Reward Receipt Research Articles

Behavioral reinforcement of pathological exercise in anorexia nervosa.

Pathological exercise in anorexia nervosa (AN) is a harmful behavior associated with a chronic course and poor prognosis. To date, no comprehensive theoretical model exists to describe pathological exercise in the context of AN, and as such, few treatments are effective at promoting direct and sustained pathological exercise extinction. Using a framework put forth by Wise & Koob (2014), debating the relative importance of positive and negative reinforcement in substance use, we present three hypotheses of behavioral reinforcement of exercise, encompassing biological, psychological, and environmental influences. Specifically, we argue that exercise is positively reinforced through receipt of biological and behavioral rewards, negatively reinforced through avoidance of aversive emotions, and that these two systems work in tandem over time to engrain pathological exercise as a habit. We then present suggestions for testing each of these hypotheses as future directions for the field.

The reward positivity is sensitive to affective liking.

The EEG feature known as the Reward Positivity (RewP) is elicited by reward receipt and appears to reflect sensitively and specifically positive prediction errors during reinforcement learning. Yet, the RewP also is modulated by state and trait affect, suggesting that it has a more complex computational role than simple reinforcement surprise. We conducted a series of experiments aimed to investigate underlying affect processing reflected in the RewP during a reinforcement learning task. In the first experiment (N = 25), we manipulated the type of rewards a person could win (simple points or hedonically-appraised pictures). Although there were no differences in the amplitudes of the RewP for different types of rewards, there was a significant correlation between the individual rating of liking for the images and RewP amplitude. In a second experiment (N = 25), we manipulated reinforcement rates (easy vs. hard) and affective picture content (liked vs. ambivalent) to examine the potential interaction of prediction error and liking on RewP amplitude. We again found a significant relationship between liking and RewP amplitude, however, only in the hard condition. These findings suggest that the RewP reflects cortical computations of reward surprise as well as hedonic liking, identifying it as a possible nexus where multidimensional value is computed.

21.4 REWARD PROCESSING IN CHILDREN WITH DISRUPTIVE BEHAVIOR DISORDERS AND CALLOUS-UNEMOTIONAL TRAITS IN THE ABCD STUDY

Disrupted reward processing is implicated in the etiology of disruptive behavior disorders (DBDs) and callous-unemotional traits. However, neuroimaging investigations of reward processing underlying these phenotypes remain sparse. The authors examined neural sensitivity in response to reward anticipation and receipt among youths with DBDs, with and without callous-unemotional traits. Data were obtained from the ABCD study (mean age = 9.51 years [SD = 0.50]; 49% female). Reward-related activation during the monetary incentive delay task was examined across 16 brain regions, including the amygdala, anterior cingulate cortex (ACC), nucleus accumbens (NAcc), and orbitofrontal cortex (OFC). Latent variable modeling was used to examine network-level coactivation. The following diagnostic groups were compared: typically developing youths (N = 693) and youths with DBDs (N = 995), subdivided into those with callous-unemotional traits (DBD+CU, n = 198) and without callous-unemotional traits (DBD only, n = 276). During reward anticipation, youths in the overall DBD group (with and without callous-unemotional traits) showed decreased dorsal ACC activation compared with typically developing youths. The DBD-only group exhibited reduced ventral and dorsal striatal activity compared with the DBD+CU and typically developing groups. During reward receipt, youths with DBDs showed increased cortical (eg, OFC) and subcortical (eg, NAcc) regional activation compared with typically developing youths. The DBD+CU group demonstrated greater activation in several regions compared with those in the typically developing (eg, amygdala) and DBD-only (eg, dorsal ACC) groups. At the network level, the DBD-only group showed reduced anticipatory reward activation compared with the typically developing and DBD+CU groups, whereas youths in the DBD+CU group showed increased activation during reward receipt compared with those in the typically developing group. These findings advance our understanding of unique neuroetiologic pathways to DBDs and callous-unemotional traits.

#3097 Temporal and spectral dynamics of reward and risk processing in the amygdala revealed with stereo-EEG recordings in epilepsy

Objectives/AimsTo examine the temporal and spectral characteristics of local field potentials recorded from the amygdala in epilepsy in the context of the anticipation and receipt of rewards and losses using an incentive learning task and a risky decision-making task.Methods16 Epilepsy patients completed two tasks. In the monetary incentive delay (MID) task, patients saw reward and loss cues which indicated whether money could be won or lost depending on whether a subsequent response was or was not quick/accurate enough, respectively. This was compared with neutral cues where responses were neither rewarded nor punished regardless of response.In the risk task, patients were presented with two face down cards with values ranging from 1 to 10. When the first card is revealed, patients have to choose whether to bet or not bet that the second card is higher. After the card is revealed, patients receive a monetary reward if it is higher and a loss if it is lower. If patients do not bet, they receive nothing.ResultsIn both tasks, patients showed larger left amygdala theta band oscillatory activity to the receipt of monetary rewards compared to no money. In contrast, there were no significant responses to monetary losses. During the decision phase of the risk task, there was increased theta activity when patients chose to bet instead of not betting and when the decision had low risk (card <= 5) compared to high risk (card above 5). There were no effects of uncertainty.ConclusionsThe combined results of these two studies embellish our understanding of the role of the amygdala in motivation and decision-making processes and lend further support for its role in reward related processes rather than its often cited fear-related functions (Baxter & Murray, 2002; Murray, 2007). Theta activation is linked to cognitive processes in frontal cortices and coupled to MTL activity (Helfrich & Knight, 2016). As left amygdala theta activation was only recruited when patients were making their bet and not just anticipating reward, the pattern of results lend support to its role in cognition-emotion interactions specific to risk and reward but not uncertainty. Indeed, the hemispheric asymmetry is highly consistent with EEG studies showing left prefrontal dominance in reward processing (Manssuer et al., 2021).

Ketamine Modulates the Neural Correlates of Reward Processing in Unmedicated Patients in Remission From Depression

BackgroundKetamine as an antidepressant improves anhedonia as early as 2 hours after infusion. These drug effects are thought to be exerted via actions on reward-related brain areas—yet these actions remain largely unknown. Our study investigates ketamine’s effects during the anticipation and receipt of an expected reward, after the psychotomimetic effects of ketamine have passed, when early antidepressant effects are reported. MethodsWe examined ketamine’s effects during the anticipation and receipt of expected rewards on predefined brain areas, namely, the dorsal and ventral striatum, ventral tegmental area, amygdala, and insula. We recruited 37 male and female participants with remitted depression who were free from symptoms and antidepressant treatments at the time of the scan. Participants were scanned 2 hours after drug administration in a double-blind crossover design (ketamine: 0.5 mg/kg and placebo) while performing a monetary reward task. ResultsA significant main effect of ketamine was observed across all regions of interest during the anticipation and feedback phases of win and no-win trials. The drug effects were particularly prominent in the nucleus accumbens and putamen, which showed increased activation on the receipt of smaller rewards compared with neutral. The levels of (2R,6R)-hydroxynorketamine 2 hours after infusion significantly correlated with the activation observed in the ventral tegmental area for that contrast. ConclusionsThese findings demonstrate that ketamine can produce detectable changes in reward-related brain areas 2 hours after infusion, which occur without symptom changes and support the idea that ketamine might improve reward-related symptoms via modulation of response to feedback.

Reward-Related Neural Circuitry in Depressed and Anxious Adolescents: A Human Connectome Project

Although depression and anxiety often have distinct etiologies, they frequently co-occur in adolescence. Recent initiatives have underscored the importance of developing new ways of classifying mental illness based on underlying neural dimensions that cut across traditional diagnostic boundaries. Accordingly, the aim of the study was to clarify reward-related neural circuitry that may characterize depressed-anxious youth. The Boston Adolescent Neuroimaging of Depression and Anxiety Human Connectome Project tested group differences regarding subcortical volume and nucleus accumbens activation during an incentive processing task among 14- to 17-year-old adolescents presenting with a primary depressive and/or anxiety disorder (n= 129) or no lifetime history of mental disorders (n= 64). In addition, multimodal modeling examined predictors of depression and anxiety symptom change over a 6-month follow-up period. Our findings highlighted considerable convergence. Relative to healthy youth, depressed-anxious adolescents exhibited reduced nucleus accumbens volume and activation following reward receipt. These findings remained when removing all medicated participants (∼59% of depressed-anxious youth). Subgroup analyses comparing anxious-only, depressed-anxious, and healthy youth also were largely consistent. Multimodal modeling showed that only structural alterations predicted depressive symptoms over time. Multimodal findings highlight alterations within nucleus accumbens structure and function that characterize depressed-anxious adolescents. In the current hypothesis-driven analyses, however, only reduced nucleus accumbens volume predicted depressive symptoms over time. An important next step will be to clarify why structural alterations have an impact on reward-related processes and associated symptoms.

Exploring Neural Mechanisms Related to Cognitive Control, Reward, and Affect in Eating Disorders: A Narrative Review of FMRI Studies.

Studies using functional magnetic resonance imaging (fMRI) have contributed to our understanding of possible neural abnormalities among individuals with eating disorders. Many of these studies have focused on three domains: 1) cognitive control, 2) reward processing, and 3) affective processing. This review attempts to summarize the recent fMRI findings across these domains among the most well-characterized eating disorders: anorexia nervosa (AN), bulimia nervosa (BN), and binge eating disorder (BED). Though the literature is a bit murky, a few major themes have emerged. Cognitive control systems are affected among individuals across eating disorder diagnoses, but effects seem least pronounced in AN. Specifically, individuals with all eating disorders appear to show decreased prefrontal activation during cognitive control, but there is less evidence in AN linking decreased prefrontal activation with behavior. There is some evidence that the reinforcing value of food is reduced in AN, but individuals with BN and BED show hyperactivation to rewarding food-related stimuli, suggesting the reinforcing value of food may be enhanced. However, more complex reward processing paradigms show that individuals with BN and BED exhibit hypoactivation to reward anticipation and provide mixed results with regards to reward receipt. There are fewer neuroimaging findings related to affective processing, yet behavioral findings suggest affective processing is important in understanding eating disorders. Though the extant literature is complicated, these studies represent a foundation from which to build and provide insight into potential neurobiological mechanisms that may contribute to the pathophysiology of eating disorders.

Motor cortex modulation and reward in children with attention-deficit/hyperactivity disorder.

Attention-deficit/hyperactivity disorder, the most prevalent developmental disorder in childhood, is a biologically heterogenous condition characterized by impaired attention and impulse control as well as motoric hyperactivity and anomalous motor skill development. Neuropsychological testing often demonstrates impairments in motivation and reward-related decision making in attention-deficit/hyperactivity disorder, believed to indicate dysfunction of the dopamine reward pathway. Development of reliable, non-invasive, easily obtained and quantitative biomarkers correlating with the presence and severity of clinical symptoms and impaired domains of function could aid in identifying meaningful attention-deficit/hyperactivity disorder subgroups and targeting appropriate treatments. To this end, 55 (37 male) 8–12-year-old children with attention-deficit/hyperactivity disorder and 50 (32 male) age-matched, typically-developing controls were enrolled in a transcranial magnetic stimulation protocol—used previously to quantify cortical disinhibition in both attention-deficit/hyperactivity disorder and Parkinson’s Disease—with a child-friendly reward motivation task. The primary outcomes were reward task-induced changes in short interval cortical inhibition and up-modulation of motor evoked potential amplitudes, evaluated using mixed model, repeated measure regression. Our results show that both reward cues and reward receipt reduce short-interval cortical inhibition, and that baseline differences by diagnosis (less inhibition in attention-deficit/hyperactivity disorder) were no longer present when reward was cued or received. Similarly, both reward cues and reward receipt up-modulated motor evoked potential amplitudes, but, differentiating the two groups, this Task-Related-Up-Modulation was decreased in children with attention-deficit/hyperactivity disorder. Furthermore, more severe hyperactive/impulsive symptoms correlated significantly with less up-modulation with success in obtaining reward. These results suggest that in children with attention-deficit/hyperactivity disorder, short interval cortical inhibition may reflect baseline deficiencies as well as processes that normalize performance under rewarded conditions. Task-Related-Up-Modulation may reflect general hypo-responsiveness in attention-deficit/hyperactivity disorder to both reward cue and, especially in more hyperactive/impulsive children, to successful reward receipt. These findings support transcranial magnetic stimulation evoked cortical inhibition and task-induced excitability as biomarkers of clinically relevant domains of dysfunction in childhood attention-deficit/hyperactivity disorder.

Sex differences in neural responses to reward and the influences of individual reward and punishment sensitivity

BackgroundMen and women show differences in sensitivity to reward and punishment, which may impact behavior in health and disease. However, the neural bases of these sex differences remain under-investigated. Here, by combining functional magnetic resonance imaging (fMRI) and a variant of the Monetary Incentive Delay Task (MIDT), we examined sex differences in the neural responses to wins and losses and how individual reward and punishment sensitivity modulates these regional activities.MethodsThirty-sex men and 27 women participated in the fMRI study. We assessed sensitivity to punishment (SP) and sensitivity to reward (SR) with the Sensitivity to Punishment and Sensitivity to Reward Questionnaire (SPSRQ). In the MIDT, participants pressed a button to collect reward ($1, 1¢, or nil), with the reaction time window titrated across trials so participants achieved a success rate of approximately 67%. We processed the Imaging data with published routines and evaluated the results with a corrected threshold.ResultsWomen showed higher SP score than men and men showed higher SR score than women. Men relative to women showed higher response to the receipt of dollar or cent reward in bilateral orbitofrontal and visual cortex. Men as compared to women also showed higher response to dollar loss in bilateral orbitofrontal cortex. Further, in whole-brain regressions, women relative to men demonstrated more significant modulation by SP in the neural responses to wins and larger wins, and the sex differences were confirmed by slope tests.ConclusionsTogether, men showed higher SR and neural sensitivity to both wins, large or small, and losses than women. Individual differences in SP were associated with diminished neural responses to wins and larger wins in women only. These findings highlight how men and women may differ in reward-related brain activations in the MIDT and add to the imaging literature of sex differences in cognitive and affective functions.

Associations between insomnia and reward learning in clinical depression.

Depression and insomnia commonly co-occur. Yet, little is known about the mechanisms through which insomnia influences depression. Recent research and theory highlight reward system dysfunction as a potential mediator of the relationship between insomnia and depression. This study is the first to examine the impact of insomnia on reward learning, a key component of reward system functioning, in clinical depression. The sample consisted of 72 veterans with unipolar depression who endorsed sleep disturbance symptoms. Participants completed the Structured Clinical Interview for DSM-IV, self-report measures of insomnia, depression, and reward processing, and a previously validated signal detection task (Pizzagalli et al., 2005, Biological Psychiatry, 57(4), 319-327). Trial-by-trial response bias (RB) estimates calculated for each of the 200 task trials were examined using linear mixed-model analyses to investigate change in reward learning. Findings demonstrated diminished rate and magnitude of reward learning in the Insomnia group relative to the Hypersomnia/Mixed Symptom group across the task. Within the Insomnia group, participants with more severe insomnia evidenced the lowest rates of reward learning, with increased RB across the task with decreasing insomnia severity. Among individuals with depression, insomnia is associated with decreased ability to learn associations between neutral stimuli and rewarding outcomes and/or modify behavior in response to differential receipt of reward. This attenuated reward learning may contribute to clinically meaningful decreases in motivation and increased withdrawal in this comorbid group. Results extend existing theory by highlighting impairments in reward learning specifically as a potential mediator of the association between insomnia and depression.

Association of Neural Reward Circuitry Function With Response to Psychotherapy in Youths With Anxiety Disorders.

Identifying neural correlates of response to psychological treatment may inform targets for interventions designed to treat psychiatric disorders. This study examined the extent to which baseline functioning in reward circuitry is associated with response to psychotherapy in youths with anxiety disorders. A randomized clinical trial of cognitive-behavioral therapy compared with supportive therapy was conducted in youths with anxiety disorders. Before treatment, 72 youths (9-14 years old) with anxiety disorders and 37 group-matched healthy comparison youths completed a monetary reward functional MRI task. Treatment response was defined categorically as at least a 35% reduction in diagnostician-rated anxiety severity from pre- to posttreatment assessment. Pretreatment neural activation in the striatum and medial prefrontal cortex (mPFC) during monetary wins relative to losses was examined in relation to treatment response. Responders, nonresponders, and healthy youths differed significantly in mPFC activation to rewards versus losses at baseline. Youths with anxiety exhibited higher mPFC activity relative to healthy youths, although this may have been driven by differences in depressive symptoms. Planned comparisons between treatment responders (N=48) and nonresponders (N=24) also revealed greater pretreatment neural activation in a cluster encompassing the subgenual anterior cingulate cortex and nucleus accumbens among responders. Striatal activation to reward receipt may not differentiate youths with anxiety from healthy youths. However, higher striatal responsivity to rewards may allow youths with anxiety to improve during treatment, potentially through greater engagement in therapy. Function in reward circuitry may guide development of treatments for youths with anxiety.

Neural mechanisms of reward processing in adolescent irritability.

Irritability is impairing and prevalent across pediatric psychiatric disorders and typical development, yet its neural mechanisms are largely unknown. This study evaluated the relation between adolescent irritability and reward-related brain function as a candidate neural mechanism. Adolescents from intervention-seeking families in the community (N=52; mean age=13.80, SD=1.94) completed a monetary incentive delay task to assess reward anticipation and feedback (reward receipt and omission) during fMRI acquisition. Whole-brain analyses, controlling for age, examined brain activation and striatal and amygdala connectivity in relation to irritability. Irritability was measured using the parent- and youth-reported Affective Reactivity Index. Irritability was associated with altered reward processing-related activation and connectivity in multiple networks during reward anticipation and feedback, including increased striatal activation and altered ventral striatum connectivity with prefrontal areas. Our findings suggest that irritability is associated with altered neural patterns during reward processing and that aberrant prefrontal cortex-mediated top-down control may be related to irritability. These findings inform our understanding of the etiology of youth irritability and the development of mechanism-based interventions.

Schizophrenia and bipolar disorder are associated with opposite brain reward anticipation-associated response.

Blunted and exaggerated neuronal response to rewards are hypothesized to be core features of schizophrenia spectrum disorders (SZ) and bipolar disorder (BD), respectively. Nonetheless, direct tests of this hypothesis, in which response between SZ and BD is compared in the same study, are lacking. Here we examined the functional correlates of reward processing during the Incentivized Control Engagement Task (ICE-T) using 3T fMRI. Reward-associated activation was examined in 49 healthy controls (HCs), 52 recent-onset individuals with SZ, and 22 recent-onset individuals with Type I BD using anterior cingulate (ACC), anterior insula, and ventral striatal regions of interest. Significant group X reward condition (neutral vs. reward) interactions were observed during reward anticipation in the dorsal ACC (F(2,120) = 4.21, P = 0.017) and right insula (F(2,120) = 4.77, P = 0.010). The ACC interaction was driven by relatively higher activation in the BD group vs. HCs (P = 0.007) and vs. individuals with SZ (P = 0.010). The insula interaction was driven by reduced activation in the SZ group relative to HCs (P = 0.018) and vs. people with BD (P = 0.008). A composite of reward anticipation-associated response across all associated ROIs also differed significantly by diagnosis (F(1,120) = 5.59, P = 0.02), BD > HC > SZ. No effects of group or group X reward interactions were observed during reward feedback. These results suggest that people with SZ and BD have opposite patterns of activation associated with reward anticipation but not reward receipt. Implications of these findings in regard to Research Domain Criteria-based classification of illness and the neurobiology of reward in psychosis are discussed.

Dopamine receptors regulate preference between high-effort and high-risk rewards.

Optimal decision-making necessitates evaluation of multiple rewards that are each offset by distinct costs, such as high effort requirement or high risk of failure. The neurotransmitter dopamine is fundamental toward these cost-benefit analyses, and D1-like and D2-like dopamine receptors differently modulate the reward-discounting effects of both effort and risk. However, measuring the role of dopamine in regulating decision-making between options associated with distinct costs exceeds the scope of traditional rodent economic decision-making paradigms. We developed the effort vs probability economic conflict task (EvP) to model multimodal economic decision-making in rats. This task measures choice between two rewards of uniform magnitude associated with either a high effort requirement or risk of reward omission. We then tested the modulatory effects of systemic cocaine and D1/D2 blockade or activation on the preference between high-effort and high-risk alternatives. In the EvP, two reinforcers of equal magnitude are associated with either (1) an effort requirement that increases throughout the session (1, 5, 10, and 20 lever presses), or (2) a low probability of reward receipt (25% of probabilistic choices). Critically, the reinforcer for each choice is comparable (one pellet), which eliminates the influence of magnitude discrimination on the decision-making process. After establishing the task, the dopamine transporter blocker cocaine and D1/D2 antagonists and agonists were administered prior to EvP performance. Preference shifted away from either effortful or probabilistic choice when either option became more costly, and this preference was highly variable between subjects and stable over time. Cocaine, D1 activation, and D2 blockade produced limited, dose-dependent shifts in choice preference contingent on high or low effort conditions. In contrast, D2 activation across multiple doses evoked a robust shift from effortful to risky choice that was evident even when clearly disadvantageous. The EvP clearly demonstrates that rats can evaluate distinct effortful or risky costs associated with rewards of comparable magnitude, and shift preference away from either option with increasing cost. This preference is more tightly linked to D2 than D1 receptor manipulation, suggesting D2-like receptors as a possible therapeutic target for maladaptive biases toward risk-taking over effort.

Proximity and Expectancy Modulate Response Vigor After Reward Omission

Both humans and some non-human animals tend to respond more vigorously after failing to obtain rewards. Such response invigoration becomes more pronounced when individuals have increased expectations of obtaining rewards during reward pursuit (expectancy), and when they perceive the eventual loss to be proximal to reward receipt (proximity). However, it was unclear whether proximity and expectancy may have distinct influences on response vigor. To investigate this question, we developed a computerized ’scratch card’ task, in which participants turned three cards one by one and won points when all three cards matched (AAA). After each game, they pressed keys to confirm the outcome and start a new game. We included three types of losses: AAB, where participants had increased expectancy of winning as the game evolved, and the final outcome was proximal to winning; ABB and ABA, with reduced expectancy, but high proximity to winning; and ABC, with reduced expectancy and low proximity to winning. In three online studies, we consistently observed that participants confirmed losses more quickly than wins. Importantly, detailed analyses of the different types of losses revealed that proximity reduced vigor, whereas expectancy increased it. Together, these findings are in line with general appraisal theories: the adjustments of response vigor may be triggered by the appraised discrepancy between the current state and a reference state (e.g., attaining one’s goal), and serve to close the gap and facilitate goal pursuit. These findings may also have implications for the effect of ‘near miss’ on gambling persistence. Further exploring how reward omission impacts response vigor may help us better understand the goal pursuit process, and how it becomes maladaptive under certain circumstances.

Executive functioning moderates neural reward processing in youth.

Although executive functioning has traditionally been studied in "cool" settings removed from emotional contexts, it is highly relevant in "hot" emotionally salient settings such as reward processing. Furthermore, brain structures related to "cool" executive functioning and "hot" reward-related processes develop simultaneously, yet little is known about how executive functioning modulates neural processes related to reward processing during adolescence, a period of time when these systems are still developing. The present study examined how performance on "cool" behavioral executive functioning measures moderates neural reward processing. Youths (N = 43, Mage = 13.74 years, SD = 1.81 years) completed a child-friendly monetary incentive delay task during fMRI acquisition that captures neural responses to reward anticipation and to reward receipt and omission. Performance on inhibitory control and cognitive flexibility measures, captured outside the scanner, was used to predict brain activation and seed-based connectivity (ventral striatum and amygdala). Across analyses, we found that executive functioning moderated youths' neural responses during both reward anticipation and performance feedback, predominantly with respect to amygdala connectivity with prefrontal/frontal and temporal structures, supporting previous theoretical models of brain development during adolescence. Overall, youths with worse executive functioning had more pronounced differences in neural activation and connectivity between task conditions compared with youths with better executive functioning. This study contributes to elucidating the relationship between "cool" and "hot" processes and our findings demonstrate that simple executive functioning skills moderate more complex processes that involve incorporation of numerous skills in an emotionally salient context, such as reward processing.

Reward Processing in Children With Disruptive Behavior Disorders and Callous-Unemotional Traits in the ABCD Study.

Disrupted reward processing is implicated in the etiology of disruptive behavior disorders (DBDs) and callous-unemotional traits. However, neuroimaging investigations of reward processing underlying these phenotypes remain sparse. The authors examined neural sensitivity in response to reward anticipation and receipt among youths with DBDs, with and without callous-unemotional traits. Data were obtained from the Adolescent Brain and Cognitive Development Study (mean age=9.51 years [SD=0.50]; 49% female). Reward-related activation during the monetary incentive delay task was examined across 16 brain regions, including the amygdala, anterior cingulate cortex (ACC), nucleus accumbens (NAcc), and orbitofrontal cortex (OFC). Latent variable modeling was used to examine network-level coactivation. The following diagnostic groups were compared: typically developing youths (N=693) and youths with DBDs (N=995), subdivided into those with callous-unemotional traits (DBD+CU, N=198) and without callous-unemotional traits (DBD only, N=276). During reward anticipation, youths in the overall DBD group (with and without callous-unemotional traits) showed decreased dorsal ACC activation compared with typically developing youths. The DBD-only group exhibited reduced ventral and dorsal striatal activity compared with the DBD+CU and typically developing groups. During reward receipt, youths with DBDs showed increased cortical (e.g., OFC) and subcortical (e.g., NAcc) regional activation compared with typically developing youths. The DBD+CU group demonstrated greater activation in several regions compared with those in the typically developing (e.g., amygdala) and DBD-only (e.g., dorsal ACC) groups. At the network level, the DBD-only group showed reduced anticipatory reward activation compared with the typically developing and DBD+CU groups, whereas youths in the DBD+CU group showed increased activation during reward receipt compared with those in the typically developing group. These findings advance our understanding of unique neuroetiologic pathways to DBDs and callous-unemotional traits.

The ventral striatum dissociates information expectation, reward anticipation, and reward receipt

Do dopaminergic reward structures represent the expected utility of information similarly to a reward? Optimal experimental design models from Bayesian decision theory and statistics have proposed a theoretical framework for quantifying the expected value of information that might result from a query. In particular, this formulation quantifies the value of information before the answer to that query is known, in situations where payoffs are unknown and the goal is purely epistemic: That is, to increase knowledge about the state of the world. Whether and how such a theoretical quantity is represented in the brain is unknown. Here we use an event-related functional MRI (fMRI) task design to disentangle information expectation, information revelation and categorization outcome anticipation, and response-contingent reward processing in a visual probabilistic categorization task. We identify a neural signature corresponding to the expectation of information, involving the left lateral ventral striatum. Moreover, we show a temporal dissociation in the activation of different reward-related regions, including the nucleus accumbens, medial prefrontal cortex, and orbitofrontal cortex, during information expectation versus reward-related processing.

Striatal activation to monetary reward is associated with alcohol reward sensitivity.

One well-known phenotypic risk factor for the development of alcohol use disorder is sensitivity to the rewarding effects of alcohol. In the present study, we examined whether individuals who are sensitive to alcohol reward are also sensitive to nondrug rewards, thereby reflecting a broader individual difference risk factor. Specifically, we tested the hypothesis that subjective response to acute rewarding effects of alcohol would be related to neural activation during monetary reward receipt relative to loss (in the absence of alcohol). Community-recruited healthy young social drinkers (N = 58) completed four laboratory sessions in which they received alcohol (0.8 g/kg) and placebo in alternating order under double-blind conditions, providing self-report measures of subjective response to alcohol at regular intervals. At a separate visit 1-3 weeks later, they completed a reward-guessing game, the 'Doors' task, during fMRI in a drug-free state. Participants who reported greater motivation (i.e., wanting) to consume more alcohol after a single moderate dose of alcohol also exhibited greater neural activation in the bilateral ventral caudate and the nucleus accumbens during reward receipt relative to loss. Striatal activation was not related to other subjective ratings including alcohol-induced sedation, stimulation, or pleasure (i.e., feeling, liking). Our study is the first to show that measures of alcohol reward are related to neural indices of monetary reward in humans. These results support growing evidence that individual differences in responses to drug and nondrug reward are linked and together form a risk profile for drug use or abuse, particularly in young adults.

The effect of concurrent reward on aversive information processing in the brain

Neural networks for the processing of appetitive and aversive information, in isolation, have been well characterized. However, how the brain integrates competing signals associated with simultaneous appetitive and aversive information is less clear. In particular, it is unknown how the presence of concurrent reward modulates the processing of an aversive event throughout the brain. Here, we utilized a four-armed bandit task in an fMRI study to measure the representation of an aversive electric shock with and without the simultaneous receipt of monetary reward. Using a region of interest (ROI) approach, we first identified regions activated by the experience of aversive electric shock, and then measured how this shock-related activation is modulated by concurrent reward using independent data. Informed by prior literature and our own preliminary data, analyses focused on the dorsolateral prefrontal cortex, anterior and posterior insula, anterior cingulate cortex, and the thalamus and somatosensory cortex. We hypothesized that the neural response to punishment in these ROIs would be attenuated by the presence of concurrent reward. However, we found no evidence of concurrent reward attenuating the neural response to punishment in any ROI and also no evidence of concurrent punishment attenuating the neural response to reward in exploratory analyses. Altogether, our findings are consistent with the idea that neural networks responsible for the processing of reward and punishment signals are largely independent of one another, and that representations of overall value or utility are arrived at through the integration of separate reward and punishment signals at later stages of information processing.