as others before us. Interestingly, negatively speed-modulated neurons were overrepresented in the dHPC>NAc population, suggestive of a role in reward approach. To actually obtain the reward, mice not only needed to remember the reward zone but also needed to lick there. Strikingly, we saw that dHPC>NAc neurons became very active around the time of appetitive (but not consummatory) licking. Also, if we zoom in on the activity of individual neurons, we saw a larger proportion of dHPC>NAc neurons tuned to appetitive licking.
Does this mean that dHPC>NAc projections could “guide” the mouse’s lick activity, or do they simply receive a motor signal from elsewhere? To test this, we optogenetically activated excitatory dHPC axons in NAc after mice learned to lick for rewards.
We found that upon stimulation of this projection, mice actually started to engage in appetitive licking. This suggests that dHPC>NAc projections seem to indeed be in the driver’s seat for reward-seeking behaviours.
How can we reconcile this with our previous findings of enhanced spatial and (negative) velocity tuning? Are there separate populations for each of these aspects or do we have “multi-tasker” neurons that can do it all?
Answering this question is not trivial because, as mice approached the reward zone (space), they tended to slow down (speed) and start licking, resulting in a lot of “collinearity” in the behavioural data. To tackle this, we built computational models (GLMs) to predict neural activity based on space, speed, and lick data. We then randomly shuffled each behavioural variable to see if our models got worse. With this approach, we found that indeed dHPC>NAc neurons were more heavily tuned to space, speed, and licking, but we also found many neurons that encoded multiple behavioural features. Indeed, among the dHPC>NAc population, this seemed to be the norm rather than the exception. We tend to cherish those one-on-one relationships like position~activity (place cells) or speed~activity (speed cells), but computationally, such mixed selectivity or conjunctive coding has been suggested to help downstream brain regions to decode action-relevant stimuli. We show that the dHPC routes a strongly conjunctive code to the action-selection relevant basal ganglia (specifically, NAc).
Indeed, we find that conjunctive coding neurons improve the performance of a linear decoder tasked with identifying the reward zone. This raises the possibility that the dHPC routes enhanced conjunctive information to action-specific brain regions such as the NAc.
Overall, we show that dHPC routes an enhanced conjunctive code of space, speed, and lick information to NAc, and that this code can guide goal-directed appetitive behaviour such as licking.
I was fortunate to be joined in this work by @petra_moce and for the unwavering support from @[email protected] and @dzne @[email protected], and @[email protected], as well as funding from @ERC_Research @dfg_public and #sfb_1089. Feel free to send comments and questions! 25/25
Also, if you're coming to NWG in Göttingen next week, please feel free to hit me up at poster ***T25-19A*** Wednesday 1-1:45pm (or write me to meet up).
-
🔥🔥🔥 PREPRINT ALERT 🔥🔥🔥
https://doi.org/10.1101/2023.03.09.531869
We used dual-colour in vivo #twophoton #imaging and #optogenetics to learn what information the #brain ’s dorsal #hippocampus sends to #NucleusAccumbens while mice navigated to a learned #reward site. What did we learn…?While we often like to think of memories as abstract mental states, they actually serve a key role for our survival and that of our ancient ancestors: Remember where there’s a dangerous place and you can avoid it; remember where there’s food and you won’t go hungry.
But how do we go from the memory of a food location to actually approaching it when we’re hungry? We know that dorsal hippocampus (dHPC) is one of the main “memory storage” sites in the brain and important for navigation, but who sits on the receiving end of this information?
Many great colleagues (like @[email protected], @marisosa @[email protected],…) have highlighted the role of projections into the nucleus accumbens (NAc), part of the basal ganglia (BG). The BG’s role revolves around action selection, while the NAc largely deals w/ reward processing.
So we know that this dHPC>NAc pathway is needed for linking rewards with locations, but what does the HPC actually tell the NAc? What would we see if we could listen in on their private conversations? As it turns out, this is technically quite challenging because we need to combine cell identity (NAc-projecting or not) with cell activity. To achieve this, we turned to dual-colour two-photon calcium imaging. We labelled NAc-projecting neurons in red and used a pan-neuronal green calcium indicator to see live neural activity in dHPC.
We trained mice to lick in a reward zone on a cued linear treadmill to receive condensed milk which they absolutely love. After 5 days, they expertly slowed down and licked ahead of this reward zone, showing us they learned this space~reward association.
So what happens inside dHPC while mice navigate to this reward location? We hypothesised that either dHPC>NAc cells would be mostly active at the reward zone, or that they would show no spatial bias. As it turned out, neither were true…
Instead, we found that dHPC>NAc neurons showed stronger spatial tuning compared to those dHPC neurons projecting elsewhere (dHPC-). They were also more strongly modulated by the texture cues we provided, suggesting privileged spatial information routing to the NAc.
What about the reward zone though? Many previous studies found place cells clustering near reward zones. When we first looked at the data, we saw little evidence of this (sad emoji), but we noticed some mice performed better than others. When we separated high- from low-success trials, we could see the reward zone being overrepresented by place cells – this effect was particularly pronounced for dHPC>NAc neurons. We could also show that these projection neurons are better at decoding the spatial location ahead of the reward zone.
This suggests that it may be less the sensory environment that determines neural coding but the behaviour with which the mouse engages with it. This is a realisation that has swept across the neurosciences: neural activity in most brain regions seems modulated by behaviour.
Better performance usually goes in hand with deceleration as mice approach the reward zone. So do neurons “care” about speed? We found neurons that were either positively (acceleration) or negatively (deceleration) modulated by speed, as others before us. Interestingly, negatively speed-modulated neurons were overrepresented in the dHPC>NAc population, suggestive of a role in reward approach. To actually obtain the reward, mice not only needed to remember the reward zone but also needed to lick there. Strikingly, we saw that dHPC>NAc neurons became very active around the time of appetitive (but not consummatory) licking. Also, if we zoom in on the activity of individual neurons, we saw a larger proportion of dHPC>NAc neurons tuned to appetitive licking.
Does this mean that dHPC>NAc projections could “guide” the mouse’s lick activity, or do they simply receive a motor signal from elsewhere? To test this, we optogenetically activated excitatory dHPC axons in NAc after mice learned to lick for rewards.
We found that upon stimulation of this projection, mice actually started to engage in appetitive licking. This suggests that dHPC>NAc projections seem to indeed be in the driver’s seat for reward-seeking behaviours.
How can we reconcile this with our previous findings of enhanced spatial and (negative) velocity tuning? Are there separate populations for each of these aspects or do we have “multi-tasker” neurons that can do it all?
Answering this question is not trivial because, as mice approached the reward zone (space), they tended to slow down (speed) and start licking, resulting in a lot of “collinearity” in the behavioural data. To tackle this, we built computational models (GLMs) to predict neural activity based on space, speed, and lick data. We then randomly shuffled each behavioural variable to see if our models got worse. With this approach, we found that indeed dHPC>NAc neurons were more heavily tuned to space, speed, and licking, but we also found many neurons that encoded multiple behavioural features. Indeed, among the dHPC>NAc population, this seemed to be the norm rather than the exception. We tend to cherish those one-on-one relationships like position~activity (place cells) or speed~activity (speed cells), but computationally, such mixed selectivity or conjunctive coding has been suggested to help downstream brain regions to decode action-relevant stimuli. We show that the dHPC routes a strongly conjunctive code to the action-selection relevant basal ganglia (specifically, NAc).
Indeed, we find that conjunctive coding neurons improve the performance of a linear decoder tasked with identifying the reward zone. This raises the possibility that the dHPC routes enhanced conjunctive information to action-specific brain regions such as the NAc.
Overall, we show that dHPC routes an enhanced conjunctive code of space, speed, and lick information to NAc, and that this code can guide goal-directed appetitive behaviour such as licking.
I was fortunate to be joined in this work by @petra_moce and for the unwavering support from @[email protected] and @dzne @[email protected], and @[email protected], as well as funding from @ERC_Research @dfg_public and #sfb_1089. Feel free to send comments and questions! 25/25
Also, if you're coming to NWG in Göttingen next week, please feel free to hit me up at poster ***T25-19A*** Wednesday 1-1:45pm (or write me to meet up).