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32,513,671 | 10.1101/cshperspect.a039792 | 2,020 | Cold Spring Harbor perspectives in medicine | Cold Spring Harb Perspect Med | Developments from Bulk Optogenetics to Single-Cell Strategies to Dissect the Neural Circuits that Underlie Aberrant Motivational States. | Motivational states are regulated by complex networks across brain regions that are composed of genetically and functionally distinct neuronal populations. Disruption within these neural circuits leads to aberrant motivational states and are thought to be the root cause of psychiatric disorders related to reward processing and addiction. Critical technological advances in the field have revolutionized the study of neural systems by allowing the use of optical strategies to precisely control and visualize neural activity within genetically identified neural populations in the brain. This review will provide a brief introduction into the history of how technological advances in single-cell strategies have been applied to elucidate the neural circuits that underlie aberrant motivational states that often lead to dysfunction in reward processing and addiction. | CognitiveConstruct | RewardProcessing |
32,512,130 | 10.1016/j.pnpbp.2020.110000 | 2,020 | Progress in neuro-psychopharmacology & biological psychiatry | Prog Neuropsychopharmacol Biol Psychiatry | Brain stimulation rewarding experience attenuates neonatal clomipramine-induced adulthood anxiety by reversal of pathological changes in the amygdala. | Major depressive disorder (MDD) is associated with enhanced anxiety and reduced reward processing leading to impaired cognitive flexibility. These pathological changes during depression are accompanied by dysfunctional hypothalamic-pituitary-adrenal (HPA) axis and its impaired regulation by the amygdala. Notably, the electrical stimulation of brain reward areas produces an antidepressant effect in both MDD patients and animal models of depression. However, the effects of chronic electrical self-stimulation of lateral hypothalamus - medial forebrain bundle (LH-MFB) on depression-associated anxiety and accompanying changes in plasma corticosterone levels, structural, and neurochemical alterations in the amygdala are unknown. Here, we used the neonatal clomipramine (CLI) model of depression. During adulthood, neonatal CLI and vehicle administered rats were subjected to bilateral electrode implantation at LH-MFB and trained to receive intracranial self-stimulation (ICSS) for 14 days. Rats were then tested for anhedonic and anxiety-like behaviors, followed by estimation of plasma corticosterone levels, assessment of amygdalar volumes and neuronal/glial numbers, levels of monoamines and their metabolites in the amygdala. We found that chronic ICSS of LH-MFB reverses CLI-induced anhedonia and anxiety. Interestingly, amelioration of CLI-induced enhanced anhedonia and anxiety in ICSS rats was associated with partial reversal of enhanced plasma corticosterone levels, hypertrophy of basolateral amygdala (BLA), and altered noradrenaline (NA) metabolism in the amygdalar complex. We suggest that beneficial effects of ICSS on CLI-induced anxiety at least in part mediated by the restoration of amygdalar and HPA axis functioning. Our results support the hypothesis that brain stimulation rewarding experience might be evolved as a therapeutic strategy for reversal of amygdalar dysfunction in depression. | CognitiveConstruct | RewardProcessing |
32,507,389 | 10.1016/j.biopsych.2020.04.009 | 2,020 | Biological psychiatry | Biol Psychiatry | Pretreatment Reward Sensitivity and Frontostriatal Resting-State Functional Connectivity Are Associated With Response to Bupropion After Sertraline Nonresponse. | Standard guidelines recommend selective serotonin reuptake inhibitors as first-line antidepressants for adults with major depressive disorder, but success is limited and patients who fail to benefit are often switched to non-selective serotonin reuptake inhibitor agents. This study investigated whether brain- and behavior-based markers of reward processing might be associated with response to bupropion after sertraline nonresponse. In a two-stage, double-blinded clinical trial, 296 participants were randomized to receive 8 weeks of sertraline or placebo in stage 1. Individuals who responded continued on another 8-week course of the same intervention in stage 2, while sertraline and placebo nonresponders crossed over to bupropion and sertraline, respectively. Data from 241 participants were analyzed. The stage 2 sample comprised 87 patients with major depressive disorder who switched medication and 38 healthy control subjects. A total of 116 participants with major depressive disorder treated with sertraline in stage 1 served as an independent replication sample. The probabilistic reward task and resting-state functional magnetic resonance imaging were administered at baseline. Greater pretreatment reward sensitivity and higher resting-state functional connectivity between bilateral nucleus accumbens and rostral anterior cingulate cortex were associated with positive response to bupropion but not sertraline. Null findings for sertraline were replicated in the stage 1 sample. Pretreatment reward sensitivity and frontostriatal connectivity may identify patients likely to benefit from bupropion following selective serotonin reuptake inhibitor failures. Results call for a prospective replication based on these biomarkers to advance clinical care. | CognitiveConstruct | RewardProcessing |
32,502,903 | 10.1016/j.cortex.2020.01.030 | 2,020 | Cortex; a journal devoted to the study of the nervous system and behavior | Cortex | Self-centered or other-directed: Neural correlates of performance monitoring are dependent on psychopathic traits and social context. | Performing in a social context can result in negative feelings when our actions harm another person, but it can also lead to positive feelings when observing an opponent fail. The extent to which individuals scoring high on psychopathic traits, often characterized as self-centered with reduced concern for others' welfare, are sensitive to own and others' success and failure is yet unknown. However, knowledge about these processes is crucial for comprehending how these traits are involved in understanding ourselves and others during social interactions. In this functional magnetic resonance imaging (fMRI) study, healthy females scoring low or high on psychopathic traits performed a cannon-shooting game in non-social, cooperative, and competitive contexts. We hypothesized group differences regarding: (1) monitoring of own actions in a non-social context (errors that only negatively affect oneself) versus cooperative context (errors that also harm others), (2) successfully performing with either positive (shared gain) or negative consequences (selfish gain) for the co-player, and (3) observing other's performance leading to shared or selfish gain for oneself. Decreased performance-monitoring-related activations were found in posterior medial frontal cortex for females scoring high on psychopathic traits in the social versus non-social context. When observing others, striatal activations were stronger for selfish gains for high scorers and for shared gains for low scorers. The current outcomes demonstrate that performance-monitoring and reward-related brain activations importantly depend on the interplay between psychopathic traits and social context. We propose that these neural mechanisms may underlie the more self-centered behavior of individuals scoring high on psychopathic traits. As such, the current findings may open up new research avenues, which could advance our understanding of how personality traits impact performance monitoring in a wide variety of social contexts and could possibly lead to the development of interventions aimed at normalizing reduced concern for others. | CognitiveConstruct | RewardProcessing |
32,496,090 | 10.1037/xge0000769 | 2,021 | Journal of experimental psychology. General | J Exp Psychol Gen | How adolescents and adults translate motivational value to action: Age-related shifts in strategic physical effort exertion for monetary rewards. | Adults titrate the degree of physical effort they are willing to expend according to the magnitude of reward they expect to obtain, a process guided by incentive motivation. However, it remains unclear whether adolescents, who are undergoing normative developmental changes in cognitive and reward processing, translate incentive motivation into action in a way that is similarly tuned to reward value and economical in effort utilization. The present study adapted a classic physical effort paradigm to quantify age-related changes in motivation-based and strategic markers of effort exertion for monetary rewards from adolescence to early adulthood. One hundred three participants aged 12-23 years completed a task that involved exerting low or high amounts of physical effort, in the form of a hand grip, to earn low or high amounts of money. Adolescents and young adults exhibited highly similar incentive-modulated effort for reward according to measures of peak grip force and speed, suggesting that motivation for monetary reward is consistent across age. However, young adults expended energy more economically and strategically: Whereas adolescents were prone to exert excess physical effort beyond what was required to earn reward, young adults were more likely to strategically prepare before each grip phase and conserve energy by opting out of low reward trials. This work extends theoretical models of development of incentive-driven behavior by demonstrating that layered on similarity in motivational value for monetary reward, there are important differences in the way behavior is flexibly adjusted in the presence of reward from adolescence to young adulthood. (PsycInfo Database Record (c) 2021 APA, all rights reserved). | CognitiveConstruct | RewardProcessing |
32,488,083 | 10.1038/s41398-020-0824-8 | 2,020 | Translational psychiatry | Transl Psychiatry | Neural responsivity to social rewards in autistic female youth. | Autism is hypothesized to be in part driven by a reduced sensitivity to the inherently rewarding nature of social stimuli. Previous neuroimaging studies have indicated that autistic males do indeed display reduced neural activity to social rewards, but it is unknown whether this finding extends to autistic females, particularly as behavioral evidence suggests that affected females may not exhibit the same reduction in social motivation as their male peers. We therefore used functional magnetic resonance imaging to examine social reward processing during an instrumental implicit learning task in 154 children and adolescents (ages 8-17): 39 autistic girls, 43 autistic boys, 33 typically developing girls, and 39 typically developing boys. We found that autistic girls displayed increased activity to socially rewarding stimuli, including greater activity in the nucleus accumbens relative to autistic boys, as well as greater activity in lateral frontal cortices and the anterior insula compared with typically developing girls. These results demonstrate for the first time that autistic girls do not exhibit the same reduction in activity within social reward systems as autistic boys. Instead, autistic girls display increased neural activation to such stimuli in areas related to reward processing and salience detection. Our findings indicate that a reduced sensitivity to social rewards, as assessed with a rewarded instrumental implicit learning task, does not generalize to affected female youth and highlight the importance of studying potential sex differences in autism to improve our understanding of the condition and its heterogeneity. | CognitiveConstruct | RewardProcessing |
32,472,419 | 10.3758/s13415-020-00804-6 | 2,020 | Cognitive, affective & behavioral neuroscience | Cogn Affect Behav Neurosci | Characterizing anhedonia: A systematic review of neuroimaging across the subtypes of reward processing deficits in depression. | Anhedonia is a key symptom of major depressive disorder (MDD) and comprises behavioural deficits in three reward processing subtypes: reward liking, reward wanting, and reward learning. However, neuroimaging findings regarding the neural abnormalities underpinning these deficits are complex. We have conducted a systematic review to update, reframe and summarize neuroimaging findings across the three subtypes of anhedonia in MDD. Using PubMed, The Cochrane Library, PsycINFO, and Web of Science databases, we identified 59 fMRI studies comparing participants with current or remitted MDD with controls, using reward processing tasks. For reward liking and wanting, striatal hypoactivation was observed, alongside hypoactivation and hyperactivation across frontal regions. For reward learning, blunted frontostriatal sensitivity to positive feedback was observed. These findings highlight the importance of studying anhedonia not only as a clinical manifestation but also as a neurobiological mechanism underlying depressive disorder and other broader psychiatric conditions. | CognitiveConstruct | RewardProcessing |
32,469,991 | 10.1371/journal.pone.0233780 | 2,020 | PloS one | PLoS One | Neurobiological influence of comorbid conditions in young patients diagnosed with gaming disorder: A whole-brain functional connectivity study based on a data driven method. | Gaming disorder, which is characterized by multiple cognitive and behavioral symptoms, often has comorbid psychiatric conditions such as depression and attention-deficit hyperactivity disorder. Neurobiological effects of the comorbid disorders so far reported are not converging, exhibiting positive and negative alterations of the connectivity in brain networks. In this study, we conducted resting-state functional magnetic-resonance imaging and whole brain functional connectivity analyses for young participants consisting of 40 patients diagnosed with the gaming disorder, with and without comorbid conditions, and 29 healthy controls. Compared to healthy controls, the gaming disorder-alone patients had partially diminished connectivities in the reward system and executive control network, within which there existed central nodes that served as a hub of diminished connections. In the gaming disorder patients who had comorbidity of autism spectrum disorder, the diminished connections were enlarged, with alteration of the hub nodes, to the entire brain areas involved in the reward system including cortical, subcortical and limbic areas that are crucial for reward processing, and to the whole cortical areas composing the executive control network. These observations suggest that the neurodevelopmental condition coexisting with the gaming disorder induced substantial impairment of the neural organizations associated with executive/cognitive and emotional functions, which are plausibly causal to the behavioral addiction, by rearranging and diminishing functional connectivities in the network. | CognitiveConstruct | RewardProcessing |
32,468,889 | 10.1177/1087054720923094 | 2,021 | Journal of attention disorders | J Atten Disord | Transcranial Direct Current Stimulation Improves Reward Processing in Children With ADHD. | Individuals with ADHD have deficits in reward processing and related cognitive tasks such as delay discounting and risky decision-making. The ventromedial prefrontal cortex (vmPFC) and dorsolateral prefrontal cortex (dlPFC) are two distinct cortical areas that are involved in reward processing. Twenty children with ADHD received transcranial direct current stimulation (tDCS) in three separate sessions with one of three montages each, including anodal/cathodal tDCS over the left dlPFC and right vmPFC respectively, the reversed montage, and a sham stimulation condition. During stimulation, in each session, participants performed the balloon analogue risk taking and chocolate delay discounting tasks. A significant effect of stimulation condition on emotional processing was observed. Specifically, anodal tDCS over the right vmPFC, coupled with cathodal tDCS over the left dlPFC, reduced risky decision-making and delay discounting. These results imply that the left dlPFC and right vmPFC are involved in reward processing in children with ADHD. This finding is discussed in the light of the delay aversion theory of ADHD. | CognitiveConstruct | RewardProcessing |
32,456,851 | 10.1016/j.euroneuro.2020.04.006 | 2,020 | European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology | Eur Neuropsychopharmacol | Cognitive modelling to assess decision-making impairments in patients with current depression and with/without suicide history. | It has been reported that decision making is impaired in suicide attempters. Decision making is a complex process and little is known about its different components. Yet, this information would help to understand the functioning of suicidal minds. In this study, the Prospect Valence-Learning (PVL) computational model was applied to the Iowa Gambling Task (IGT) to investigate and compare decision-making components in patients with affective disorder and with/without history of suicide attempts and in healthy controls. To this aim, 116 inpatients with current major depressive episode (among whom 62 suicide attempters) and 38 healthy controls were recruited. Decision-making performance was measured using the IGT. The Bayesian computational PVL model was applied to compare the feedback sensitivity, loss aversion, learning/memory, and choice consistency components of decision making in the different groups. Depressive symptomatology was assessed using the Beck Depression Inventory short form (BDI-SF). The total IGT net score and the loss aversion and learning/memory scores were lower in suicide attempters than in healthy controls. The choice consistency score was low in all patients (with/without suicide history) compared with healthy controls. Moreover, patients with high BDI score showed a positive relationship between the choice consistency score and suicide attempt. These findings suggest that decision-making impairment in depressed patients with and without suicidal history might be the result of underlying problems in feedback processing and task learning, which influence the building of long-term strategies. All these impairments should be targeted in therapeutic strategies for suicidal patients. | CognitiveConstruct | RewardProcessing |
32,451,322 | 10.1523/JNEUROSCI.2841-19.2020 | 2,020 | The Journal of neuroscience : the official journal of the Society for Neuroscience | J Neurosci | Behavioral and Neural Signatures of Working Memory in Childhood. | Working memory function changes across development and varies across individuals. The patterns of behavior and brain function that track individual differences in working memory during human development, however, are not well understood. Here, we establish associations between working memory, other cognitive abilities, and functional MRI (fMRI) activation in data from over 11,500 9- to 10-year-old children (both sexes) enrolled in the Adolescent Brain Cognitive Development (ABCD) Study, an ongoing longitudinal study in the United States. Behavioral analyses reveal robust relationships between working memory, short-term memory, language skills, and fluid intelligence. Analyses relating out-of-scanner working memory performance to memory-related fMRI activation in an emotional -back task demonstrate that frontoparietal activity during a working memory challenge indexes working memory performance. This relationship is domain specific, such that fMRI activation related to emotion processing during the emotional -back task, inhibitory control during a stop-signal task (SST), and reward processing during a monetary incentive delay (MID) task does not track memory abilities. Together, these results inform our understanding of individual differences in working memory in childhood and lay the groundwork for characterizing the ways in which they change across adolescence. Working memory is a foundational cognitive ability that changes over time and varies across individuals. Here, we analyze data from over 11,500 9- to 10-year-olds to establish relationships between working memory, other cognitive abilities, and frontoparietal brain activity during a working memory challenge, but not during other cognitive challenges. Our results lay the groundwork for assessing longitudinal changes in working memory and predicting later academic and other real-world outcomes. | CognitiveConstruct | RewardProcessing |
32,440,002 | 10.1038/s41598-020-65345-x | 2,020 | Scientific reports | Sci Rep | Autistic Traits Affect Reward Anticipation but not Reception. | Autism spectrum conditions (ASC) have been linked to aberrant reward processing, but it remains unclear whether it is a general dysfunction or limited to social stimuli, and whether it affects both phases of reward processing, namely anticipation and reception. We used event-related brain potentials and a population-based approach to investigate reward anticipation and reception to socially relevant (i.e., picture of experimenter's face showing approval/disapproval) and monetary rewards in 51 neurotypical individuals with varying levels of autistic traits. Higher autistic traits were associated with enhanced reward anticipation across reward types in the early anticipation phase (triggered by incentive cues), but not in the late anticipation phase (directly before reward reception), as reflected by the CNV component. The P3 component in response to reward reception showed a general increase for monetary outcomes, which was not modulated by autistic traits. These results suggest that higher autistic traits are related to enhanced reward anticipation, but do not modulate reward reception. No interaction between reward types and autistic traits was observed. We propose that the relevance of social rewards had higher reward value than commonly used pictures of strangers, which specifically normalised responses for individuals with high autistic traits. | CognitiveConstruct | RewardProcessing |
32,437,204 | 10.1037/abn0000528 | 2,020 | Journal of abnormal psychology | J Abnorm Psychol | Sacrificing reward to avoid threat: Characterizing PTSD in the context of a trauma-related approach-avoidance conflict task. | Posttraumatic stress disorder (PTSD) is characterized by heightened avoidance, cognitive inflexibility, and impaired reward processing. Maladaptive behavior in PTSD may reflect an imbalance between approach and avoidance, but no research has investigated approach-avoidance conflict (AAC) in PTSD. The current study investigated approach-avoidance behavior in PTSD using a trauma-related AAC (trAAC) task in two independent samples. In Study 1, 43 women with a current diagnosis of PTSD and 18 healthy comparison subjects were recruited from the community. In Study 2, 53 women with trauma exposure and a range of PTSD symptoms were recruited from a correctional institution. Trials were separated into two phases: conflict (the option most likely to win points was most likely to show a trauma-related image) and congruent (the option most likely to win points was least likely to show a trauma-related image). In Study 1, reward obtainment varied with the task manipulation (i.e., fewer points earned during conflict compared to congruent Phase) in PTSD but not healthy subjects. These results indicate that when avoidance is advantageous (congruent phase), individuals with PTSD show increased task performance, whereas when avoidance is maladaptive (conflict phase), individuals with PTSD show increased sacrifice of reward. In Study 2, higher PTSD symptoms predicted decreased reward earning during the conflict phase, again indicating a sacrifice of reward when avoidance is maladaptive. Across both studies, PTSD associated with increased AAC and sacrifice of reward in the presence of trauma-related stimuli. These studies shed light on AAC in PTSD and could inform more targeted therapy approaches. (PsycInfo Database Record (c) 2020 APA, all rights reserved). | CognitiveConstruct | RewardProcessing |
32,436,626 | 10.1111/adb.12919 | 2,021 | Addiction biology | Addict Biol | Increased striatal functional connectivity is associated with improved smoking cessation outcomes: A preliminary study. | The striatum is the critical area of reward processing and has been repeatedly linked to nicotine addiction. However, it remains unclear whether different smoking cessation outcomes (relapse or not) are associated with different functional connectivity changes of the striatum during smoking cessation treatment. A total of 30 treatment-seeking smokers were recruited in the study and underwent magnetic resonance imaging (MRI) scans immediately before and after a 12-week treatment with varenicline. After the 12-week treatment with varenicline, 14 subjects relapsed to smoking (relapsers), whereas 16 not relapsed (nonrelapsers). Changes in resting-state functional connectivity (rsFC) across groups and visits were assessed using repeated measures analysis of covariance (ANCOVA). Significant interaction effects were detected: (1) between left nucleus accumbens (NAc) and left orbitofrontal cortex (OFC), insula, inferior frontal gyrus (IFG), and bilateral precuneus; (2) between right NAc and left insula, IFG, and bilateral dorsolateral prefrontal cortex (DLPFC); and (3) between bilateral putamen and left precuneus. Post hoc region-of-interest analyses in brain areas showing interaction effects indicated significantly decreased rsFC after treatment compared with before treatment in relapsers but opposite longitudinal changes in nonrelapers. These novel findings suggest that increased striatal rsFC is associated with improved smoking cessation outcomes. These striatal functional circuits may serve as potential therapeutic targets for more efficacious treatment of nicotine addiction. | CognitiveConstruct | RewardProcessing |
32,435,818 | 10.1007/s00213-020-05541-9 | 2,020 | Psychopharmacology | Psychopharmacology (Berl) | Comparison of acute treatment with delayed-onset versus rapid-acting antidepressants on effort-related choice behaviour. | Reward-related impairments are common in major depressive disorder (MDD) and may contribute to the loss of interest in pleasurable activities. A novel approach to studying reward-related decision-making are effort-based tasks; however, direct comparisons between delayed-onset and rapid-acting antidepressants (ADs) have not yet been carried out. To investigate the effects of conventional delayed-onset ADs versus rapid-acting ADs, ketamine and scopolamine, on effort-related choice behaviour. Female Lister hooded rats were trained in an operant effort for reward task (EfRT) where animals choose between working for a high value-high effort reward and consuming low value-low effort chow. Using a within-subject study design, animals were then tested following acute treatment with different monoaminergic ADs, and the rapid-acting ADs ketamine or scopolamine. Consistent with previous findings, we found choice behaviour was sensitive to dopaminergic manipulations. We observed that pre-feeding altered choice behaviour and that the use of high or low value reward differentially affected behaviour. Monoamine re-uptake inhibitors and rapid-acting ADs resulted in similar, general patterns of reduced motivation without any evidence for specific effects, and we did not observe any clear differences between these classes of antidepressant. Motivational changes induced by dopaminergic manipulations and pre-feeding differentially affect effort choice behaviour. However, both conventional delayed-onset ADs and ketamine and scopolamine appear to have detrimental effects on motivation in this task at the higher doses tested without any evidence of specificity for effort-related choice behaviour, in contrast to their specificity in tasks which look at more cognitive aspects of reward processing. | CognitiveConstruct | RewardProcessing |
32,430,200 | 10.1016/j.biopsych.2020.03.012 | 2,020 | Biological psychiatry | Biol Psychiatry | Aberrant Salience, Information Processing, and Dopaminergic Signaling in People at Clinical High Risk for Psychosis. | The aberrant salience hypothesis proposes that striatal dopamine dysregulation causes misattribution of salience to irrelevant stimuli leading to psychosis. Recently, new lines of preclinical evidence on information coding by subcortical dopamine coupled with computational models of the brain's ability to predict and make inferences about the world (predictive processing) provide a new perspective on this hypothesis. We review these and summarize the evidence for dopamine dysfunction, reward processing, and salience abnormalities in people at clinical high risk of psychosis (CHR) relative to findings in patients with psychosis. This review identifies consistent evidence for dysregulated subcortical dopamine function in people at CHR, but also indicates a number of areas where neurobiological processes are different in CHR subjects relative to patients with psychosis, particularly in reward processing. We then consider how predictive processing models may explain psychotic symptoms in terms of alterations in prediction error and precision signaling using Bayesian approaches. We also review the potential role of environmental risk factors, particularly early adverse life experiences, in influencing the prior expectations that individuals have about their world in terms of computational models of the progression from being at CHR to frank psychosis. We identify a number of key outstanding questions, including the relative roles of prediction error or precision signaling in the development of symptoms and the mechanism underlying dopamine dysfunction. Finally, we discuss how the integration of computational psychiatry with biological investigation may inform the treatment for people at CHR of psychosis. | CognitiveConstruct | RewardProcessing |
32,428,002 | 10.1371/journal.pone.0232813 | 2,020 | PloS one | PLoS One | Effects of hunger on mood and affect reactivity to monetary reward in women with obesity - A pilot study. | Worldwide, nearly 3 million people die every year because of being overweight or obese. Although obesity is a metabolic disease, behavioral aspects are important in its etiology. Hunger changes the rewarding potential of food in normal-weight controls. In obesity, impairments related to reward processing are present, but it is not clear whether these are due to mental disorders more common among this population. Therefore, in this pilot study, we aimed at investigating whether fasting influence mood reactivity to reward in people with obesity. Women with obesity (n = 11, all mentally healthy) and normal weight controls (n = 17) were compared on a computerized monetary reward task (the wheel of fortune), using self-reports of mood and affect (e.g., PANAS and mood evaluation during the task) as dependent variables. This task was done in 2 satiety conditions, during fasting and after eating. Partially, in line with our expectation of a reduced affect and mood reactivity to monetary reward in participants with obesity accentuated by fasting, our results indicated a significant within-group difference across time (before and after the task), with monetary gains significantly improving positive affect in healthy controls (p>0.001), but not in individuals with obesity (p = 0.32). There were no significant between-group differences in positive affect before (p = 0.328) and after (p = 0.70) the task. In addition, women with obesity, compared to controls, reported more negative affect in general (p < 0.05) and less mood reactivity during the task in response to risky gains (p < 0.001) than healthy controls. The latter was independent of the level of satiety. These preliminary results suggest an impairment in mood reactivity to monetary reward in women with obesity which is not connected to the fasting state. Increasing the reinforcing potential of rewards other than food in obesity may be one target of intervention in order to verify if that could reduce overeating. | CognitiveConstruct | RewardProcessing |
32,424,057 | 10.1523/ENEURO.0061-20.2020 | 2,020 | eNeuro | eNeuro | Differential Rapid Plasticity in Auditory and Visual Responses in the Primarily Multisensory Orbitofrontal Cortex. | Given the connectivity of orbitofrontal cortex (OFC) with the sensory areas and areas involved in goal execution, it is likely that OFC, along with its function in reward processing, also has a role to play in perception-based multisensory decision-making. To understand mechanisms involved in multisensory decision-making, it is important to first know the encoding of different sensory stimuli in single neurons of the mouse OFC. Ruling out effects of behavioral state, memory, and others, we studied the anesthetized mouse OFC responses to auditory, visual, and audiovisual/multisensory stimuli, multisensory associations and sensory-driven input organization to the OFC. Almost all, OFC single neurons were found to be multisensory in nature, with sublinear to supralinear integration of the component unisensory stimuli. With a novel multisensory oddball stimulus set, we show that the OFC receives both unisensory as well as multisensory inputs, further corroborated by retrograde tracers showing labeling in secondary auditory and visual cortices, which we find to also have similar multisensory integration and responses. With long audiovisual pairing/association, we show rapid plasticity in OFC single neurons, with a strong visual bias, leading to a strong depression of auditory responses and effective enhancement of visual responses. Such rapid multisensory association driven plasticity is absent in the auditory and visual cortices, suggesting its emergence in the OFC. Based on the above results, we propose a hypothetical local circuit model in the OFC that integrates auditory and visual information which participates in computing stimulus value in dynamic multisensory environments. | CognitiveConstruct | RewardProcessing |
32,423,530 | 10.7554/eLife.50654 | 2,020 | eLife | Elife | Alterations in the amplitude and burst rate of beta oscillations impair reward-dependent motor learning in anxiety. | Anxiety results in sub-optimal motor learning, but the precise mechanisms through which this effect occurs remain unknown. Using a motor sequence learning paradigm with separate phases for initial exploration and reward-based learning, we show that anxiety states in humans impair learning by attenuating the update of reward estimates. Further, when such estimates are perceived as unstable over time (volatility), anxiety constrains adaptive behavioral changes. Neurally, anxiety during initial exploration increased the amplitude and the rate of long bursts of sensorimotor and prefrontal beta oscillations (13-30 Hz). These changes extended to the subsequent learning phase, where phasic increases in beta power and burst rate following reward feedback were linked to smaller updates in reward estimates, with a higher anxiety-related increase explaining the attenuated belief updating. These data suggest that state anxiety alters the dynamics of beta oscillations during reward processing, thereby impairing proper updating of motor predictions when learning in unstable environments. | CognitiveConstruct | RewardProcessing |
32,420,985 | 10.3791/60886 | 2,020 | Journal of visualized experiments : JoVE | J Vis Exp | Combined Infusion and Stimulation with Fast-Scan Cyclic Voltammetry (CIS-FSCV) to Assess Ventral Tegmental Area Receptor Regulation of Phasic Dopamine. | Phasic dopamine (DA) release from the ventral tegmental area (VTA) to the nucleus accumbens plays a pivotal role in reward processing and reinforcement learning. Understanding how the diverse neuronal inputs into the VTA control phasic DA release can provide a better picture of the circuitry that controls reward processing and reinforcement learning. Here, we describe a method that combines intra-VTA cannula infusions of pharmacological agonists and antagonists with stimulation-evoked phasic DA release (combined infusion and stimulation, or CIS) as measured by in vivo fast-scan cyclic voltammetry (FSCV). Using CIS-FSCV in anesthetized rats, a phasic DA response can be evoked by electrically stimulating the VTA with a bipolar electrode fitted with a cannula while recording in the nucleus accumbens core. Pharmacological agonists or antagonists can be infused directly at the stimulation site to investigate specific VTA receptors' roles in driving phasic DA release. A major benefit of CIS-FSCV is that VTA receptor function can be studied in vivo, building on in vitro studies. | CognitiveConstruct | RewardProcessing |
32,405,316 | 10.5334/jcr.193 | 2,020 | Journal of circadian rhythms | J Circadian Rhythms | Diurnal Preference and Grey Matter Volume in a Large Population of Older Adults: Data from the UK Biobank. | Eveningness (a diurnal preference for evening time) is associated with a number of negative health outcomes and risk and prevalence for psychiatric disorder. Our understanding of the anatomical substrates of diurnal preference, however, is limited. The current study used Voxel-Based Morphometry to compare grey matter volume in a large sample ( = 3730) of healthy adults determined by questionnaire to be either definite morning-type or definite evening-type. Eveningness was associated with increased grey matter volume in precuneus, brain regions implicated in risk and reward processing (bilateral nucleus accumbens, caudate, putamen and thalamus) and orbitofrontal cortex. These results indicate an anatomical-basis for diurnal preference which may underlie reported differences in behaviour and brain function observed in these individuals. | CognitiveConstruct | RewardProcessing |
32,397,250 | 10.3390/brainsci10050283 | 2,020 | Brain sciences | Brain Sci | Event-Related Potentials (ERP) Indices of Motivation during the Effort Expenditure for Reward Task. | Dynamic and temporal facets of the various constructs that comprise motivation remain to be explored. Here, we adapted the Effort Expenditure for Reward Task, a well-known laboratory task used to evaluate motivation, to study the event-related potentials associated with reward processing. The Stimulus Preceding Negativity (SPN) and the P300 were utilized as motivation indicators with high density electroencephalography. The SPN was found to be more negative for difficult choices compared to easy choices, suggesting a greater level of motivation, at a neurophysiological level. The insula, a structure previously associated with both effort discounting and prediction error, was concomitantly activated during the generation of the SPN. Processing a gain significantly altered the amplitude of the P300 compared to an absence of gain, particularly on centroparietal electrodes. One of the generators of the P300 was located on the vmPFC, a cerebral structure involved in the choice between two positive results and their predictions, during loss processing. Both the SPN and the P300 appear to be reliable neural markers of motivation. We postulate that the SPN represents the strength of the motivational level, while the P300 represents the impact of motivation on updating memories of the feedback. | CognitiveConstruct | RewardProcessing |
32,393,358 | 10.1186/s12888-020-02541-z | 2,020 | BMC psychiatry | BMC Psychiatry | The biological classification of mental disorders (BeCOME) study: a protocol for an observational deep-phenotyping study for the identification of biological subtypes. | A major research finding in the field of Biological Psychiatry is that symptom-based categories of mental disorders map poorly onto dysfunctions in brain circuits or neurobiological pathways. Many of the identified (neuro) biological dysfunctions are "transdiagnostic", meaning that they do not reflect diagnostic boundaries but are shared by different ICD/DSM diagnoses. The compromised biological validity of the current classification system for mental disorders impedes rather than supports the development of treatments that not only target symptoms but also the underlying pathophysiological mechanisms. The Biological Classification of Mental Disorders (BeCOME) study aims to identify biology-based classes of mental disorders that improve the translation of novel biomedical findings into tailored clinical applications. BeCOME intends to include at least 1000 individuals with a broad spectrum of affective, anxiety and stress-related mental disorders as well as 500 individuals unaffected by mental disorders. After a screening visit, all participants undergo in-depth phenotyping procedures and omics assessments on two consecutive days. Several validated paradigms (e.g., fear conditioning, reward anticipation, imaging stress test, social reward learning task) are applied to stimulate a response in a basic system of human functioning (e.g., acute threat response, reward processing, stress response or social reward learning) that plays a key role in the development of affective, anxiety and stress-related mental disorders. The response to this stimulation is then read out across multiple levels. Assessments comprise genetic, molecular, cellular, physiological, neuroimaging, neurocognitive, psychophysiological and psychometric measurements. The multilevel information collected in BeCOME will be used to identify data-driven biologically-informed categories of mental disorders using cluster analytical techniques. The novelty of BeCOME lies in the dynamic in-depth phenotyping and omics characterization of individuals with mental disorders from the depression and anxiety spectrum of varying severity. We believe that such biology-based subclasses of mental disorders will serve as better treatment targets than purely symptom-based disease entities, and help in tailoring the right treatment to the individual patient suffering from a mental disorder. BeCOME has the potential to contribute to a novel taxonomy of mental disorders that integrates the underlying pathomechanisms into diagnoses. Retrospectively registered on June 12, 2019 on ClinicalTrials.gov (TRN: NCT03984084). | CognitiveConstruct | RewardProcessing |
32,392,573 | 10.1038/s41386-020-0702-3 | 2,020 | Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology | Neuropsychopharmacology | The role of dopaminergic and serotonergic transmission in the processing of primary and monetary reward. | Natural rewards such as erotic stimuli activate common neural pathways with monetary rewards. In human studies, the manipulation of dopamine and serotonin play an important role in the processing of monetary rewards with less understood on its role on erotic stimuli. In this study, we investigate the neuromodulatory effects of dopaminergic and serotonergic transmission in the processing of erotic versus monetary visual stimuli. We scanned one hundred and two (N = 102) healthy volunteers using functional magnetic resonance imaging while performing a modified version of the well-validated monetary incentive delay task consisting of erotic, monetary and neutral visual stimuli. We show a role for enhanced central dopamine and lowered central serotonin levels in increasing activity in the right caudate and left anterior insula during anticipation of erotic relative to monetary rewards in healthy controls. We further show differential activation in the anticipation of natural versus monetary rewards with the former associated with ventromesial and dorsomesial activity and the latter with dorsal cingulate, striatal and anterior insular activity. These findings are consistent with preclinical and clinical findings of a role for dopaminergic and serotonergic mechanisms in the processing of natural rewards. Our study provides further insights into the neural substrates underlying reward processing for natural primary erotic rewards and yields importance for the neurochemical systems of addictive disorders including gambling disorder. | CognitiveConstruct | RewardProcessing |
32,390,943 | 10.3389/fendo.2020.00231 | 2,020 | Frontiers in endocrinology | Front Endocrinol (Lausanne) | Avoidance Learning Across the Menstrual Cycle: A Conceptual Replication. | Hormonal transitions across the menstrual cycle may modulate human reward processing and reinforcement learning, but previous results were contradictory. Studies assessed relatively small samples ( < 30) and exclusively used within-subject designs to compare women in hormonally distinct menstrual cycle phases. This increased the risk of sporadic findings and results may have been disproportionally affected by expectancy effects. Also, replication studies are widely missing, which currently precludes any reliable inferences. The present study was intended as a conceptual replication of a previous study [(1), Neuropsychologia 84; = 15]. There, we had observed a reduction in avoidance learning capacity when women were in the high estradiol state of the late follicular phase as compared to the mid luteal phase with enhanced progesterone influence. These results conformed to the idea that estradiol and progesterone may antagonistically modulate dopaminergic transmission as a dopamine agonist and antagonist, respectively. Heightened progesterone in the luteal phase thereby supported the ability to learn from the negative outcomes of one's actions, while the follicular rise in estradiol interfered with this capacity. Here, we re-examined the above described within-subject difference between the follicular and the luteal phase in a between-subjects design. Seventy-five women were tested once with a probabilistic feedback learning task, while being either in the follicular (36 women) or luteal phase (39 women), and were compared for phase-related differences in behavior. Secondly, we combined the new data with data from three previous studies from our laboratory that used the same task and menstrual cycle phases. This meta-analysis included only data from the first test day, free of any biasing expectancy effects. Both analyses demonstrated the consistency of the decline in avoidance learning in the follicular relative to the luteal phase. We also showed that this decline reliably occurred in all of the included samples. Altogether, these results provide evidence for the consistency of a behavioral difference and its apparent association with a transient change in hormonal state that occurs in the natural menstrual cycle. Our findings may also open new avenues for the development of reliable between-subjects test protocols in menstrual cycle research. | CognitiveConstruct | RewardProcessing |
32,381,649 | 10.1523/ENEURO.0433-19.2020 | 2,020 | eNeuro | eNeuro | Targeting Morphine-Responsive Neurons: Generation of a Knock-In Mouse Line Expressing Cre Recombinase from the Mu-Opioid Receptor Gene Locus. | The mu-opioid receptor (MOR) modulates nociceptive pathways and reward processing, and mediates the strong analgesic and addictive properties of both medicinal as well as abused opioid drugs. MOR function has been extensively studied, and tools to manipulate or visualize the receptor protein are available. However, circuit mechanisms underlying MOR-mediated effects are less known, because genetic access to MOR-expressing neurons is lacking. Here we report the generation of a knock-in -Cre mouse line, which allows targeting and manipulating MOR opioid-responsive neurons. A cDNA encoding a T2A cleavable peptide and Cre recombinase fused to enhanced green fluorescent protein (EGFP/Cre) was inserted downstream of the gene sequence. The resulting Cre line shows intact gene transcription. MOR and EGFP/Cre proteins are coexpressed in the same neurons, and localized in cytoplasmic and nuclear compartments, respectively. MOR signaling is unaltered, demonstrated by maintained DAMGO-induced G-protein activation, and MOR function is preserved as indicated by normal morphine-induced analgesia, hyperlocomotion, and sensitization. The Cre recombinase efficiently drives the expression of Cre-dependent reporter genes, shown by local virally mediated expression in the medial habenula and brain-wide fluorescence on breeding with tdTomato reporter mice, the latter showing a distribution patterns typical of MOR expression. Finally, we demonstrate that optogenetic activation of MOR neurons in the ventral tegmental area of -Cre mice evokes strong avoidance behavior, as anticipated from the literature. The -Cre line is therefore an excellent tool for both mapping and functional studies of MOR-positive neurons, and will be of broad interest for opioid, pain, and addiction research. | CognitiveConstruct | RewardProcessing |
32,371,614 | 10.1097/FPC.0000000000000403 | 2,020 | Pharmacogenetics and genomics | Pharmacogenet Genomics | The effect of SLC6A3 variable number of tandem repeats and methylation levels on individual susceptibility to start tobacco smoking and on the ability of smokers to quit smoking. | Nicotine acts through the dopamine pathway in the brain affecting reward processing through cigarette consumption. Thus, both genetic and epigenetic factors related to dopamine metabolism may influence individual's smoking behavior. We studied variations of two variable numbers of tandem repeats (VNTRs), 40 and 30 bp in length, in SLC6A3 gene together with six DNA methylation sites located in a first intron of the gene in relation to several smoking-related phenotypes in a study population consisting of 1230 Whites of Russian origin. Both the 5R allele of 30 bp VNTR and the 9R allele of 40 bp VNTR in SLC6A3 were associated with a reduced risk to tobacco smoking [odds ratio (OR) 0.53, 95% confidence interval (CI) 0.37-0.75; OR 0.62, 95% CI 0.43-0.88]. Although the carriers of 9R allele also had high Fagerström test for nicotine dependence scores (OR 1.65, 95% CI 1.04-2.60), they were still more likely to succeed in smoking cessation (OR 0.59, 95% CI 0.40-0.88). Also, current smokers had more than 2.5-fold likelihood to have increased SLC6A3 methylation levels than former smokers (OR 2.72, 95% CI 1.63-4.53). The SLC6A3 5R of 30 bp and 9R of 40 bp VNTR variants may lead to a reduced risk to start smoking through decreased dopamine availability, and can also affect the success in subsequent smoking cessation attempts. Moreover, the elevated mean methylation values in the first intron of SLC6A3 may be related to nicotine dependence via a more active dopamine transporter. | CognitiveConstruct | RewardProcessing |
32,367,265 | 10.1007/s00429-020-02069-8 | 2,020 | Brain structure & function | Brain Struct Funct | Untangling the dorsal diencephalic conduction system: a review of structure and function of the stria medullaris, habenula and fasciculus retroflexus. | The often-overlooked dorsal diencephalic conduction system (DDCS) is a highly conserved pathway linking the basal forebrain and the monoaminergic brainstem. It consists of three key structures; the stria medullaris, the habenula and the fasciculus retroflexus. The first component of the DDCS, the stria medullaris, is a discrete bilateral tract composed of fibers from the basal forebrain that terminate in the triangular eminence of the stalk of the pineal gland, known as the habenula. The habenula acts as a relay hub where incoming signals from the stria medullaris are processed and subsequently relayed to the midbrain and hindbrain monoaminergic nuclei through the fasciculus retroflexus. As a result of its wide-ranging connections, the DDCS has recently been implicated in a wide range of behaviors related to reward processing, aversion and motivation. As such, an understanding of the structure and connections of the DDCS may help illuminate the pathophysiology of neuropsychiatric disorders such as depression, addiction and pain. This is the first review of all three components of the DDCS, the stria medullaris, the habenula and the fasciculus retroflexus, with particular focus on their anatomy, function and development. | CognitiveConstruct | RewardProcessing |
32,362,843 | 10.3389/fpsyt.2020.00281 | 2,020 | Frontiers in psychiatry | Front Psychiatry | The Role of Interoception in the Pathogenesis and Treatment of Anorexia Nervosa: A Narrative Review. | Anorexia nervosa (AN) is a psychiatric illness characterized by extreme overvaluation of weight and disturbed eating. Despite having the highest mortality rate of any psychiatric illness, the etiology and neurobiology of AN are poorly understood. A growing body of research has begun to elucidate the role of reward processing, as well as cognitive and limbic networks, in the symptomology of AN. However, these advances have so far failed to contribute therapeutically, suggesting a new understanding may be necessary. A disturbance in the interoceptive system, involved in perceiving and interpreting the physiological condition of the body, has recently been proposed as a central mechanism of pathology in AN, through links to hunger and satiety, risk prediction errors, emotional awareness, and body dysmorphia. This review summarizes the existing literature in order to clarify possible underlying mechanisms and proposes a novel model of the neuro-circuitry of AN. Detailed neuroanatomical studies and new methods for studying interoception may allow further refinement of this model and the development of improved treatment. | CognitiveConstruct | RewardProcessing |
32,349,119 | 10.1038/s41386-020-0688-x | 2,020 | Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology | Neuropsychopharmacology | Clinical, behavioral, and neural measures of reward processing correlate with escitalopram response in depression: a Canadian Biomarker Integration Network in Depression (CAN-BIND-1) Report. | Anhedonia is thought to reflect deficits in reward processing that are associated with abnormal activity in mesocorticolimbic brain regions. It is expressed clinically as a deficit in the interest or pleasure in daily activities. More severe anhedonia in major depressive disorder (MDD) is a negative predictor of antidepressant response. It is unknown, however, whether the pathophysiology of anhedonia represents a viable avenue for identifying biological markers of antidepressant treatment response. Therefore, this study aimed to examine the relationships between reward processing and response to antidepressant treatment using clinical, behavioral, and functional neuroimaging measures. Eighty-seven participants in the first Canadian Biomarker Integration Network in Depression (CAN-BIND-1) protocol received 8 weeks of open-label escitalopram. Clinical correlates of reward processing were assessed at baseline using validated scales to measure anhedonia, and a monetary incentive delay (MID) task during functional neuroimaging was completed at baseline and after 2 weeks of treatment. Response to escitalopram was associated with significantly lower self-reported deficits in reward processing at baseline. Activity during the reward anticipation, but not the reward consumption, phase of the MID task was correlated with clinical response to escitalopram at week 8. Early (baseline to week 2) increases in frontostriatal connectivity during reward anticipation significantly correlated with reduction in depressive symptoms after 8 weeks of treatment. Escitalopram response is associated with clinical and neuroimaging correlates of reward processing. These results represent an important contribution towards identifying and integrating biological, behavioral, and clinical correlates of treatment response. ClinicalTrials.gov: NCT01655706. | CognitiveConstruct | RewardProcessing |
32,338,128 | 10.1177/1073858420907591 | 2,021 | The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry | Neuroscientist | Dopamine, Prediction Error and Beyond. | A large body of work has linked dopaminergic signaling to learning and reward processing. It stresses the role of dopamine in reward prediction error signaling, a key neural signal that allows us to learn from past experiences, and that facilitates optimal choice behavior. Latterly, it has become clear that dopamine does not merely code prediction error size but also signals the difference between the expected value of rewards, and the value of rewards actually received, which is obtained through the integration of reward attributes such as the type, amount, probability and delay. More recent work has posited a role of dopamine in learning beyond rewards. These theories suggest that dopamine codes absolute or unsigned prediction errors, playing a key role in how the brain models associative regularities within its environment, while incorporating critical information about the reliability of those regularities. Work is emerging supporting this perspective and, it has inspired theoretical models of how certain forms of mental pathology may emerge in relation to dopamine function. Such pathology is frequently related to disturbed inferences leading to altered internal models of the environment. Thus, it is critical to understand the role of dopamine in error-related learning and inference. | CognitiveConstruct | RewardProcessing |
32,329,565 | 10.1111/adb.12911 | 2,021 | Addiction biology | Addict Biol | Maternal separation increases cocaine intake through a mechanism involving plasticity in glutamate signalling. | Early-life stress (ELS) is associated with negative consequences, including maladaptive long-lasting brain effects. These alterations seem to increase the likelihood of developing substance use disorders. However, the molecular consequences of ELS are poorly understood. In the present study, we tested the impact of ELS induced by maternal separation with early weaning (MSEW) in CD1 male mice at different phases of cocaine self-administration (SA). We also investigated the subsequent alterations on GluR2, GluR1, cAMP response element-binding (CREB), and CREB-phosphorylation (pCREB) in ventral tegmental area (VTA) and nucleus accumbens (NAc) induced by both MSEW and cocaine SA. Our results show that MSEW animals expressed a higher cocaine intake, an increased vulnerability to the acquisition of cocaine SA, and incapacity to extinguish cocaine SA behaviour. MSEW mice showed decreased GluR2 and increased GluR1 and pCREB in NAc. Also, results displayed reduction of basal levels of GluR1 and CREB and an elevation of GluR1/GluR2 ratio in the VTA. Such results hint at an enhanced glutamatergic function in NAc and increased excitability of VTA DA neurons in maternally separated mice. Altogether, our results suggest that MSEW induces molecular alterations in the brain areas related to reward processing, increasing the vulnerability to depression and cocaine-seeking behaviour. | CognitiveConstruct | RewardProcessing |
32,325,424 | 10.1016/j.nicl.2020.102249 | 2,020 | NeuroImage. Clinical | Neuroimage Clin | Attenuated activation of the anterior rostral medial prefrontal cortex on self-relevant social reward processing in individuals with autism spectrum disorder. | The social motivation hypothesis posits that people with autism spectrum disorder (ASD) find social stimuli less rewarding and are therefore less motivated towards social interaction than people with neuro-typical development (TD). However, the less rewarding social stimuli characteristics during social interaction for people with ASD are largely unknown. The contingent positive responsiveness of others relevant to self-action motivates the early development of social interaction, thus representing a social reward. As individuals with ASD often exhibit atypical responses to self-relevant stimuli in their early life, we hypothesized that the self-relevant responses of others are less rewarding for individuals with ASD. To test this hypothesis, we conducted a functional magnetic resonance imaging study using a social contingency task. During the task, the participants attempted to make the audience laugh by telling funny jokes and thus activating the anterior rostral medial prefrontal cortex (arMPFC) of TD individuals (Sumiya et al., 2017). We explicitly predicted that the atypical activation of the arMPFC is related to the reduced reward value of self-relevant responses to others in individuals with ASD. Thirty-one adults with ASD and 24 age- and intelligence quotient-matched TD adults participated in the study. Participants with ASD reported significantly lower pleasure after the audience's responses to their own actions than those in the TD group. Correspondingly, the self-related activation of the arMPFC, defined by the results of our previous study, was attenuated in the ASD group compared to the TD group. The present findings indicate that weak self-relevant outcome processing mediated by the arMPFC of individuals with ASD dampens the rewarding nature of social interaction. | CognitiveConstruct | RewardProcessing |
32,321,745 | 10.1523/JNEUROSCI.3003-19.2020 | 2,020 | The Journal of neuroscience : the official journal of the Society for Neuroscience | J Neurosci | Acute Stress Enhances Associative Learning via Dopamine Signaling in the Ventral Lateral Striatum. | Acute stress transiently increases vigilance, enhancing the detection of salient stimuli in one's environment. This increased perceptual sensitivity is thought to promote the association of rewarding outcomes with relevant cues. The mesolimbic dopamine system is critical for learning cue-reward associations. Dopamine levels in the ventral striatum are elevated following exposure to stress. Together, this suggests that the mesolimbic dopamine system could mediate the influence of acute stress on cue-reward learning. To address this possibility, we examined how a single stressful experience influenced learning in an appetitive pavlovian conditioning task. Male rats underwent an episode of restraint prior to the first conditioning session. This acute stress treatment augmented conditioned responding in subsequent sessions. Voltammetry recordings of mesolimbic dopamine levels demonstrated that acute stress selectively increased reward-evoked dopamine release in the ventral lateral striatum (VLS), but not in the ventral medial striatum. Antagonizing dopamine receptors in the VLS blocked the stress-induced enhancement of conditioned responding. Collectively, these findings illustrate that stress engages dopamine signaling in the VLS to facilitate appetitive learning. Acute stress influences learning about aversive and rewarding outcomes. Dopamine neurons are sensitive to stress and critical for reward learning. However, it is unclear whether stress regulates reward learning via dopamine signaling. Using fast-scan cyclic voltammetry as rats underwent pavlovian conditioning, we demonstrate that a single stressful experience increases reward-evoked dopamine release in the ventral lateral striatum. This enhanced dopamine signal accompanies a long-lasting increase in conditioned behavioral responding. These findings highlight that the ventral lateral striatum is a node for mediating the effect of stress on reward processing. | CognitiveConstruct | RewardProcessing |
32,313,235 | 10.1038/s41562-020-0846-5 | 2,020 | Nature human behaviour | Nat Hum Behav | Neurobehavioural characterisation and stratification of reinforcement-related behaviour. | Reinforcement-related cognitive processes, such as reward processing, inhibitory control and social-emotional regulation are critical components of externalising and internalising behaviours. It is unclear to what extent the deficit in each of these processes contributes to individual behavioural symptoms, how their neural substrates give rise to distinct behavioural outcomes and whether neural activation profiles across different reinforcement-related processes might differentiate individual behaviours. We created a statistical framework that enabled us to directly compare functional brain activation during reward anticipation, motor inhibition and viewing emotional faces in the European IMAGEN cohort of 2,000 14-year-old adolescents. We observe significant correlations and modulation of reward anticipation and motor inhibition networks in hyperactivity, impulsivity, inattentive behaviour and conduct symptoms, and we describe neural signatures across cognitive tasks that differentiate these behaviours. We thus characterise shared and distinct functional brain activation patterns underling different externalising symptoms and identify neural stratification markers, while accounting for clinically observed comorbidity. | CognitiveConstruct | RewardProcessing |
32,305,169 | 10.1016/j.schres.2020.03.072 | 2,020 | Schizophrenia research | Schizophr Res | Impulsive decision making, brain cortical thickness and familial schizophrenia risk. | Schizophrenia (SZ) patients and their biological relatives are more impulsive than controls. Although greater impulsivity in SZ has been associated with dysfunction in prefrontal neural circuits implicated in reward processing, little is known regarding brain structural correlates of heightened impulsivity in unaffected adolescent relatives of SZ patients. Impulsive decision-making was assessed using the delay discounting task in 174 adolescents: 36 first-degree relatives (FDR) and 50 second-degree relatives (SDR) of SZ patients, and 88 healthy controls with no SZ family history (NSFH). We contrasted MRI brain gray matter cortical thickness-discounting constant (k) relationships between these 3 comparison groups using well-validated statistical approaches. FDR had a distinct pattern in cortical thickness-k associations when compared to NSFH and SDR. Preference for immediate rewards (i.e. greater impulsivity) among FDR correlated with less cortical thickness within diffuse brain regions, including dorsolateral prefrontal (cognitive control network and motor/premotor cortex) and lateral temporal (auditory and visual association cortex) brain areas. Adolescent impulsive decision-making may serve as an informative phenotype of underlying brain circuitry dysfunction associated with SZ risk. Future research focusing on impulsivity in SZ will likely help advance understanding how dysfunctional interactions between cognitive and reward neural circuits contribute to the neurobiological basis of SZ. | CognitiveConstruct | RewardProcessing |
32,302,475 | 10.1021/acschemneuro.0c00100 | 2,020 | ACS chemical neuroscience | ACS Chem Neurosci | Classics in Chemical Neuroscience: Buprenorphine. | Buprenorphine has not only had an interdisciplinary impact on our understanding of key neuroscience topics like opioid pharmacology, pain signaling, and reward processing but has also been a key influence in changing the way that substance use disorders are approached in modern medical systems. From its leading role in expanding outpatient treatment of opioid use disorders to its continued influence on research into next-generation analgesics, buprenorphine has been a continuous player in the ever-evolving societal perception of opioids and substance use disorder. To provide a multifaceted account on the enormous diversity of areas where this molecule has made an impact, this article discusses buprenorphine's chemical properties, synthesis and development, pharmacology, adverse effects, manufacturing information, and historical place in the field of chemical neuroscience. | CognitiveConstruct | RewardProcessing |
32,301,215 | 10.1111/bdi.12915 | 2,020 | Bipolar disorders | Bipolar Disord | Abnormal prefrontal cortex processing of reward prediction errors in recently diagnosed patients with bipolar disorder and their unaffected relatives. | Bipolar disorder (BD) has been associated with abnormal reward functioning including pleasure-seeking and impulsivity. Here we sought to clarify whether these changes can be attributed to abnormalities in the neural processing of reward valuation or error prediction. Moreover, we tested whether abnormalities in these processes are associated with familial vulnerability to BD. We obtained functional magnetic resonance imaging data from patients with recently diagnosed BD (n = 85), their unaffected first-degree relatives (n = 44), and healthy control participants (n = 66) while they were performing a monetary card game. We used a region-of-interest approach to test for group differences in the activation of the midbrain, the ventral striatum, and the prefrontal cortex during reward valuation and error prediction. Patients with BD showed decreased prediction error signal in ventrolateral prefrontal cortex and the unaffected relatives showed decreased prediction error signal in the supplementary motor area in comparison to healthy controls. There were no significant group differences in the activation of the ventral striatum during the task. In healthy controls, prediction error signal in dorsal anterior cingulate cortex correlated with an out-of-scanner measure of motor inhibition but this association was absent in patients and relatives. The findings indicate that abnormal reward processing in BD is primarily related to deficits in the engagement of prefrontal regions involved in inhibitory control during error prediction. In contrast, deficient activation in supplementary motor cortex involved in planning of movement emerged as a familial vulnerability to BD. | CognitiveConstruct | RewardProcessing |
32,257,439 | 10.1155/2020/8014248 | 2,020 | Autism research and treatment | Autism Res Treat | Neural Mechanisms of Vicarious Reward Processing in Adults with Autism Spectrum Disorder. | Previous studies examining the neural substrates of reward processing in ASD have explored responses to rewards for oneself but not rewards earned for others (i.e., vicarious reward). This omission is notable given that vicarious reward processing is a critical component of creating and maintaining social relationships. The current study examined the neural mechanisms of vicarious reward processing in 15 adults with ASD and 15 age- and gender-matched typically developing controls. Individuals with ASD demonstrated attenuated activation of reward-related regions during vicarious reward processing. Altered connectivity was also observed in individuals with ASD during reward receipt. These findings of altered neural sensitivity to vicarious reward processing may represent a mechanism that hinders the development of social abilities in ASD. | CognitiveConstruct | RewardProcessing |
32,252,540 | 10.1176/appi.ajp.2019.19030281 | 2,020 | The American journal of psychiatry | Am J Psychiatry | Brain Reward System Dysfunction in Adolescence: Current, Cumulative, and Developmental Periods of Depression. | Reward system dysfunction is a well-known correlate and predictor of depression in adults and adolescents, with depressed individuals showing blunted (hyporeactive) striatal response to monetary rewards. Furthermore, studies of remitted depression suggest network-wide hyporeactivity of striatal (caudate, putamen, nucleus accumbens) and cortical (insula, anterior cingulate cortex [ACC]) regions even in the absence of current symptoms. Thus, it remains unclear which patterns of hyporeactivity represent a trait-like indicator of depression and which represent a current depressed state. The authors examined the relationships between regions of a cortico-striatal circuit supporting reward processing and both current depression and cumulative depression history. Using a functional MRI monetary reward task, the authors measured brain response to monetary gains and losses in a longitudinal sample of adolescents (N=131) who had been annually assessed for psychiatric symptoms since ages 3-5 years. Current depression severity was associated with hyporeactivity exclusively in the nucleus accumbens in response to the anticipation of a reward, while cumulative depression severity was associated with blunted response to anticipation across a cortico-striatal circuit (striatum, ACC, insula). Follow-up analyses investigating the effects of depression on reward processing at different developmental stages revealed a similar pattern: recent depression severity during adolescence was associated with more focal hyporeactivity in the nucleus accumbens, while depression severity during early childhood (i.e., preschool) was associated with more global hyporeactivity across the cortico-striatal circuit. The study findings indicate important distinctions between disruptions in reward system neural circuitry associated with a history of depression (particularly early-onset depression) and current depression. These results have implications for understanding the etiology and treatment of reward processing deficits in depression. | CognitiveConstruct | RewardProcessing |
32,248,851 | 10.1017/S0033291720000677 | 2,021 | Psychological medicine | Psychol Med | Delay discounting in youth at clinical high-risk for psychosis and adults with schizophrenia. | Schizophrenia (SZ) is typically preceded by a prodromal (i.e. pre-illness) period characterized by attenuated positive symptoms and declining functional outcome. Negative symptoms are prominent among individuals at clinical high-risk (CHR) for psychosis (i.e. those with prodromal syndromes) and highly predictive of conversion to illness. Mechanisms underlying negative symptoms in the CHR population are unclear. Two studies were conducted to evaluate whether abnormalities in a reward processing mechanism thought to be core to negative symptoms in SZ, value representation, also exist in CHR individuals and whether they are associated with negative symptoms transphasically. Study 1 included 33 individuals in the chronic phase of illness who have been diagnosed with schizophrenia or schizoaffective disorder (SZ) and 40 healthy controls (CN). Study 2 included 37 CHR participants and 45 CN. In both studies, participants completed the delay discounting (DD) task as a measure of value representation and the Brief Negative Symptom Scale was rated to measure negative symptoms. Results indicated that patients with SZ had steeper discounting rates than CN, indicating impairments in value representation. However, CHR participants were unimpaired on the DD task. In both studies, steeper discounting was associated with greater severity of negative symptoms. These findings suggest that deficits in value representation are associated with negative symptoms transphasically. | CognitiveConstruct | RewardProcessing |
32,248,234 | 10.1093/scan/nsaa041 | 2,020 | Social cognitive and affective neuroscience | Soc Cogn Affect Neurosci | Exposure to negative stereotypes influences representations of monetary incentives in the nucleus accumbens. | Contemporary society is saturated with negative representations of racial and ethnic minorities. Social science research finds that exposure to such negative stereotypes creates stress above and beyond pre-existing effects of income inequality and structural racism. Neuroscience studies in animals and humans show that life stress modulates brain responses to rewards. However, it is not known whether contending with negative representations of one's social group spills overs to influence reward processing. We used functional magnetic resonance imaging to examine the effects of stigmatizing negative stereotypes on neural responding to the anticipation and consumption of monetary gains and losses in a Mexican American sample. Machine learning analyses indicated that incentive-related patterns of brain activity within the nucleus accumbens differed between Mexican Americans subjected to negative stereotypes and those who were not. This effect occurred for anticipating both gains and losses. Our work suggests that rhetoric stigmatizing Latinos and other minorities could alter how members of such groups process incentives in their environment. These findings contribute to our understanding of the linkage between stigmatizing experiences and motivated behavior, with implications for well-being and health. | CognitiveConstruct | RewardProcessing |
32,245,184 | 10.3390/ijms21062160 | 2,020 | International journal of molecular sciences | Int J Mol Sci | The Role of Dorsal Raphe Serotonin Neurons in the Balance between Reward and Aversion. | Reward processing is fundamental for animals to survive and reproduce. Many studies have shown the importance of dorsal raphe nucleus (DRN) serotonin (5-HT) neurons in this process, but the strongly correlative link between the activity of DRN 5-HT neurons and rewarding/aversive potency is under debate. Our primary objective was to reveal this link using two different strategies to transduce DRN 5-HT neurons. For transduction of 5-HT neurons in wildtype mice, adeno-associated virus (AAV) bearing the mouse tryptophan hydroxylase 2 (TPH2) gene promoter was used. For transduction in Tph2-tTA transgenic mice, AAVs bearing the tTA-dependent TetO enhancer were used. To manipulate the activity of 5-HT neurons, optogenetic actuators (CheRiff, eArchT) were expressed by AAVs. For measurement of rewarding/aversive potency, we performed a nose-poke self-stimulation test and conditioned place preference (CPP) test. We found that stimulation of DRN 5-HT neurons and their projections to the ventral tegmental area (VTA) increased the number of nose-pokes in self-stimulation test and CPP scores in both targeting methods. Concomitantly, CPP scores were decreased by inhibition of DRN 5-HT neurons and their projections to VTA. Our findings indicate that the activity of DRN 5-HT neurons projecting to the VTA is a key modulator of balance between reward and aversion. | CognitiveConstruct | RewardProcessing |
32,219,179 | 10.1177/2398212820907177 | 2,020 | Brain and neuroscience advances | Brain Neurosci Adv | Comparison of conventional and rapid-acting antidepressants in a rodent probabilistic reversal learning task. | Deficits in reward processing are a central feature of major depressive disorder with patients exhibiting decreased reward learning and altered feedback sensitivity in probabilistic reversal learning tasks. Methods to quantify probabilistic learning in both rodents and humans have been developed, providing translational paradigms for depression research. We have utilised a probabilistic reversal learning task to investigate potential differences between conventional and rapid-acting antidepressants on reward learning and feedback sensitivity. We trained 12 rats in a touchscreen probabilistic reversal learning task before investigating the effect of acute administration of citalopram, venlafaxine, reboxetine, ketamine or scopolamine. Data were also analysed using a Q-learning reinforcement learning model to understand the effects of antidepressant treatment on underlying reward processing parameters. Citalopram administration decreased trials taken to learn the first rule and increased win-stay probability. Reboxetine decreased win-stay behaviour while also decreasing the number of rule changes animals performed in a session. Venlafaxine had no effect. Ketamine and scopolamine both decreased win-stay probability, number of rule changes performed and motivation in the task. Insights from the reinforcement learning model suggested that reboxetine led animals to choose a less optimal strategy, while ketamine decreased the model-free learning rate. These results suggest that reward learning and feedback sensitivity are not differentially modulated by conventional and rapid-acting antidepressant treatment in the probabilistic reversal learning task. | CognitiveConstruct | RewardProcessing |
32,218,141 | 10.3390/jcm9040900 | 2,020 | Journal of clinical medicine | J Clin Med | Strengthened Default Mode Network Activation During Delay Discounting in Adolescents with Anorexia Nervosa After Partial Weight Restoration: A Longitudinal fMRI Study. | The capacity of patients with anorexia nervosa (AN) to resist food-based rewards is often assumed to reflect excessive self-control. Previous cross-sectional functional magnetic resonance imaging (fMRI) studies utilizing the delay discounting (DD) paradigm, an index of impulsivity and self-control, suggested altered neural efficiency of decision-making in acutely underweight patients (acAN) and a relative normalization in long-term, weight-recovered individuals with a history of AN (recAN). The current longitudinal study tested for changes in functional magnetic resonance imaging (fMRI) activation during DD associated with intensive weight restoration treatment. A predominately adolescent cohort of 22 female acAN patients (mean age-15.5 years) performed an established DD paradigm during fMRI at the beginning of hospitalization and again after partial weight restoration (≥12% body mass index (BMI) increase). Analyses investigated longitudinal changes in both reward valuation and executive decision-making processes. Additional exploratory analyses included comparisons with data acquired in aged-matched healthy controls (HC) as well as probes of functional connectivity between empirically identified nodes of the "task-positive" frontoparietal control network (FPN) and "task-negative" default-mode network (DMN). While treatment was not associated with changes in behavioral DD parameters or activation, specific to reward processing, deactivation of the DMN during decision-making was significantly less pronounced following partial weight restoration. Strengthened DMN activation during DD might reflect a relative relaxation of cognitive overcontrol or improved self-referential, decision-making. Together, our findings present further evidence that aberrant decision-making in AN might be remediable by treatment and, therefore, might constitute an acute effect rather than a core trait variable of the disorder. | CognitiveConstruct | RewardProcessing |
32,198,016 | 10.1016/j.bbi.2020.03.015 | 2,020 | Brain, behavior, and immunity | Brain Behav Immun | Gene signatures in peripheral blood immune cells related to insulin resistance and low tyrosine metabolism define a sub-type of depression with high CRP and anhedonia. | Inflammation and altered glucose metabolism are two pathways implicated in the pathophysiology of major depressive disorder (MDD). We have previously shown that high inflammation as measured by C-reactive protein (CRP) in MDD patients is associated with symptoms of anhedonia, a core symptom of MDD, along with deficits in dopaminergic reward circuitry. Increased inflammation can shift metabolic demand and reprogram cellular energy sources, which may collectively impact the brain and reward processing to contribute to symptoms of anhedonia. To determine whether immunometabolic gene signatures were enriched in immune cells of depressed patients with increased inflammation and anhedonia, we examined whole-blood gene expression microarray (Illumina HumanHT-12) data from unmedicated, medically-stable patients with MDD (n = 93). Patients were considered to have increased inflammation based on High (>3mg/L) versus Low (≤3mg/L) plasma CRP, and further classified as having a self-reported phenotype of High (n = 30, 33rd percentile) versus Low (n = 32, 67th percentile) Anhedonia. Functional enrichment of gene pathways was assessed by Gene Set Enrichment Analysis (GSEA) using the KEGG pathway database. Pathways related to glucose metabolism (insulin signaling, insulin resistance, HIF-1, PI3K/AKT signaling), cancer (e.g., genes related to insulin and PI3K/AKT signaling), and inflammation (B cell, T cell and Fc receptor signaling) were specifically enriched in patients with both High CRP and High Anhedonia (all FDR q < 0.25). Within patients with High CRP in GSEA, the insulin signaling pathway was the top enriched pathway in patients with High versus Low Anhedonia (n = 10 and 9 respectively), which was driven by genes expressed predominantly in monocytes (z = 2.95, p < 0.01). Conversely, within patients with High Anhedonia, in addition to enrichment of immunometabolic pathways, the tyrosine metabolism pathway was also reduced in patients with High versus Low CRP (n = 20 and 10 respectively). Of note, enrichment of immunometabolic pathways was confirmed in complementary linear regression analyses examining pathways associated with a CRP-by-Anhedonia interaction term while controlling for clinical covariates in all patients (n = 93). These results indicate that increased glucose and low tyrosine metabolism define a subset of depressed patients with high inflammation and anhedonia. Enrichment of cancer-related pathways driven by metabolic genes also suggests a shift in immune cell metabolism from oxidative phosphorylation to glycolysis. Together these data suggest that anhedonia in MDD with high CRP involves both immunometabolic shifts and reduced dopamine precursor availability. | CognitiveConstruct | RewardProcessing |
32,194,279 | 10.1016/j.neuroimage.2020.116757 | 2,020 | NeuroImage | Neuroimage | An insight-related neural reward signal. | Moments of insight, a phenomenon of creative cognition in which an idea suddenly emerges into awareness as an "Aha!" are often reported to be affectively positive experiences. We tested the hypothesis that problem-solving by insight is accompanied by neural reward processing. We recorded high-density EEGs while participants solved a series of anagrams. For each solution, they reported whether the answer had occurred to them as a sudden insight or whether they had derived it deliberately and incrementally (i.e., "analytically'). Afterwards, they filled out a questionnaire that measures general dispositional reward sensitivity. We computed the time-frequency representations of the EEGs for trials with insight (I) solutions and trials with analytic (A) solutions and subtracted them to obtain an I-A time-frequency representation for each electrode. Statistical Parametric Mapping (SPM) analyses tested for significant I-A and reward-sensitivity effects. SPM revealed the time, frequency, and scalp locations of several I > A effects. No A > I effect was observed. The primary neural correlate of insight was a burst of (I > A) gamma-band oscillatory activity over prefrontal cortex approximately 500 ms before participants pressed a button to indicate that they had solved the problem. We correlated the I-A time-frequency representation with reward sensitivity to discover insight-related effects that were modulated by reward sensitivity. This revealed a separate anterior prefrontal burst of gamma-band activity, approximately 100 ms after the primary I-A insight effect, which we interpreted to be an insight-related reward signal. This interpretation was supported by source reconstruction showing that this signal was generated in part by orbitofrontal cortex, a region associated with reward learning and hedonically pleasurable experiences such as food, positive social experiences, addictive drugs, and orgasm. These findings support the notion that for many people insight is rewarding. Additionally, these results may explain why many people choose to engage in insight-generating recreational and vocational activities such as solving puzzles, reading murder mysteries, creating inventions, or doing research. This insight-related reward signal may be a manifestation of an evolutionarily adaptive mechanism for the reinforcement of exploration, problem solving, and creative cognition. | CognitiveConstruct | RewardProcessing |
32,184,386 | 10.1038/s41398-020-0775-0 | 2,020 | Translational psychiatry | Transl Psychiatry | Neural substrates of smoking and reward cue reactivity in smokers: a meta-analysis of fMRI studies. | Smoking is partly attributed to alterations of reward processing. However, findings on the neurobiological mechanisms that underlie smoking-related and smoking-unrelated reward processing in smokers have been inconsistent. Neuroimaging experiments that used functional magnetic resonance imaging (fMRI) and reported brain responses to smoking-related cues and nonsmoking reward-related cues in smokers and healthy controls as coordinates in a standard anatomic reference space were identified by searching the PubMed, Embase, and Web of Science databases up to December 2018. Three meta-analyses were performed using random-effect nonparametric statistics with Seed-based d Mapping software, with brain activity contrast from individual studies as the input. The striatum showed higher activation in response to smoking-related cues compared with neutral cues in 816 smokers from 28 studies and lower activation in response to nonsmoking reward-related cues in 275 smokers compared with 271 healthy control individuals from 13 studies. The relative reactivity of the putamen to smoking-related cues increased in 108 smokers compared with 107 healthy controls from seven studies. Meta-regression showed that smokers with a greater severity of nicotine dependence exhibited less engagement of the striatum in response to both smoking-related cues and nonsmoking reward-related cues. The present results reveal the disruption of reward system function in smokers and provide new insights into diverging theories of addiction. With the escalation of nicotine dependence, nicotine appears to exert dynamic effects on reward processing, based on incentive sensitization theory and reward deficiency syndrome theory. | CognitiveConstruct | RewardProcessing |
32,164,847 | 10.1016/B978-0-444-63934-9.00010-X | 2,020 | Handbook of clinical neurology | Handb Clin Neurol | Video games as rich environments to foster brain plasticity. | This chapter highlights the key role of two main factors, attentional control and reward processing, in unlocking brain plasticity. We first review the evidence for the role that each of these mechanisms plays in neuroplasticity, and then make the case that tools and technologies that combine these two are likely to result in maximal and broad, generalized benefits. In this context, we review the evidence concerning the impact of video game play on brain plasticity, with an eye toward plasticity-driving methods such as the seamless integration of neurofeedback into the video game platforms. | CognitiveConstruct | RewardProcessing |
32,160,766 | 10.1176/appi.ajp.2019.19030261 | 2,020 | The American journal of psychiatry | Am J Psychiatry | Neural Insensitivity to the Effects of Hunger in Women Remitted From Anorexia Nervosa. | Anorexia nervosa has the highest mortality rate of any psychiatric condition, yet the pathophysiology of this disorder and its primary symptom, extreme dietary restriction, remains poorly understood. In states of hunger relative to satiety, the rewarding value of food stimuli normally increases to promote eating, yet individuals with anorexia nervosa avoid food despite emaciation. This study's aim was to examine potential neural insensitivity to these effects of hunger in anorexia nervosa. At two scanning sessions scheduled 24 hours apart, one after a 16-hour fast and one after a standardized meal, 26 women who were in remission from anorexia nervosa (to avoid the confounding effects of malnutrition) and 22 matched control women received tastes of sucrose solution or ionic water while functional MRI data were acquired. Within a network of interest responsible for food valuation and transforming taste signals into motivation to eat, the authors compared groups across conditions on blood-oxygen-level-dependent (BOLD) signal and task-based functional connectivity. Participants in the two groups had similar BOLD responses to sucrose and water tastants. A group-by-condition interaction in the ventral caudal putamen indicated that hunger had opposite effects on tastant response in the control group and the remitted anorexia nervosa group, with an increase and a decrease, respectively, in BOLD response when hungry. Hunger had a similar opposite effect on insula-to-ventral caudal putamen functional connectivity in the remitted anorexia nervosa group compared with the control group. Exploratory analyses indicated that lower caudate response to tastants when hungry was associated with higher scores on harm avoidance among participants in the remitted anorexia nervosa group. Reduced recruitment of neural circuitry that translates taste stimulation to motivated eating behavior when hungry may facilitate food avoidance and prolonged periods of extremely restricted food intake in anorexia nervosa. | CognitiveConstruct | RewardProcessing |
32,150,009 | 10.1097/PSY.0000000000000782 | 2,020 | Psychosomatic medicine | Psychosom Med | Obesity and the Brain: Another Brain-Body Versus Body-Brain Conundrum. | Midlife obesity has been associated with poor cognitive functioning in older age, but the bidirectional pathways linking the brain and excessive adipose tissue require further research. In this issue of Psychosomatic Medicine, two investigations address the brain responses to food-related cues and psychological stressors relevant to obesity. Moazzami and colleagues document the relationship between abdominal obesity and brain responses to stress among patients with coronary artery disease and find that stress-related brain activity plays a potentially important role in the link between psychological distress, food cravings, and eating patterns relevant to obesity. Donofry and colleagues compare food cue-evoked functional connectivity in adults with obesity and report that brain areas involved in impaired self-regulation and reward processing may increase the risk of obesity by influencing decisions regarding diet and exercise. In this editorial, these findings are discussed in the context of brain-obesity interactions and the need for personalized multidisciplinary interventions for obesity. It is possible that functional magnetic resonance imaging and other indices of brain functioning will be useful in tailoring interventions that target weight reduction and/or cognitive functioning and monitoring treatment progress. | CognitiveConstruct | RewardProcessing |
32,148,214 | 10.1017/S0033291720000264 | 2,021 | Psychological medicine | Psychol Med | Aberrant salience and reward processing: a comparison of measures in schizophrenia and anxiety. | Aberrant salience may contribute to the development of schizophrenia symptoms via alterations in reward processing and motivation. However, tests of this hypothesis have yielded inconsistent results. These inconsistencies may reflect problems with the validity and specificity of measures of aberrant salience in schizophrenia. Therefore, we investigated relationships among measures of aberrant salience, reward, and motivation in schizophrenia and anxiety. Individuals with schizophrenia (n = 30), anxiety (n = 33) or unaffected by mental disorder (n = 30) completed measures of aberrant salience [Aberrant Salience Inventory (ASI), Salience Attribution Test (SAT)], motivation (Effort Expenditure for Reward Task), and reinforcer sensitivity (Stimulus Chase Task). Schizophrenia participants scored higher than anxiety (d = 0.71) and unaffected (d = 1.54) groups on the ASI and exhibited greater aberrant salience (d = 0.60) and lower adaptive salience (d = 0.98) than anxious participants on the SAT. There was no evidence of a correlation between measures of aberrant salience. Schizophrenia was associated with related deficits in motivated behaviour and maladaptive reward processing. However, these differences in reward processing did not correlate with aberrant salience measures. The results suggest that key measures of aberrant salience have limited specificity and validity. These problems may account for inconsistent findings reported in the literature. | CognitiveConstruct | RewardProcessing |
32,142,670 | 10.1016/j.cmet.2020.02.012 | 2,020 | Cell metabolism | Cell Metab | Causal Link between n-3 Polyunsaturated Fatty Acid Deficiency and Motivation Deficits. | Reward-processing impairment is a common symptomatic dimension of several psychiatric disorders. However, whether the underlying pathological mechanisms are common is unknown. Herein, we asked if the decrease in the n-3 polyunsaturated fatty acid (PUFA) lipid species, consistently described in these pathologies, could underlie reward-processing deficits. We show that reduced n-3 PUFA biostatus in mice leads to selective motivational impairments. Electrophysiological recordings revealed increased collateral inhibition of dopamine D2 receptor-expressing medium spiny neurons (D2-MSNs) onto dopamine D1 receptor-expressing MSNs in the nucleus accumbens, a main brain region for the modulation of motivation. Strikingly, transgenically preventing n-3 PUFA deficiency selectively in D2-expressing neurons normalizes MSN collateral inhibition and enhances motivation. These results constitute the first demonstration of a causal link between a behavioral deficit and n-3 PUFA decrease in a discrete neuronal population and suggest that lower n-3 PUFA biostatus in psychopathologies could participate in the etiology of reward-related symptoms. | CognitiveConstruct | RewardProcessing |
32,135,427 | 10.1016/j.neuropharm.2020.107993 | 2,020 | Neuropharmacology | Neuropharmacology | The hypocretin (orexin) system: from a neural circuitry perspective. | Hypocretin/orexin neurons are distributed restrictively in the hypothalamus, a brain region known to orchestrate diverse functions including sleep, reward processing, food intake, thermogenesis, and mood. Since the hypocretins/orexins were discovered more than two decades ago, extensive studies have accumulated concrete evidence showing the pivotal role of hypocretin/orexin in diverse neural modulation. New method of viral-mediated tracing system offers the possibility to map the monosynaptic inputs and detailed anatomical connectivity of Hcrt neurons. With the development of powerful research techniques including optogenetics, fiber-photometry, cell-type/pathway specific manipulation and neuronal activity monitoring, as well as single-cell RNA sequencing, the details of how hypocretinergic system execute functional modulation of various behaviors are coming to light. In this review, we focus on the function of neural pathways from hypocretin neurons to target brain regions. Anatomical and functional inputs to hypocretin neurons are also discussed. We further briefly summarize the development of pharmaceutical compounds targeting hypocretin signaling. This article is part of the special issue on Neuropeptides. | CognitiveConstruct | RewardProcessing |
32,116,845 | 10.3389/fpsyt.2020.00028 | 2,020 | Frontiers in psychiatry | Front Psychiatry | Reduced Reward Responsiveness in Women With Moderate - to - Severe Premenstrual Syndrome: Evidence From a Probabilistic Reward Task. | Nearly 50% of women of reproductive age worldwide experience premenstrual syndrome (PMS). Women with PMS exhibit low positive affect and low frontal electroencephalography asymmetry scores, both of which are associated with reward processing. These findings suggest that women with PMS may exhibit deficiencies in reward processing. A probabilistic reward task based on signal detection approach was used to assess reward responsiveness in 30 women with moderate-to-severe PMS and 31 controls without PMS. The results revealed that in the late luteal phase, the women with moderate-to-severe PMS exhibited lower response bias and lower hit rate toward more frequently rewarded stimuli (rich stimuli) than the controls. By contrast, the response bias and hit rate did not differ between the two groups in the follicular phase. The group differences still remained after controlling for anhedonic symptoms. Furthermore, trial-by-trial probability analyses revealed that women with moderate-to-severe PMS exhibited a trend of having a higher miss rate for rich stimuli than the controls. In particular, when a rich stimulus was preceded by an infrequently rewarded stimulus (a rewarded lean stimulus), participants in the PMS group exhibited a trend for higher miss rate than those in the control group in the late luteal and follicular phases. However, group differences in the probability analyses were nonsignificant after controlling for anhedonic symptoms. These results provide preliminary evidence that women with moderate-to-severe PMS exhibit dysfunctional reward responsiveness and impaired ability to modulate their behavior as a function of prior reinforcement. | CognitiveConstruct | RewardProcessing |
32,112,695 | 10.1530/JOE-19-0386 | 2,020 | The Journal of endocrinology | J Endocrinol | Sucrose consumption alters steroid and dopamine signalling in the female rat brain. | Sucrose consumption is associated with type 2 diabetes, cardiovascular disease, and cognitive deficits. Sucrose intake during pregnancy might have particularly prominent effects on metabolic, endocrine, and neural physiology. It remains unclear how consumption of sucrose affects parous females, especially in brain circuits that mediate food consumption and reward processing. Here, we examine whether a human-relevant level of sucrose before, during, and after pregnancy (17-18 weeks total) influences metabolic and neuroendocrine physiology in female rats. Females were fed either a control diet or a macronutrient-matched, isocaloric sucrose diet (25% of kcal from sucrose). Metabolically, sucrose impairs glucose tolerance, increases liver lipids, and increases a marker of adipose inflammation, but has no effect on body weight or overall visceral adiposity. Sucrose also decreases corticosterone levels in serum but not in the brain. Sucrose increases progesterone levels in serum and in the brain and increases the brain:serum ratio of progesterone in the mesocorticolimbic system and hypothalamus. These data suggest a dysregulation of systemic and local steroid signalling. Moreover, sucrose decreases tyrosine hydroxylase (TH), a catecholamine-synthetic enzyme, in the medial prefrontal cortex. Finally, sucrose consumption alters the expression pattern of FOSB, a marker of phasic dopamine signalling, in the nucleus accumbens. Overall, chronic consumption of sucrose at a human-relevant level alters metabolism, steroid levels, and brain dopamine signalling in a female rat model. | CognitiveConstruct | RewardProcessing |
32,102,722 | 10.1017/S003329172000032X | 2,021 | Psychological medicine | Psychol Med | Disrupted prefrontal regulation of striatum-related craving in Internet gaming disorder revealed by dynamic causal modeling: results from a cue-reactivity task. | Studies of Internet gaming disorder (IGD) suggest an imbalanced relationship between cognitive control and reward processing in people with IGD. However, it remains unclear how these two systems interact with each other, and whether they could serve as neurobiological markers for IGD. Fifty IGD subjects and matched individuals with recreational game use (RGU) were selected and compared when they were performing a cue-craving task. Regions of interests [anterior cingulate cortex (ACC), lentiform nucleus] were selected based on the comparison between brain responses to gaming-related cues and neutral cues. Directional connectivities among these brain regions were determined using Bayesian estimation. We additionally examined the posterior cingulate cortex (PCC) in a separate analysis based on data implicating the PCC in craving in addiction. During fixed-connectivity analyses, IGD subjects showed blunted ACC-to-lentiform and lentiform-to-ACC connectivity relative to RGU subjects, especially in the left hemisphere. When facing gaming cues, IGD subjects trended toward lower left-hemispheric modulatory effects in ACC-to-lentiform connectivity than RGU subjects. Self-reported cue-related craving prior to scanning correlated inversely with left-hemispheric modulatory effects in ACC-to-lentiform connectivity. The results suggesting that prefrontal-to-lentiform connectivity is impaired in IGD provides a possible neurobiological mechanism for difficulties in controlling gaming-cue-elicited cravings. Reduced connectivity ACC-lentiform connectivity may be a useful neurobiological marker for IGD. | CognitiveConstruct | RewardProcessing |
32,100,312 | 10.1111/psyp.13550 | 2,020 | Psychophysiology | Psychophysiology | Time of day differences in neural reward responsiveness in children. | The Reward Positivity (∆RewP) event-related potential (ERP), generally quantified as the difference between neural responsiveness to monetary gains (RewP-Gain) and losses (RewP-Loss) is commonly used as an index of neural reward responsiveness. Despite the popularity of this ERP component in studies of reward processing, knowledge about the role of state-related influences on the ∆RewP is limited. The present study examined whether ∆RewP amplitudes may differ based on when during the day they are assessed and whether age or sex would moderate this link. Participants were 188 children between the ages of 7 and 11 (47.3% female) without a lifetime history of a major depressive disorder or any anxiety disorder recruited from the community. Children completed the Doors task during which continuous electroencephalography was recorded to isolate the ∆RewP. To better isolate this ERP component from other temporally or spatially overlapping ERPs, we used temporospatial principal component analysis. We found that time of day (ToD) differences in the ∆RewP amplitude varied based on children's age. Specifically, older, compared to younger, children exhibited stronger responses to gains versus losses between 11:15 a.m. and 12:30 p.m. and after around 5:15 p.m. Further, these age-related differences appeared to be driven specifically by older children's reduced neural responsiveness to losses. The findings have methodological implications by highlighting the importance of accounting for the ToD at which ∆RewP-focused study sessions are conducted as well as for demographic characteristics of the participants, such as their age. | CognitiveConstruct | RewardProcessing |
32,098,756 | 10.1016/j.orcp.2020.02.004 | 2,020 | Obesity research & clinical practice | Obes Res Clin Pract | Food cue recruits increased reward processing and decreased inhibitory control processing in the obese/overweight: An activation likelihood estimation meta-analysis of fMRI studies. | Growing researches have shown that obese/overweight and healthy weight individuals exhibit different neural responses to food-related stimuli. Accordingly, researchers proposed several theories to explain these differences. Hereon, meta-analyses were conducted using activation likelihood estimation (ALE) to verify these theories and specify the reason of overeating from two aspects. Pubmed, Web of Science and Neurosynth were searched for the current study and screened according to inclusion criteria. Firstly, neural responses to visual food cues versus non-food images were compared between obese/overweight and healthy weight individuals. Then, neural activation to high-calorie food images versus low-calorie food/non-food visual stimuli was further investigated among the two populations. Coordinates in included studies were recorded and analysed by Ginger ALE software under threshold at uncorrected p < 0.001 with cluster-level p < 0.05 (cFWE). Eleven and seven studies were found in the first and second set of meta-analysis, respectively. The first meta-analysis showed that obese/overweight have hyper-responsivity in reward area and hypo-responsivity in both gustatory processing and inhibitory control area. The second meta-analysis indicated that the reward responsivity in the obese/overweight individuals was amplified and healthy weight individuals had higher activation in areas associated with gustatory processing in response to high-calorie food images. Our results showed that the obese/overweight exhibit hyper-responsivity in brain regions involved in reward processing for visual food cue which provide strong support for incentive-sensitization theory of obesity and healthy weight individuals showed higher response in inhibitory control region which support the inhibitory control deficit theory of obesity. | CognitiveConstruct | RewardProcessing |
32,088,112 | 10.1016/j.euroneuro.2020.01.019 | 2,020 | European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology | Eur Neuropsychopharmacol | Unpacking common and distinct neuroanatomical alterations in cocaine dependent versus pathological gambling. | Pathological gambling and cocaine dependence are highly pervasive disorders. Functional neuroimaging evidence implicates aberrant activity of prefrontal striatal pathways in both disorders. It is unclear if the neuroanatomy of these areas is also affected. Participants with pathological gambling (n = 18), cocaine dependence (n = 19) and controls (n = 21) underwent high-resolution structural MRI scan and cognitive assessments. In line with emerging functional neuroimaging findings, we hypothesised (i) lower volumes of corticostriatal areas ascribed to decision-making/inhibitory control, craving and reward processing (i.e., orbitofrontal cortex, inferior frontal gyrus, amygdala, striatum, insula) in both pathological gamblers and cocaine dependent participants versus controls; (ii) selected dopaminergic/glutamatergic pathways directly taxed by cocaine (i.e., superior, dorsolateral and anterior cingulate cortices) would be altered in cocaine dependent versus control participants only. Analyses were conducted with a bonferroni correction. Our results showed that both pathological gambling and cocaine dependent participants, compared to controls, had larger volumes of the right inferior frontal gyrus (ps <.01, ds = 0.66 and 0.62). Cocaine dependent participants had lower nucleus accumbens and medial orbitofrontal cortex volumes than pathological gamblers (ps <.05, ds = 0.51 and 0.72), with the latter being predicted by higher negative urgency scores. Inferior frontal gyrus volume may reflect common alterations of cocaine and gambling addictions, whereas cocaine dependence may be uniquely associated with reduced volume in dorsolateral and middle frontal regions. Cocaine's supra-physiological effects on mesolimbic neurons may explain reduced accumbens-orbitofrontal structure compared to gambling. | CognitiveConstruct | RewardProcessing |
32,067,136 | 10.1007/s00213-020-05478-z | 2,020 | Psychopharmacology | Psychopharmacology (Berl) | Methylphenidate affects task-switching and neural signaling in non-human primates. | Low doses of psychostimulants such as methylphenidate (MPH), which increase extracellular dopamine and norepinephrine by inhibiting their reuptake, are the most commonly used treatment for attention deficit hyperactivity disorder (ADHD). Therapeutic doses of these drugs may improve focused attention at the expense of hindering other cognitive functions, including the ability to adapt behavior in response to changing circumstances-cognitive flexibility. Cognitive flexibility is thought to depend on proper operation of the prefrontal cortex (PFC) and is also linked to reward processing, which is dopamine-dependent. Additionally, reward outcome signals have been recorded from the PFC. This study tested the hypothesis that therapeutic doses of MPH impair cognitive flexibility and that this impairment in performance resulted from interference in reward signals within the PFC. Four rhesus monkeys were given therapeutically relevant doses of oral MPH (0, 3, and 6 mg/kg) while performing an oculomotor switching task to evaluate its effect on task performance. Single-unit recordings in the PFC of two monkeys were taken before and after MPH administration during task performance. The results show that MPH does hinder switching task performance, an effect that was correlated with a reduction in the amplitude of outcome signals found in the discharges of some neurons in the PFC. Methylphenidate impaired task-switching performance, which can be used as a measure of cognitive flexibility. This detriment may result from degraded outcome signaling within the PFC. This study has implications for the use of MPH in the treatment of ADHD. | CognitiveConstruct | RewardProcessing |
32,058,065 | 10.1016/j.neuroscience.2020.01.038 | 2,020 | Neuroscience | Neuroscience | Gender Differences in the Associations Between Gray Matter Volume and the Centrality of Visual Product Aesthetics. | Visual aesthetics influence consumers' perception, acquisition, and usage of products, but the level of significance that a commercial product's visual aesthetics hold for each consumer varies from one person to another. Such individual difference is referred to as the centrality of visual product aesthetics (CVPA). Previous research has revealed that female adults scored higher than male adults in the self-reported CVPA scale. In order to identify the neuroanatomical correlates of this gender difference, we conducted a voxel-based morphometry (VBM) study to examine the association between the CVPA and gray matter volume (GMV) in a large sample of healthy adults from mainland China. The results revealed positive correlations between the female participants' CVPA scores and the GMV in two brain areas liked to reward processing, namely the left medial orbitofrontal cortex (mOFC) and the left dorsal striatum. By contrast, the results revealed a negative correlation between the male participants' CVPA scores and their GMV in the left mOFC. Collectively, these findings suggest that the level of significance that a commercial product's visual aesthetics hold for consumers may be associated with the rewards that they are able to receive from them. These findings also provide empirical evidence about the neuroanatomical correlates of self-reported values. | CognitiveConstruct | RewardProcessing |
32,055,822 | 10.1093/ijnp/pyaa007 | 2,020 | The international journal of neuropsychopharmacology | Int J Neuropsychopharmacol | A Neurofunctional Domains Approach to Evaluate D1/D5 Dopamine Receptor Partial Agonism on Cognition and Motivation in Healthy Volunteers With Low Working Memory Capacity. | Dopamine D1 receptor signaling plays key roles in core domains of neural function, including cognition and reward processing; however, many questions remain about the functions of circuits modulated by dopamine D1 receptor, largely because clinically viable, selective agonists have yet to be tested in humans. Using a novel, exploratory neurofunctional domains study design, we assessed the safety, tolerability, pharmacodynamics, and pharmacokinetics of PF-06412562, a selective D1/D5R partial agonist, in healthy male volunteers who met prespecified criteria for low working memory capacity. Functional magnetic resonance imaging, electrophysiologic endpoints, and behavioral paradigms were used to assess working memory, executive function, and motivation/reward processing following multiple-dose administration of PF-06412562. A total of 77 patients were assigned PF-06412562 (3 mg twice daily and 15 mg twice daily) or placebo administered for 5 to 7 days. Due to the exploratory nature of the study, it was neither powered for any specific treatment effect nor corrected for multiple comparisons. Nominally significant improvements from baseline in cognitive endpoints were observed in all 3 groups; however, improvements in PF-06412562-treated patients were less than in placebo-treated participants. Motivation/reward processing endpoints were variable. PF-06412562 was safe and well tolerated, with no serious adverse events, severe adverse events, or adverse events leading to dose reduction or temporary discontinuation except for 1 permanent discontinuation due to increased orthostatic heart rate. PF-06412562, in the dose range and patient population explored in this study, did not improve cognitive function or motivation/reward processing more than placebo over the 5- to 7-day treatment period. NCT02306876. | CognitiveConstruct | RewardProcessing |
32,054,621 | 10.1523/ENEURO.0356-19.2020 | 2,020 | eNeuro | eNeuro | Arousal State-Dependent Alterations in VTA-GABAergic Neuronal Activity. | Decades of research have implicated the ventral tegmental area (VTA) in motivation, learning and reward processing. We and others recently demonstrated that it also serves as an important node in sleep/wake regulation. Specifically, VTA-dopaminergic neuron activation is sufficient to drive wakefulness and necessary for the maintenance of wakefulness. However, the role of VTA-GABAergic neurons in arousal regulation is not fully understood. It is still unclear whether VTA-GABAergic neurons predictably alter their activity across arousal states, what is the nature of interactions between VTA-GABAergic activity and cortical oscillations, and how activity in VTA-GABAergic neurons relates to VTA-dopaminergic neurons in the context of sleep/wake regulation. To address these, we simultaneously recorded population activity from VTA subpopulations and electroencephalography/electromyography (EEG/EMG) signals during spontaneous sleep/wake states and in the presence of salient stimuli in freely-behaving mice. We found that VTA-GABAergic neurons exhibit robust arousal-state-dependent alterations in population activity, with high activity and transients during wakefulness and REM sleep. During wakefulness, population activity of VTA-GABAergic neurons, but not VTA-dopaminergic neurons, was positively correlated with EEG γ power and negatively correlated with θ power. During NREM sleep, population activity in both VTA-GABAergic and VTA-dopaminergic neurons negatively correlated with δ, θ, and σ power bands. Salient stimuli, with both positive and negative valence, activated VTA-GABAergic neurons. Together, our data indicate that VTA-GABAergic neurons, like their dopaminergic counterparts, drastically alter their activity across sleep-wake states. Changes in their activity predicts cortical oscillatory patterns reflected in the EEG, which are distinct from EEG spectra associated with dopaminergic neural activity. | CognitiveConstruct | RewardProcessing |
32,051,656 | 10.1007/s10862-018-9712-4 | 2,019 | Journal of psychopathology and behavioral assessment | J Psychopathol Behav Assess | Disentangling Reward Processing in Trichotillomania: 'Wanting' and 'Liking' Hair Pulling Have Distinct Clinical Correlates. | Trichotillomania (TTM; hair-pulling disorder) is characterized by an irresistible urge or desire to pull out one's own hair, and a sense of pleasure when hair is pulled out. Evidence from translational neuroscience has shown that 'wanting' (motivation to seek a reward) and 'liking' (enjoyment when reward is received) are each mediated by overlapping but distinct neural circuitry, and that 'wanting' contributes to addictive/compulsive behaviors more so than 'liking'. In the present study, we developed the Hair Pulling Reward Scale (HPRS), a self-report measure that consists of two subscales designed to assess (a) cue-triggered urges and appetitive motivation to pull hair (i.e., putative correlates of 'wanting'), and (b) momentary pleasure and gratification during pulling episodes (i.e., putative correlates of 'liking'). We administered the HPRS to 259 individuals with TTM and examined its psychometric properties. Confirmatory factor analysis supported a two-factor model reflecting correlated Wanting and Liking scales. Consistent with predictions, Wanting, much more than Liking, had robust correlations with TTM severity, impulsiveness, difficulties in emotion regulation, psychiatric symptoms, and sleep dysfunction. The results suggest that the HPRS is a psychometrically sound instrument that can be used as a symptom-level measure of reward processing in TTM. | CognitiveConstruct | RewardProcessing |
32,047,245 | 10.1038/s41598-020-59329-0 | 2,020 | Scientific reports | Sci Rep | Effects of exogenous testosterone application on network connectivity within emotion regulation systems. | Studies with steroid hormones underlined the vital role of testosterone on social-emotional processing. However, there is still a lack of studies investigating whether testosterone modulates network connectivity during resting-state. Here, we tested how the exogenous application of testosterone would affect functional connectivity between regions implicated in emotion regulation. In total, 96 male participants underwent resting-state fMRI scanning. Before the measurement, half of the subjects received 5 g Testim gel (containing 50 mg testosterone) and the other half a corresponding amount of placebo gel. Seeds for the connectivity analysis were meta-analytically defined. First, all regions associated with emotion regulation were chosen via Neurosynth (data driven). Among those, specific seeds were selected and categorized based on the neural model of emotion regulation by Etkin and colleagues (Etkin et al., 2015) (theory-guided). Resting-state connectivity analysis revealed decreased connectivity between the right DLPFC and the right amygdala as well as between the VMPFC and the left IPL for the testosterone group compared to the placebo group. A complementary dynamic causal modeling (DCM) analysis on findings from the resting-state connectivity analysis underlined a bidirectional coupling which was decreased close to zero by testosterone administration. Our results demonstrate that testosterone administration disrupts resting-state connectivity within fronto-subcortical and fronto-parietal circuits. The findings suggest that even without a specific task (e.g. challenge, reward processing) testosterone modulates brain networks important for social-emotional processing. | CognitiveConstruct | RewardProcessing |
32,046,333 | 10.3390/jcm9020468 | 2,020 | Journal of clinical medicine | J Clin Med | Microglial Function in the Effects of Early-Life Stress on Brain and Behavioral Development. | The putative effects of early-life stress (ELS) on later behavior and neurobiology have been widely investigated. Recently, microglia have been implicated in mediating some of the effects of ELS on behavior. In this review, findings from preclinical and clinical literature with a specific focus on microglial alterations induced by the exposure to ELS (i.e., exposure to behavioral stressors or environmental agents and infection) are summarized. These studies were utilized to interpret changes in developmental trajectories based on the time at which the stress occurred, as well as the paradigm used. ELS and microglial alterations were found to be associated with a wide array of deficits including cognitive performance, memory, reward processing, and processing of social stimuli. Four general conclusions emerged: (1) ELS interferes with microglial developmental programs, including their proliferation and death and their phagocytic activity; (2) this can affect neuronal and non-neuronal developmental processes, which are dynamic during development and for which microglial activity is instrumental; (3) the effects are extremely dependent on the time point at which the investigation is carried out; and (4) both pre- and postnatal ELS can prime microglial reactivity, indicating a long-lasting alteration, which has been implicated in behavioral abnormalities later in life. | CognitiveConstruct | RewardProcessing |
32,045,732 | 10.1016/j.nicl.2020.102202 | 2,020 | NeuroImage. Clinical | Neuroimage Clin | Is monetary reward processing altered in drug-naïve youth with a behavioral addiction? Findings from internet gaming disorder. | Current models of addiction biology highlight altered neural responses to non-drug rewards as a central feature of addiction. However, given that drugs of abuse can directly impact reward-related dopamine circuitry, it is difficult to determine the extent to which reward processing alterations are a trait feature of individuals with addictions, or primarily a consequence of exogenous drug exposure. Examining individuals with behavioral addictions is one promising approach for disentangling neural features of addiction from the direct effects of substance exposure. The current fMRI study compared neural responses during monetary reward processing between drug naïve young adults with a behavioral addiction, internet gaming disorder (IGD; n = 22), and healthy controls (n = 27) using a monetary incentive delay task. Relative to controls, individuals with IGD exhibited blunted caudate activity associated with loss magnitude at the outcome stage, but did not differ from controls in neural activity at other stages. These findings suggest that decreased loss sensitivity might be a critical feature of IGD, whereas alterations in gain processing may be less characteristic of individuals with IGD, relative to those with substance use disorders. Therefore, classic theories of altered reward processing in substance use disorders should be translated to behavioral addictions with caution. | CognitiveConstruct | RewardProcessing |
32,043,206 | 10.3758/s13415-019-00764-6 | 2,020 | Cognitive, affective & behavioral neuroscience | Cogn Affect Behav Neurosci | Modulatory effects of positive mood and approach motivation on reward processing: Two sides of the same coin? | In a previous study (Paul & Pourtois, 2017), we found that positive mood substantially influenced the neural processing of reward, mostly by altering expectations and creating an optimistic bias. Under positive mood, the Reward Positivity (RewP) component and fronto-medial theta activity (FMθ) in response to monetary feedback were both changed compared with neutral mood. Nevertheless, whether positive valence per se or motivational intensity drove these neurophysiological effects remained unclear. To address this question, we combined a mindset manipulation with an imagery procedure to create and maintain three different affective states using a between-subjects design: a neutral mood, and positive mood with either high or low motivational intensity. After mood induction, 161 participants performed a simple gambling task while 64-channel EEG was recorded. FMθ activity results showed that irrespective of motivational intensity, positive compared with neutral mood altered reward expectancy. By comparison, RewP was not affected by positive mood nor motivational intensity. These results suggest that positive mood, rather than motivational intensity, is likely driving the change in reward expectation during gambling, which could reflect the presence of an optimistic bias. Moreover, at the methodological level, they confirm that the RewP ERP component and FMθ activity can capture dissociable effects during reward processing. | CognitiveConstruct | RewardProcessing |
32,040,562 | 10.1093/brain/awaa002 | 2,020 | Brain : a journal of neurology | Brain | Baseline reward processing and ventrostriatal dopamine function are associated with pramipexole response in depression. | The efficacy of dopamine agonists in treating major depressive disorder has been hypothesized to stem from effects on ventrostriatal dopamine and reward function. However, an important question is whether dopamine agonists are most beneficial for patients with reward-based deficits. This study evaluated whether measures of reward processing and ventrostriatal dopamine function predicted response to the dopamine agonist, pramipexole (ClinicalTrials.gov Identifier: NCT02033369). Individuals with major depressive disorder (n = 26) and healthy controls (n = 26) (mean ± SD age = 26.5 ± 5.9; 50% female) first underwent assessments of reward learning behaviour and ventrostriatal prediction error signalling (measured using functional MRI). 11C-(+)-PHNO PET before and after oral amphetamine was used to assess ventrostriatal dopamine release. The depressed group then received open-label pramipexole treatment for 6 weeks (0.5 mg/day titrated to a maximum daily dose of 2.5 mg). Symptoms were assessed weekly, and reward learning was reassessed post-treatment. At baseline, relative to controls, the depressed group showed lower reward learning (P = 0.02), a trend towards blunted reward-related prediction error signals (P = 0.07), and a trend towards increased amphetamine-induced dopamine release (P = 0.07). Despite symptom improvements following pramipexole (Cohen's d ranging from 0.51 to 2.16 across symptom subscales), reward learning did not change after treatment. At a group level, baseline reward learning (P = 0.001) and prediction error signalling (P = 0.004) were both associated with symptom improvement, albeit in a direction opposite to initial predictions: patients with stronger pretreatment reward learning and reward-related prediction error signalling improved most. Baseline D2/3 receptor availability (P = 0.02) and dopamine release (P = 0.05) also predicted improvements in clinical functioning, with lower D2/3 receptor availability and lower dopamine release predicting greater improvements. Although these findings await replication, they suggest that measures of reward-related mesolimbic dopamine function may hold promise for identifying depressed individuals likely to respond favourably to dopaminergic pharmacotherapy. | CognitiveConstruct | RewardProcessing |
32,036,303 | 10.1016/j.nicl.2020.102193 | 2,020 | NeuroImage. Clinical | Neuroimage Clin | Striatal reactivity to reward under threat-of-shock and working memory load in adults at increased familial risk for major depression: A preliminary study. | Anhedonia, a core symptom of Major Depressive Disorder (MDD), manifests as a lack or loss of motivation as reflected by decreased reward responsiveness, at both behavioral and neural (i.e., striatum) levels. Exposure to stressful life events is another important risk factor for MDD. However, the mechanisms linking reward-deficit and stress to MDD remain poorly understood. Here, we explore whether the effects of stress exposure on reward processing might differentiate between Healthy Vulnerable adults (HVul, i.e., positive familial MDD) from Healthy Controls (HCon). Furthermore, the well-described reduction in cognitive resources in MDD might facilitate the stress-induced decrease in reward responsiveness in HVul individuals. Accordingly, this study includes a manipulation of cognitive resources to address the latter possibility. 16 HVul (12 females) and 16 gender- and age-matched HCon completed an fMRI study, during which they performed a working memory reward task. Three factors were manipulated: reward (reward, no-reward), cognitive resources (working memory at low and high load), and stress level (no-shock, unpredictable threat-of-shock). Only the reward anticipation phase was analyzed. Imaging analyses focused on striatal function. Compared to HCon, HVul showed lower activation in the caudate nucleus across all conditions. The HVul group also exhibited lower stress-related activation in the nucleus accumbens, but only in the low working memory (WM) load condition. Moreover, while stress potentiated putamen reactivity to reward cues in HVul when the task was more demanding (high WM load), stress blunted putamen reactivity in both groups when no reward was at stake. Findings suggest that HVul might be at increased risk of developing anhedonic symptoms due to weaker encoding of reward value, higher difficulty to engage in goal-oriented behaviors and increased sensitivity to negative feedback, particularly in stressful contexts. These findings open new avenues for a better understanding of the mechanisms underlying how the complex interaction between the systems of stress and reward responsiveness contribute to the vulnerability to MDD, and how cognitive resources might modulate this interaction. | CognitiveConstruct | RewardProcessing |
32,028,083 | 10.1016/j.psyneuen.2020.104589 | 2,020 | Psychoneuroendocrinology | Psychoneuroendocrinology | Effects of hydrocortisone and yohimbine on decision-making under risk. | Many studies have investigated the influence of stress on decision-making. However, results are equivocal and the exact role of increased noradrenaline and cortisol after stress remains unclear. Using pharmacological manipulation, we investigated the influence of noradrenergic and glucocorticoid activity on risky decision-making in a gambling task that included mixed-gamble trials (gains and losses are possible) and gain-only trials. One hundred-and-four healthy young men participated in our randomized, double-blind, placebo-controlled, between-group study. Participants were randomly assigned to one of four groups: (A) yohimbine, (B) hydrocortisone, (C) yohimbine and hydrocortisone, or (D) placebo. Frequency of risky choices, i.e., monetary risk taking, was the dependent variable. We also investigated the influence of hydrocortisone and yohimbine on loss aversion, which is the tendency to overweigh losses compared with gains. Participants chose the risky option less often after receiving hydrocortisone compared with no hydrocortisone. This effect was strongest in the gain-only trials. Yohimbine had no effect. Loss aversion was not affected by hydrocortisone or yohimbine. Decreased reward processing may explain the reduction of risk taking by hydrocortisone in gain-only trials. The effects of stress hormones on different decision-related constructs and processes hence require further investigation. | CognitiveConstruct | RewardProcessing |
31,998,210 | 10.3389/fneur.2019.01338 | 2,019 | Frontiers in neurology | Front Neurol | Behavioral and Neuroanatomical Account of Impulsivity in Parkinson's Disease. | Impulse control disorder (ICD) is a major non-motor complication of Parkinson's disease (PD) with often devastating consequences for patients' quality of life. In this study, we aimed to characterize the phenotype of impulsivity in PD and its neuroanatomical correlates. Thirty-seven PD patients (15 patients with ICD, 22 patients without ICD) and 36 healthy controls underwent a neuropsychological battery. The test battery consisted of anxiety and depression scales, self-report measures of impulsivity (Barratt scale and UPPS-P), behavioral measures of impulsive action (Go/No-Go task, Stop signal task) and impulsive choice (Delay discounting, Iowa gambling task), and measures of cognitive abilities (working memory, attention, executive function). Patients and controls underwent structural MRI scanning. Patients with ICD had significantly higher levels of self-reported impulsivity (Barratt scale and Lack of perseverance from UPPS-P) in comparison with healthy controls and non-impulsive PD patients, but they performed similarly in behavioral tasks, except for the Iowa gambling task. In this task, patients with ICD made significantly less risky decisions than patients without ICD and healthy controls. Patients without ICD did not differ from healthy controls in self-reported impulsivity or behavioral measurements. Both patient groups were more anxious and depressive than healthy controls. MRI scanning revealed structural differences in cortical areas related to impulse control in both patient groups. Patients without ICD had lower volumes and cortical thickness of bilateral inferior frontal gyrus. Patients with ICD had higher volumes of right caudal anterior cingulate and rostral middle frontal cortex. Despite the presence of ICD as confirmed by both clinical follow-up and self-reported impulsivity scales and supported by structural differences in various neural nodes related to inhibitory control and reward processing, patients with ICD performed no worse than healthy controls in various behavioral tasks previously hypothesized as robust impulsivity measures. These results call for caution against impetuous interpretation of behavioral tests, since various factors may and will influence the ultimate outcomes, be it the lack of sensitivity in specific, limited ICD subtypes, excessive caution of ICD patients during testing due to previous negative experience rendering simplistic tasks insufficient, or other, as of now unknown aspects, calling for further research. | CognitiveConstruct | RewardProcessing |
31,993,667 | 10.1093/scan/nsaa005 | 2,019 | Social cognitive and affective neuroscience | Soc Cogn Affect Neurosci | Behavioral and neural evidence for an evaluative bias against other people's mundane interracial encounters. | Evaluating other people's social encounters from a third-person perspective is an ubiquitous activity of daily life. Yet little is known about how these evaluations are affected by racial bias. To overcome this empirical lacuna, two experiments were conducted. The first experiment used evaluative priming to show that both Black (n = 44) and White Americans (n = 44) assess the same mundane encounters (e.g. two people chatting) less favorably when they involve a Black and a White individual rather than two Black or two White individuals. The second experiment used functional magnetic resonance imaging to demonstrate that both Black (n = 46) and White Americans (n = 42) respond with reduced social reward processing (i.e. lower activity in the ventral striatum) and enhanced mentalizing (e.g. higher activity in the bilateral temporal-parietal junction) toward so-called cross-race relative to same-race encounters. By combining unobtrusive measures from social psychology and social neuroscience, this work demonstrates that racial bias can affect impression formation even at the level of the dyad. | CognitiveConstruct | RewardProcessing |
31,989,721 | 10.1111/ejn.14688 | 2,020 | The European journal of neuroscience | Eur J Neurosci | Mitogen-activated protein kinase phosphatase-2 deletion modifies ventral tegmental area function and connectivity and alters reward processing. | Mitogen-activated protein kinases (MAPKs) regulate normal brain functioning, and their dysfunction is implicated in a number of brain disorders. Thus, there is great interest in understanding the signalling systems that control MAPK functioning. One family of proteins that contribute to this process, the mitogen-activated protein kinase phosphatases (MKPs), directly inactivate MAPKs through dephosphorylation. Recent studies have identified novel functions of MKPs in foetal development, the immune system, cancer and synaptic plasticity and memory. In the present study, we performed an unbiased investigation using MKP-2 mice to assess whether MKP-2 plays a global role in modulating brain function. Local cerebral glucose utilization is significantly increased in the ventral tegmental area (VTA) of MKP-2 mice, with connectivity analysis revealing alterations in VTA functional connectivity, including a significant reduction in connectivity to the nucleus accumbens and hippocampus. In addition, spontaneous excitatory postsynaptic current frequency, but not amplitude, onto putative dopamine neurons in the VTA is increased in MKP-2 mice, which indicates that increased excitatory drive may account for the increased VTA glucose utilization. Consistent with modified VTA function and connectivity, in behavioural tests MKP-2 mice exhibited increased sucrose preference and impaired amphetamine-induced hyperlocomotion. Overall, these data reveal that MKP-2 plays a role in modulating VTA function and that its dysfunction may contribute to brain disorders in which altered reward processing is present. | CognitiveConstruct | RewardProcessing |
31,948,895 | 10.1016/j.schres.2019.12.041 | 2,020 | Schizophrenia research | Schizophr Res | Reward anticipation in schizophrenia: A coordinate-based meta-analysis. | Reward processing impairments have been linked with positive and negative symptoms of schizophrenia. Here, we performed a coordinate-based meta-analysis that combined eleven BOLD-fMRI studies comparing reward anticipation signals between schizophrenia patients and healthy controls. We observed a reduced difference in activation in schizophrenia patients within a frontal-striatal network. Meta-regressions revealed that this functional signature was linked to the severity of psychotic symptoms and persisted even after controlling for the dose of antipsychotic medications. | CognitiveConstruct | RewardProcessing |
31,932,769 | 10.1038/s41593-019-0567-0 | 2,020 | Nature neuroscience | Nat Neurosci | Temporally restricted dopaminergic control of reward-conditioned movements. | Midbrain dopamine (DA) neurons encode both reward- and movement-related events and are implicated in disorders of reward processing as well as movement. Consequently, disentangling the contribution of DA neurons in reinforcing versus generating movements is challenging and has led to lasting controversy. In this study, we dissociated these functions by parametrically varying the timing of optogenetic manipulations in a Pavlovian conditioning task and examining the influence on anticipatory licking before reward delivery. Inhibiting both ventral tegmental area and substantia nigra pars compacta DA neurons in the post-reward period had a significantly greater behavioral effect than inhibition in the pre-reward period of the task. Furthermore, the contribution of DA neurons to behavior decreased linearly as a function of elapsed time after reward. Together, the results indicate a temporally restricted role of DA neurons primarily related to reinforcing stimulus-reward associations and suggest that directly generating movements is a comparatively less important function. | CognitiveConstruct | RewardProcessing |
31,931,509 | 10.1038/s41386-020-0611-5 | 2,020 | Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology | Neuropsychopharmacology | The acute effects of nicotine on corticostriatal responses to distinct phases of reward processing. | Nicotine enhances the reinforcement of non-drug rewards by increasing nucleus accumbens (NAcc) reactivity to anticipatory cues. This anticipatory effect is selective as no clear evidence has emerged showing that nicotine acutely changes reward receipt reactivity. However, repeated rewarding experiences shift peak brain reactivity from hedonic reward outcome to the motivational anticipatory cue yielding more habitual cue-induced behavior. Given nicotine's influence on NAcc reactivity and connectivity, it is plausible that nicotine acutely induces this shift and alters NAcc functional connectivity during reward processing. To evaluate this currently untested hypothesis, a randomized crossover design was used in which healthy non-smokers were administered placebo and nicotine (2-mg lozenge). Brain activation to monetary reward anticipation and outcome was evaluated with functional magnetic resonance imaging. Relative to placebo, nicotine induced more NAcc reactivity to reward anticipation. Greater NAcc activation during anticipation was significantly associated with lower NAcc activation to outcome. During outcome, nicotine reduced NAcc functional connectivity with cortical regions including the anterior cingulate cortex, orbitofrontal cortex, and insula. These regions showed the same negative relationship between reward anticipation and outcome as noted in the NAcc. The current findings significantly improve our understanding of how nicotine changes corticostriatal circuit function and communication during distinct phases of reward processing and critically show that these alterations happen acutely following a single dose. The implications of this work explain nicotinic modulation of general reward function, which offer insights into the initial drive to smoke and the subsequent difficulty in cessation. | CognitiveConstruct | RewardProcessing |
31,931,508 | 10.1038/s41386-020-0610-6 | 2,020 | Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology | Neuropsychopharmacology | Epigenetic modification of the oxytocin receptor gene: implications for autism symptom severity and brain functional connectivity. | The role of oxytocin in social cognition has attracted tremendous interest in social neuroscience and psychiatry. Some studies have reported improvement in social symptoms following oxytocin treatment in autism spectrum disorders (ASD), while others point to endogenous factors influencing its efficiency and to mixed results in terms of long-term clinical benefits. Epigenetic modification to the oxytocin receptor gene (OXTR) in ASD could be an informative biomarker of treatment efficacy. Yet, little is known about the relationship between OXTR methylation, clinical severity, and brain function in ASD. Here, we investigated the relationship between OXTR methylation, ASD diagnosis (in N = 35 ASD and N = 64 neurotypical group), measures of social responsiveness, and resting-state functional connectivity (rsFC) between areas involved in social cognition and reward processing (in a subset of ASD, N = 30). Adults with ASD showed higher OXTR methylation levels in the intron 1 area compared with neurotypical subjects. This hypermethylation was related to clinical symptoms and to a hypoconnectivity between cortico-cortical areas involved in theory of mind. Methylation at a CpG site in the exon 1 area was positively related to social responsiveness deficits in ASD and to a hyperconnectivity between striatal and cortical brain areas. Taken together, these findings provide initial evidence for OXTR hypermethylation in the intron area as a potential biomarker for adults with ASD with less severe developmental communication deficits, but with impairments in theory of mind and self-awareness. Also, OXTR methylation in the exon 1 area could be a potential biomarker of sociability sensitive to life experiences. | CognitiveConstruct | RewardProcessing |
31,930,153 | 10.1117/1.NPh.6.2.025011 | 2,019 | Neurophotonics | Neurophotonics | Functional near-infrared spectroscopy-informed neurofeedback: regional-specific modulation of lateral orbitofrontal activation and cognitive flexibility. | Cognitive flexibility and reward processing critically rely on the orbitofrontal cortex (OFC). Dysregulations in these domains and orbitofrontal activation have been reported in major psychiatric disorders. Hemodynamic brain imaging-informed neurofeedback allows regional-specific control over brain activation and thus may represent an innovative intervention to regulate orbitofrontal dysfunctions. Against this background the present proof-of-concept study evaluates the feasibility and behavioral relevance of functional near-infrared spectroscopy (fNIRS)-assisted neurofeedback training of the lateral orbitofrontal cortex (lOFC). In a randomized sham-controlled between-subject design, 60 healthy participants have undergone four subsequent runs of training to enhance the lOFC activation. Training-induced changes in the lOFC, attentional set-shifting performance, and reward experience have served as primary outcomes. Feedback from the target channel significantly increases the regional-specific lOFC activation over the four training runs in comparison with sham neurofeedback. The real-time OFC neurofeedback group demonstrates a trend for faster responses during the set-shifting relative to the sham neurofeedback group. Within the real-time OFC neurofeedback group, stronger training-induced lOFC increases are associated with higher reward experience. The present results demonstrate that fNIRS-informed neurofeedback allows regional-specific regulation of lOFC activation and may have the potential to modulate the associated behavioral domains. As such fNIRS-informed neurofeedback may represent a promising strategy to regulate OFC dysfunctions in psychiatric disorders. | CognitiveConstruct | RewardProcessing |
31,928,716 | 10.1016/j.biopsych.2019.11.001 | 2,020 | Biological psychiatry | Biol Psychiatry | From Signaling Molecules to Circuits and Behaviors: Cell-Type-Specific Adaptations to Psychostimulant Exposure in the Striatum. | Addiction is characterized by a compulsive pattern of drug seeking and consumption and a high risk of relapse after withdrawal that are thought to result from persistent adaptations within brain reward circuits. Drugs of abuse increase dopamine (DA) concentration in these brain areas, including the striatum, which shapes an abnormal memory trace of drug consumption that virtually highjacks reward processing. Long-term neuronal adaptations of gamma-aminobutyric acidergic striatal projection neurons (SPNs) evoked by drugs of abuse are critical for the development of addiction. These neurons form two mostly segregated populations, depending on the DA receptor they express and their output projections, constituting the so-called direct (D receptor) and indirect (D receptor) SPN pathways. Both SPN subtypes receive converging glutamate inputs from limbic and cortical regions, encoding contextual and emotional information, together with DA, which mediates reward prediction and incentive values. DA differentially modulates the efficacy of glutamate synapses onto direct and indirect SPN pathways by recruiting distinct striatal signaling pathways, epigenetic and genetic responses likely involved in the transition from casual drug use to addiction. Herein we focus on recent studies that have assessed psychostimulant-induced alterations in a cell-type-specific manner, from remodeling of input projections to the characterization of specific molecular events in each SPN subtype and their impact on long-lasting behavioral adaptations. We discuss recent evidence revealing the complex and concerted action of both SPN populations on drug-induced behavioral responses, as these studies can contribute to the design of future strategies to alleviate specific behavioral components of addiction. | CognitiveConstruct | RewardProcessing |
31,927,758 | 10.1007/s11682-019-00215-3 | 2,020 | Brain imaging and behavior | Brain Imaging Behav | Basal ganglia lateralization in different types of reward. | Reward processing is a fundamental human activity. The basal ganglia are recognized for their role in reward processes; however, specific roles of the different nuclei (e.g., nucleus accumbens, caudate, putamen and globus pallidus) remain unclear. Using quantitative meta-analyses we assessed whole-brain and basal ganglia specific contributions to money, erotic, and food reward processing. We analyzed data from 190 fMRI studies which reported stereotaxic coordinates of whole-brain, within-group results from healthy adult participants. Results showed concordance in overlapping and distinct cortical and sub-cortical brain regions as a function of reward type. Common to all reward types was concordance in basal ganglia nuclei, with distinct differences in hemispheric dominance and spatial extent in response to the different reward types. Food reward processing favored the right hemisphere; erotic rewards favored the right lateral globus pallidus and left caudate body. Money rewards engaged the basal ganglia bilaterally including its most anterior part, nucleus accumbens. We conclude by proposing a model of common reward processing in the basal ganglia and separate models for money, erotic, and food rewards. | CognitiveConstruct | RewardProcessing |
31,927,083 | 10.1016/j.nlm.2020.107162 | 2,020 | Neurobiology of learning and memory | Neurobiol Learn Mem | Instrumental learning in a mouse model for obsessive-compulsive disorder: Impaired habit formation in Sapap3 mutants. | It has been hypothesized that maladaptive habit formation contributes to compulsivity in psychiatric disorders such as obsessive-compulsive disorder (OCD). Here, we used an established animal model of OCD, Sapap3 knockout mice (SAPAP3), to investigate the balance of goal-directed and habitual behavior in compulsive individuals and if altered habit formation is associated with compulsive-like behavior. We subjected 24 SAPAP3 and 24 wildtype littermates (WT) to two different schedules of reinforcement in a within-subjects design: a random-ratio (RR) schedule to promote goal-directedness, and a random-interval (RI) schedule, known to facilitate habitual responding. SAPAP3 acquired responding under both schedules, but showed lower response rates and fewer attempts to collect food pellets than WT, indicative of altered reward processing. As expected, WT were sensitive to sensory-specific satiety (outcome devaluation) following RR training, but not RI training, demonstrating schedule-specific acquisition of goal-directed and habitual responding, respectively. In contrast, SAPAP3 were sensitive to outcome devaluation after both RR and RI training, suggesting decreased engagement of a habitual response strategy. No linear relation was observed between increased grooming and behavior during the outcome devaluation test in SAPAP3. Together, our findings demonstrate altered reward processing and impaired habit learning in SAPAP3. We report a diminished propensity to form habits in these mice, which albeit inconsistent with the predominant idea of excessive habit formation in OCD, nonetheless points at dysregulation of behavioral automation in the context of compulsivity. Thus, the habit hypothesis of compulsivity should be updated to state that an imbalance of habitual and goal-directed responding in either direction can contribute to the development of compulsive behavior. | CognitiveConstruct | RewardProcessing |
31,924,324 | 10.1016/j.biopsych.2019.10.027 | 2,020 | Biological psychiatry | Biol Psychiatry | A Critical Role of Basolateral Amygdala-to-Nucleus Accumbens Projection in Sleep Regulation of Reward Seeking. | Sleep impacts reward-motivated behaviors partly by retuning the brain reward circuits. The nucleus accumbens (NAc) is a reward processing hub sensitive to acute sleep deprivation. Glutamatergic transmission carrying reward-associated signals converges in the NAc and regulates various aspects of reward-motivated behaviors. The basolateral amygdala projection (BLAp) innervates broad regions of the NAc and critically regulates reward seeking. Using slice electrophysiology, we measured how acute sleep deprivation alters transmission at BLAp-NAc synapses in male C57BL/6 mice. Moreover, using SSFO (stabilized step function opsin) and DREADDs (designer receptors exclusively activated by designer drugs) (Gi) to amplify and reduce transmission, respectively, we tested behavioral consequences following bidirectional manipulations of BLAp-NAc transmission. Acute sleep deprivation increased sucrose self-administration in mice and altered the BLAp-NAc transmission in a topographically specific manner. It selectively reduced glutamate release at the rostral BLAp (rBLAp) onto ventral and lateral NAc (vlNAc) synapses, but spared caudal BLAp onto medial NAc synapses. Furthermore, experimentally facilitating glutamate release at rBLAp-vlNAc synapses suppressed sucrose reward seeking. Conversely, mimicking sleep deprivation-induced reduction of rBLAp-vlNAc transmission increased sucrose reward seeking. Finally, facilitating rBLAp-vlNAc transmission per se did not promote either approach motivation or aversion. Sleep acts on rBLAp-vINAc transmission gain control to regulate established reward seeking but does not convey approach motivation or aversion on its own. | CognitiveConstruct | RewardProcessing |
31,921,421 | 10.1186/s40337-019-0276-9 | 2,020 | Journal of eating disorders | J Eat Disord | Food related attention bias modification training for anorexia nervosa and its potential underpinning mechanisms. | Treatment outcomes in anorexia nervosa (AN) remain suboptimal, evidencing the need for better and more targeted treatments. Whilst the aetiology of AN is complex, cognitive processes such as attention bias (AB) have been proposed to contribute to maintaining food restriction behaviour. Attention bias modification raining (ABMT) has been investigated in other eating disorders (EDs) such as binge eating disorder (BED) as a means of modifying AB for food and of changing eating behaviour. Promising findings have been reported, but the mechanisms underlying ABMT are poorly understood. We hypothesise that in AN, ABMT has the potential to modify maladaptive eating behaviours related to anxiety around food and eating and propose two mechanistic models; (1) ABMT increases general attentional control (which will improve control over disorder-relevant thoughts) or (2) ABMT promotes stimulus re-evaluation. In this second case, the effects of ABMT might arise via changes in the subjective value of food stimuli (i.e. reward processing) or via habituation, with both resulting in a reduced threat response. Investigating the clinical potential of ABMT in AN holds the promise of a novel, evidence-based adjunctive treatment approach. Importantly, understanding ABMT's underlying mechanisms will help tailor treatment protocols and improve understanding of the cognitive characteristics of AN and other EDs. | CognitiveConstruct | RewardProcessing |
31,913,979 | 10.1097/HRP.0000000000000241 | 2,020 | Harvard review of psychiatry | Harv Rev Psychiatry | Using Neuroscience to Augment Behavioral Interventions for Depression. | Depression is both prevalent and costly, and many individuals do not adequately respond to existing psychopharmacological and behavioral interventions. The current article describes the use of neuroscience in augmenting behavioral interventions for depression in two primary areas: anhedonia and cognitive deficits/biases. Neuroscience research has increased our understanding of the neural bases of reward processing and regulation of positive affect, and anhedonia among depressed samples can be related to deficits in each of these domains. Treatments that specifically target reward processing and regulation of positive affect in order to reduce anhedonia represent a recent advance in the field. Depression is also associated with aberrant processes relating to working memory, autobiographical memory, attentional bias, and interpretive bias. Neuroscience findings have increasingly been leveraged to augment the efficacy of cognitive-training and bias-modification interventions in these domains. The use of neuroscience to inform the development and augmentation of behavioral interventions for depression is a promising avenue of continued research. | CognitiveConstruct | RewardProcessing |
31,908,976 | 10.1016/j.scog.2019.100171 | 2,020 | Schizophrenia research. Cognition | Schizophr Res Cogn | Six month durability of targeted cognitive training supplemented with social cognition exercises in schizophrenia. | Deficits in cognition, social cognition, and motivation are significant predictors of poor functional outcomes in schizophrenia. Evidence of durable benefit following social cognitive training is limited. We previously reported the effects of 70 h of targeted cognitive training supplemented with social cognitive exercises (TCT + SCT) verses targeted cognitive training alone (TCT). Here, we report the effects six months after training. 111 participants with schizophrenia spectrum disorders were randomly assigned to TCT + SCT or TCT-only. Six months after training, thirty-four subjects (18 TCT + SCT, 16 TCT-only) were assessed on cognition, social cognition, reward processing, symptoms, and functioning. Intent to treat analyses was used to test the durability of gains, and the association of gains with improvements in functioning and reward processing were tested. Both groups showed durable improvements in multiple cognitive domains, symptoms, and functional capacity. Gains in global cognition were significantly associated with gains in functional capacity. In the TCT + SCT group, participants showed durable improvements in prosody identification and reward processing, relative to the TCT-only group. Gains in reward processing in the TCT + SCT group were significantly associated with improvements in social functioning. Both TCT + SCT and TCT-only result in durable improvements in cognition, symptoms, and functional capacity six months post-intervention. Supplementing TCT with social cognitive training offers greater and enduring benefits in prosody identification and reward processing. These results suggest that novel cognitive training approaches that integrate social cognitive exercises may lead to greater improvements in reward processing and functioning in individuals with schizophrenia. | CognitiveConstruct | RewardProcessing |
31,908,107 | 10.1111/adb.12863 | 2,021 | Addiction biology | Addict Biol | Investigation of brain functional connectivity to assess cognitive control over cue-processing in Alcohol Use Disorder. | Alcohol Use Disorder has been associated with impairments of functional connectivity between neural networks underlying reward processing and cognitive control. Evidence for aberrant functional connectivity between the striatum, insula, and frontal cortex in alcohol users exists at rest, but not during cue-exposure. In this study, we investigated functional connectivity changes during a cue-reactivity task across different subgroups of alcohol consumers. Ninety-six participants (ranging from light social to heavy social drinkers and nonabstinent dependent to abstinent dependent drinkers) were examined. A functional magnetic resonance imaging cue-reactivity paradigm was administered, during which alcohol-related and neutral stimuli were presented. Applying psychophysiological interaction analyses, we found: (a) Abstinent alcohol-dependent patients compared with non-abstinent dependent drinkers showed a greater increase of functional connectivity of the ventral striatum and anterior insula with the anterior cingulate cortex and dorsolateral prefrontal cortex during the presentation of alcohol cues compared with neutral cues. (b) Subjective craving correlated positively with functional connectivity change between the posterior insula and the medial orbitofrontal cortex and negatively with functional connectivity change between the ventral striatum and the anterior cingulate cortex, dorsolateral prefrontal cortex, and lateral orbitofrontal cortex. (c) Compulsivity of alcohol use correlated positively with functional connectivity change between the dorsolateral prefrontal cortex and the ventral striatum, anterior insula, and posterior insula. Results suggest increased cognitive control over cue-processing in abstinent alcohol-dependent patients, compensating high levels of cue-provoked craving and compulsive use. Clinical trial registration details: ClinicalTrials.gov ID: NCT00926900. | CognitiveConstruct | RewardProcessing |
31,907,094 | 10.1017/S0033291719003659 | 2,021 | Psychological medicine | Psychol Med | Reduced neural response to reward and pleasant pictures independently relate to depression. | Multiple studies have found a reduced reward positivity (RewP) among individuals with major depressive disorder (MDD). Event-related potential studies have also reported blunted neural responses to pleasant pictures in MDD as reflected by the late positive potential (LPP). These deficits have been interpreted broadly in terms of anhedonia and decreased emotional engagement characteristic of depression. In the current study, a community-based sample of 83 participants with current MDD and 45 healthy individuals performed both a guessing task and a picture viewing paradigm with neutral and pleasant pictures to assess the RewP and the LPP, respectively. We found that both RewP and LPP to pleasant pictures were reduced in the MDD group; moreover, RewP and LPP were both independent predictors of MDD status. Within the MDD group, a smaller RewP predicted impaired mood reactivity in younger but not older participants. Smaller LPP amplitudes were associated with increased anhedonia severity in the MDD group. These data replicate and merge separate previous lines of research, and suggest that a blunted RewP and LPP reflect independent neural deficits in MDD - which could be used in conjunction to improve the classification of depression. | CognitiveConstruct | RewardProcessing |
31,907,032 | 10.1186/s13063-019-3802-9 | 2,020 | Trials | Trials | Protocol for a randomized controlled trial examining multilevel prediction of response to behavioral activation and exposure-based therapy for generalized anxiety disorder. | Only 40-60% of patients with generalized anxiety disorder experience long-lasting improvement with gold standard psychosocial interventions. Identifying neurobehavioral factors that predict treatment success might provide specific targets for more individualized interventions, fostering more optimal outcomes and bringing us closer to the goal of "personalized medicine." Research suggests that reward and threat processing (approach/avoidance behavior) and cognitive control may be important for understanding anxiety and comorbid depressive disorders and may have relevance to treatment outcomes. This study was designed to determine whether approach-avoidance behaviors and associated neural responses moderate treatment response to exposure-based versus behavioral activation therapy for generalized anxiety disorder. We are conducting a randomized controlled trial involving two 10-week group-based interventions: exposure-based therapy or behavioral activation therapy. These interventions focus on specific and unique aspects of threat and reward processing, respectively. Prior to and after treatment, participants are interviewed and undergo behavioral, biomarker, and neuroimaging assessments, with a focus on approach and avoidance processing and decision-making. Primary analyses will use mixed models to examine whether hypothesized approach, avoidance, and conflict arbitration behaviors and associated neural responses at baseline moderate symptom change with treatment, as assessed using the Generalized Anxiety Disorder-7 item scale. Exploratory analyses will examine additional potential treatment moderators and use data reduction and machine learning methods. This protocol provides a framework for how studies may be designed to move the field toward neuroscience-informed and personalized psychosocial treatments. The results of this trial will have implications for approach-avoidance processing in generalized anxiety disorder, relationships between levels of analysis (i.e., behavioral, neural), and predictors of behavioral therapy outcome. The study was retrospectively registered within 21 days of first participant enrollment in accordance with FDAAA 801 with ClinicalTrials.gov, NCT02807480. Registered on June 21, 2016, before results. | CognitiveConstruct | RewardProcessing |
31,892,542 | 10.1073/pnas.1913079117 | 2,020 | Proceedings of the National Academy of Sciences of the United States of America | Proc Natl Acad Sci U S A | Reward does not facilitate visual perceptual learning until sleep occurs. | A growing body of evidence indicates that visual perceptual learning (VPL) is enhanced by reward provided during training. Another line of studies has shown that sleep following training also plays a role in facilitating VPL, an effect known as the offline performance gain of VPL. However, whether the effects of reward and sleep interact on VPL remains unclear. Here, we show that reward interacts with sleep to facilitate offline performance gains of VPL. First, we demonstrated a significantly larger offline performance gain over a 12-h interval including sleep in a reward group than that in a no-reward group. However, the offline performance gains over the 12-h interval without sleep were not significantly different with or without reward during training, indicating a crucial interaction between reward and sleep in VPL. Next, we tested whether neural activations during posttraining sleep were modulated after reward was provided during training. Reward provided during training enhanced rapid eye movement (REM) sleep time, increased oscillatory activities for reward processing in the prefrontal region during REM sleep, and inhibited neural activation in the untrained region in early visual areas in non-rapid eye movement (NREM) and REM sleep. The offline performance gains were significantly correlated with oscillatory activities of visual processing during NREM sleep and reward processing during REM sleep in the reward group but not in the no-reward group. These results suggest that reward provided during training becomes effective during sleep, with excited reward processing sending inhibitory signals to suppress noise in visual processing, resulting in larger offline performance gains over sleep. | CognitiveConstruct | RewardProcessing |
31,891,238 | 10.1002/ajmg.b.32777 | 2,020 | American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics | Am J Med Genet B Neuropsychiatr Genet | Genetic meta-analysis of obsessive-compulsive disorder and self-report compulsive symptoms. | We investigated whether obsessive-compulsive (OC) symptoms from a population-based sample could be analyzed to detect genetic variants influencing obsessive-compulsive disorder (OCD). We performed a genome-wide association studies (GWAS) on the obsession (rumination and impulsions) and compulsion (checking, washing, and ordering/precision) subscales of an abbreviated version of the Padua Inventory (N = 8,267 with genome-wide genotyping and phenotyping). The compulsion subscale showed a substantial and significant positive genetic correlation with an OCD case-control GWAS (r = 0.61, p = .017) previously published by the Psychiatric Genomics Consortium (PGC-OCD). The obsession subscale and the total Padua score showed no significant genetic correlations (r = -0.02 and r = 0.42, respectively). A meta-analysis of the compulsive symptoms GWAS with the PGC-OCD revealed no genome-wide significant Single-Nucleotide Polymorphisms (SNPs combined N = 17,992, indicating that the power is still low for individual SNP effects). A gene-based association analysis, however, yielded two novel genes (WDR7 and ADCK1). The top 250 genes in the gene-based test also showed a significant increase in enrichment for psychiatric and brain-expressed genes. S-Predixcan testing showed that for genes expressed in hippocampus, amygdala, and caudate nucleus significance increased in the meta-analysis with compulsive symptoms compared to the original PGC-OCD GWAS. Thus, the inclusion of dimensional symptom data in genome-wide association on clinical case-control GWAS of OCD may be useful to find genes for OCD if the data are based on quantitative indices of compulsive behavior. SNP-level power increases were limited, but aggregate, gene-level analyses showed increased enrichment for brain-expressed genes related to psychiatric disorders, and increased association with gene expression in brain tissues with known emotional, reward processing, memory, and fear-formation functions. | CognitiveConstruct | RewardProcessing |
31,884,055 | 10.1016/j.neuroimage.2019.116493 | 2,020 | NeuroImage | Neuroimage | Early life stress and brain function: Activity and connectivity associated with processing emotion and reward. | Investigating the developmental sequelae of early life stress has provided researchers the opportunity to examine adaptive responses to extreme environments. A large body of work has established mechanisms by which the stressful experiences of childhood poverty, maltreatment, and institutional care can impact the brain and the distributed stress systems of the body. These mechanisms are reviewed briefly to lay the foundation upon which the current neuroimaging literature has been built. More recently, developmental cognitive neuroscientists have identified a number of the effects of early adversity, including differential behavior and brain function. Among the most consistent of these findings are differences in the processing of emotion and reward-related information. The neural correlates of emotion processing, particularly frontolimbic functional connectivity, have been well studied in early life stress samples with results indicating accelerated maturation following early adversity. Reward processing has received less attention, but here the evidence suggests a deficit in reward sensitivity. It is as yet unknown whether the accelerated maturation of emotion-regulation circuits comes at the cost of delayed development in other systems, most notably the reward system. This review addresses the early life stress neuroimaging literature that has investigated emotion and reward processing, identifying important next steps in the study of brain function following adversity. | CognitiveConstruct | RewardProcessing |
31,872,334 | 10.3758/s13415-019-00763-7 | 2,020 | Cognitive, affective & behavioral neuroscience | Cogn Affect Behav Neurosci | Meta-analytic clustering dissociates brain activity and behavior profiles across reward processing paradigms. | Reward learning is a ubiquitous cognitive mechanism guiding adaptive choices and behaviors, and when impaired, can lead to considerable mental health consequences. Reward-related functional neuroimaging studies have begun to implicate networks of brain regions essential for processing various peripheral influences (e.g., risk, subjective preference, delay, social context) involved in the multifaceted reward processing construct. To provide a more complete neurocognitive perspective on reward processing that synthesizes findings across the literature while also appreciating these peripheral influences, we used emerging meta-analytic techniques to elucidate brain regions, and in turn networks, consistently engaged in distinct aspects of reward processing. Using a data-driven, meta-analytic, k-means clustering approach, we dissociated seven meta-analytic groupings (MAGs) of neuroimaging results (i.e., brain activity maps) from 749 experimental contrasts across 176 reward processing studies involving 13,358 healthy participants. We then performed an exploratory functional decoding approach to gain insight into the putative functions associated with each MAG. We identified a seven-MAG clustering solution that represented dissociable patterns of convergent brain activity across reward processing tasks. Additionally, our functional decoding analyses revealed that each of these MAGs mapped onto discrete behavior profiles that suggested specialized roles in predicting value (MAG-1 & MAG-2) and processing a variety of emotional (MAG-3), external (MAG-4 & MAG-5), and internal (MAG-6 & MAG-7) influences across reward processing paradigms. These findings support and extend aspects of well-accepted reward learning theories and highlight large-scale brain network activity associated with distinct aspects of reward processing. | CognitiveConstruct | RewardProcessing |
31,862,207 | 10.1016/j.neuropsychologia.2019.107311 | 2,020 | Neuropsychologia | Neuropsychologia | Decomposing the effort paradox in reward processing: Time matters. | Effort expenditure not only discounts reward value prospectively but also accrues reward value retrospectively. To decompose the effort paradox in reward processing, the current event-related potential study investigated the neural dynamics underlying effects of effort expenditure on subsequent reward processing. Participants exerted one of two levels of effort to obtain an opportunity of winning a high or low amount of monetary reward, and we focused on electrophysiological activity during the anticipatory and consummatory phases of reward processing. During the anticipatory phase, the stimulus-preceding negativity was enhanced when potential high rewards were anticipated, but this reward effect disappeared following high-effort expenditure. During the consummatory phase, feedback-related ERPs were increased for high relative to low rewards, and this reward effect was enlarged following effort expenditure during the early stage (200-300 ms) as indexed by the reward positivity but not the late stage (400-600 ms) as indexed by the P3. Our findings provide a strong support for the psychological contrast theory and indicate that time matters in decomposing the effort paradox for reward processing such that effort expenditure reduces reward sensitivity during the anticipatory phase but enhances reward sensitivity during the consummatory phase. | CognitiveConstruct | RewardProcessing |
31,853,427 | 10.1177/2167702619838480 | 2,019 | Clinical psychological science : a journal of the Association for Psychological Science | Clin Psychol Sci | Blunted Reward Sensitivity and Trait Disinhibition Interact to Predict Substance Use Problems. | Reward deficit models of addiction posit weaknesses in reward sensitivity to be promotive of substance dependence, while the externalizing spectrum model views substance problems as arising in large part from a general disinhibitory liability. The current study sought to integrate these perspectives by testing for separate and interactive associations of disinhibition and reward dysfunction with interview-assessed substance use disorders (SUDs). Community and college adults ( = 199) completed a scale measure of trait disinhibition and performed a gambling-feedback task yielding a neural index of reward sensitivity, the 'Reward Positivity' (RewP). Disinhibition and blunted RewP independently predicted SUDs, and also operated such that participants - in particular, men - with high levels of disinhibition together with blunted RewP exhibited especially severe substance problems. Though limited by its cross-sectional design, this work provides new information about the interplay of disinhibition, reward processing, and gender in SUDs and suggests important directions for future research. | CognitiveConstruct | RewardProcessing |
31,837,472 | 10.1016/j.neuroimage.2019.116413 | 2,020 | NeuroImage | Neuroimage | Sensitivity to sweetness correlates to elevated reward brain responses to sweet and high-fat food odors in young healthy volunteers. | Taste sensitivity relates to food preferences and macronutrients intake. The current study investigated whether the neural responses to food odors varied in sensory quality (sweet or non-sweet) and their associations with macronutrient content (high- or low-fat) in young healthy participants varied in sweet taste sensitivity. Thirty-eight participants were assessed for their sensitivity to sucrose solutions using a modified "taste strip" test. They were divided into high sweetness sensitive (HS, n = 15) and low sweetness sensitive (LS, n = 15) groups using the median split approach. Brain responses to four food-related odors (chocolate, peach, peanut, and bread) and one non-food odor (rose) were assessed using functional magnetic resonance imaging (fMRI). Preferences for tastes and macronutrients were measured using a computer-based task. Behavioral results showed that HS group, compared to LS group, had a higher preference for carbohydrate-dominated foods and liking for sweet foods, but a lower liking for protein-dominated foods. The food odors, in comparison to non-food odors, produced greater brain-activations in the gustatory and reward regions. Compared to LS group, the HS group showed a higher level of activation in the frontal inferior operculum in response to sweet vs. savory food odors, and stronger insular activations to high-fat vs. low-fat food odors. In addition, individual sweetness sensitivity was positively associated with activation of the insula in response to chocolate odor, suggesting an overlap of neural responses to food odor with high sugar and fat content. Our findings highlight that high sensitivity to sweetness can be associated with increased preference for carbohydrate-dominated or sweet foods, and elevated brain activations to sweet or high-fat food odors in the areas related to food reward processing. | CognitiveConstruct | RewardProcessing |
31,822,658 | 10.1038/s41398-019-0674-4 | 2,019 | Translational psychiatry | Transl Psychiatry | Chronic corticosterone administration induces negative valence and impairs positive valence behaviors in mice. | Behavioral approaches utilizing rodents to study mood disorders have focused primarily on negative valence behaviors associated with potential threat (anxiety-related behaviors). However, for disorders such as depression, positive valence behaviors that assess reward processing may be more translationally valid and predictive of antidepressant treatment outcome. Chronic corticosterone (CORT) administration is a well-validated pharmacological stressor that increases avoidance in negative valence behaviors associated with anxiety. However, whether chronic stress paradigms such as CORT administration also lead to deficits in positive valence behaviors remains unclear. We treated male C57BL/6J mice with chronic CORT and assessed both negative and positive valence behaviors. We found that CORT induced avoidance in the open field and NSF. Interestingly, CORT also impaired instrumental acquisition, reduced sensitivity to a devalued outcome, reduced breakpoint in progressive ratio, and impaired performance in probabilistic reversal learning. Taken together, these results demonstrate that chronic CORT administration at the same dosage both induces avoidance in negative valence behaviors associated with anxiety and impairs positive valence behaviors associated with reward processing. These data suggest that CORT administration is a useful experimental system for preclinical approaches to studying stress-induced mood disorders. | CognitiveConstruct | RewardProcessing |
31,821,832 | 10.1016/j.neubiorev.2019.12.007 | 2,020 | Neuroscience and biobehavioral reviews | Neurosci Biobehav Rev | Opioid receptor modulation of neural circuits in depression: What can be learned from preclinical data? | Major depressive disorder (MDD) is a heterogeneous clinical syndrome involving distinct pathological processes. Core features of MDD include anhedonia, reduced motivation, increased anxiety, negative affective bias, cognitive impairments, and dysregulated neuroplasticity mechanisms. There are multiple biological hypotheses related to MDD, including dysfunction of the opioid system. Although opium was abandoned as an antidepressant after the introduction of monoaminergic drugs, there has been renewed interest in targeting the opioid system for MDD. In this review, we discuss the preclinical support of this idea using a neurocircuitry- and molecular neuroplasticity-based approach. This article highlights how the opioid system potently modulates mesolimbic circuitry underlying motivation and reward processing, limbic circuitry underlying fear and anxiety responses, cortical and hippocampal circuitry underlying a variety of cognitive functions, as well as broad functional and structural plasticity mechanisms. Ultimately, a more thorough understanding of how the opioid system modulates these core functional domains may lead to novel treatment strategies and molecular targets in the treatment of MDD. | CognitiveConstruct | RewardProcessing |
31,799,907 | 10.1152/physiol.00013.2019 | 2,020 | Physiology (Bethesda, Md.) | Physiology (Bethesda) | Ovarian Hormones and Reward Processes in Palatable Food Intake and Binge Eating. | Ovarian hormones are associated with risk for binge eating in women. Recent animal and human studies suggest that food-related reward processing may be one set of neurobiological factors that contribute to these relationships, but additional studies are needed to confirm and extend findings. | CognitiveConstruct | RewardProcessing |