Reward Processing Research Articles

Aerobic Exercise and Endocannabinoids: A Narrative Review of Stress Regulation and Brain Reward Systems.

Aerobic exercise is a widely adopted practice, not solely for enhancing fitness and reducing the risk of various diseases but also for its ability to uplift mood and aid in addressing depression and anxiety disorders. Within the scope of this narrative review, we seek to consolidate current insights into the endocannabinoid-mediated regulation of stress and the brain's reward mechanism resulting from engaging in aerobic exercise. A comprehensive search was conducted across Medline, SPORTDiscus, Pubmed, and Scopus, encompassing data available until November 30, 2023. This review indicates that a bout of aerobic exercise, particularly of moderate intensity, markedly augments circulating levels of endocannabinoids-N-arachidonoyl-ethanolamine (AEA) and 2-acylglycerol (2-AG), that significantly contributes to mood elevation and reducing stress in healthy individuals. The current understanding of how aerobic exercise impacts mental health and mood improvement is still unclear. Moderate and high-intensity aerobic exercise modulatesstress through a negative feedback mechanism targeting both the hypothalamus-pituitary-adrenal (HPA) axis and the sympathetic nervous system, thereby facilitating stress regulation crucial role in endocannabinoid synthesis, ultimately culminating in the orchestration of negative feedback across multiple tiers of the HPA axis, coupled with its influence over cortical and subcortical brain structures. The endocannabinoid has been observed to govern the release of neurotransmitters from diverse neuronal populations, implying a universal mechanism that fine-tunes neuronal activity and consequently modulates both emotional and stress-related responses. Endocannabinoids further assume a pivotal function within brain reward mechanisms, primarily mediated by CB1 receptors distributed across diverse cerebral centers. Notably, these endocannabinoids partake in natural reward processes, as exemplified in aerobic exercise, by synergizing with the dopaminergic reward system. The genesis of this reward pathway can be traced to the ventral tegmental area, with dopamine neurons predominantly projecting to the nucleus accumbens, thereby inciting dopamine release in response to rewarding stimuli.

Neural substrates of marriage on self-parents processing and the association with a parents-oriented perspective shift in a collectivistic culture

Relationship with parents is a special bond that shapes self-other representations and have an impact on adult-child’s marriage, especially in the early stages of marriage. This study sought to investigate the neural mechanisms underlying self-parents processing as well as their relationship with marriage. Seventy-eight premarital Korean participants were scanned in functional MRI while evaluating traits of the self and parents. Then, 21 of them returned after being married to engage in the identical task three years later. The precuneus and temporoparietal junction were identified to activate stronger for parents than self at both marital statuses. The dorsal anterior cingulate cortex, posterior cingulate cortex, parietal operculum, and caudate activated more for self than parents before marriage, but their activities changed during marriage. The activation increase of the parietal operculum between marital statuses in the parents condition was negatively correlated with the level of marital dissatisfaction, and this association only appeared among participants with a child. Self-parents processing may recruit brain regions involved in autobiographical memory and self-other distinction, and marriage has an impact on the way individuals process rewards and multimodal sensory information during this processing. Marriage may lead to changes in brain function that affect the processing of emotions toward parents and a more parents-oriented perspective shift in collectivistic societies.

The roots of polarization in the individual reward system.

Polarization raises concerns for democracy and society, which have expanded in the internet era where (mis)information has become ubiquitous, its transmission faster than ever, and the freedom and means of opinion expressions are expanding. The origin of polarization however remains unclear, with multiple social and emotional factors and individual reasoning biases likely to explain its current forms. In the present work, we adopt a principled approach and show that polarization tendencies can take root in biased reward processing of new information in favour of choice confirmatory evidence. Through agent-based simulations, we show that confirmation bias in individual learning is an independent mechanism and could be sufficient for creating polarization at group level independently of any additional assumptions about the opinions themselves, a priori beliefs about them, information transmission mechanisms or the structure of social relationship between individuals. This generative process can interact with polarization mechanisms described elsewhere, but constitutes an entrenched biological tendency that helps explain the extraordinary resilience of polarization against mitigating efforts such as dramatic informational change in the environment.

Stimulant medications in children with ADHD normalize the structure of brain regions associated with attention and reward.

Children with ADHD show abnormal brain function and structure. Neuroimaging studies found that stimulant medications may improve brain structural abnormalities in children with ADHD. However, prior studies on this topic were conducted with relatively small sample sizes and wide age ranges and showed inconsistent results. In this cross-sectional study, we employed latent class analysis and linear mixed-effects models to estimate the impact of stimulant medications using demographic, clinical measures, and brain structure in a large and diverse sample of children aged 9-11 from the Adolescent Brain and Cognitive Development Study. We studied 273 children with low ADHD symptoms and received stimulant medication (Stim Low-ADHD), 1002 children with high ADHD symptoms and received no medications (No-Med ADHD), and 5378 typically developing controls (TDC). After controlling for the covariates, compared to Stim Low-ADHD and TDC, No-Med ADHD showed lower cortical thickness in the right insula (INS, d = 0.340, PFDR = 0.003) and subcortical volume in the left nucleus accumbens (NAc, d = 0.371, PFDR = 0.003), indicating that high ADHD symptoms were associated with structural abnormalities in these brain regions. In addition, there was no difference in brain structural measures between Stim Low-ADHD and TDC children, suggesting that the stimulant effects improved both ADHD symptoms and ADHD-associated brain structural abnormalities. These findings together suggested that children with ADHD appear to have structural abnormalities in brain regions associated with saliency and reward processing, and treatment with stimulant medications not only improve the ADHD symptoms but also normalized these brain structural abnormalities.

Ghrelin decreases sensitivity to negative feedback and increases prediction-error related caudate activity in humans, a randomized controlled trial

The stomach-derived hormone ghrelin plays not only a role in feeding, starvation, and survival, but it has been suggested to also be involved in the stress response, in neuropsychiatric conditions, and in alcohol and drug use disorders. Mechanisms related to reward processing might mediate ghrelin’s broader effects on complex behaviors, as indicated by animal studies and mostly correlative human studies. Here, using a within-subject double-blind placebo-controlled design with intravenous ghrelin infusion in healthy volunteers (n = 30), we tested whether ghrelin alters sensitivity to reward and punishment in a reward learning task. Parameters were derived from a computational model of participants’ task behavior. The reversal learning task with monetary rewards was performed during functional brain imaging to investigate ghrelin effects on brain signals related to reward prediction errors. Compared to placebo, ghrelin decreased punishment sensitivity (t = −2.448, p = 0.021), while reward sensitivity was unaltered (t = 0.8, p = 0.43). We furthermore found increased prediction-error related activity in the dorsal striatum during ghrelin administration (region of interest analysis: t-values ≥ 4.21, p-values ≤ 0.044). Our results support a role for ghrelin in reward processing that extends beyond food-related rewards. Reduced sensitivity to negative outcomes and increased processing of prediction errors may be beneficial for food foraging when hungry but could also relate to increased risk taking and impulsivity in the broader context of addictive behaviors.

Exploring transgenerational inheritance in epigenotypes of DAT heterozygous rats: Circadian anomalies and attentional vulnerability

Dopamine (DA) is mainly involved in locomotor activity, reward processes and maternal behaviors. Rats with KO gene for dopamine transporter (DAT), coding for a truncated DAT protein, are in hyperdopaminergic conditions and thus develop stereotyped behaviors and hyperactivity. Our aim was to test the prior transgenerational modulation of wild and truncated alleles as expressed in heterozygous DAT rats: specifically, we addressed the possible sequelae due to genotype and gender of the ancestors, with regard to behavioral differences in F1, F2, F3 rats. We studied non-classical DAT heterozygotes (HETs) based on two specular lines, with putative grand-maternal vs. grand-paternal imprinting. MAT females (F1; offspring of KO male and WT female) mated with a KO male to generate MIX offspring (F2). Specularly, PAT females (F1; offspring of KO female and WT male) mated with a KO male to generate PIX offspring (F2). Similarly to PAT, we obtained MUX (F2; HET offspring of MAT sire and KO dam); we also observed the F3 (MYX: HET offspring of KO male and MUX female, thus with DAT-KO maternal grandmother like also for PIX). We studied their circadian cycle of locomotor activity and their behavior in the elevated-plus-maze (EPM). Locomotor hyper-activity occurs in F1, the opposite occurs in F2, with MYX rats appearing undistinguishable from WT ones. Open-arm preference emerged in PIX and MIX rats. Only MAT and MYX rats showed a significant vulnerability for ADHD-like inattentive symptoms (duration of rearing in the EPM; Viggiano et al., 2002). A risk-taking profile is evident in the F2 phenotype, while inattentiveness from F1 progeny tends to be transferred to F3. We hypothesize that DAT-related phenotypes result from effective inheritance through pedigree of imprints that are dependent on grandparents, suggesting a protective role for gestation within a hyperdopaminergic uterus. For major features, similar odd (F1, F3) generations appear opposed to even (F2) ones; for minor specific features, the phenotype transfer may affect the progenies with a male but not a female DAT-KO ancestor.

Fractional amplitude of low-frequency fluctuations associated with μ-opioid and dopamine receptor distributions in the central nervous system after high-intensity exercise bouts.

Dopaminergic, opiod and endocannabinoid neurotransmission are thought to play an important role in the neurobiology of acute exercise and, in particular, in mediating positive affective responses and reward processes. Recent evidence indicates that changes in fractional amplitude of low-frequency fluctuations (zfALFF) in resting-state functional MRI (rs-fMRI) may reflect changes in specific neurotransmitter systems as tested by means of spatial correlation analyses. Here, we investigated this relationship at different exercise intensities in twenty young healthy trained athletes performing low-intensity (LIIE), high-intensity (HIIE) interval exercises, and a control condition on three separate days. Positive And Negative Affect Schedule (PANAS) scores and rs-fMRI were acquired before and after each of the three experimental conditions. Respective zfALFF changes were analyzed using repeated measures ANOVAs. We examined the spatial correspondence of changes in zfALFF before and after training with the available neurotransmitter maps across all voxels and additionally, hypothesis-driven, for neurotransmitter maps implicated in the neurobiology of exercise (dopaminergic, opiodic and endocannabinoid) in specific brain networks associated with "reward" and "emotion." Elevated PANAS Positive Affect was observed after LIIE and HIIE but not after the control condition. HIIE compared to the control condition resulted in differential zfALFF decreases in precuneus, temporo-occipital, midcingulate and frontal regions, thalamus, and cerebellum, whereas differential zfALFF increases were identified in hypothalamus, pituitary, and periaqueductal gray. The spatial alteration patterns in zfALFF during HIIE were positively associated with dopaminergic and μ-opioidergic receptor distributions within the 'reward' network. These findings provide new insight into the neurobiology of exercise supporting the importance of reward-related neurotransmission at least during high-intensity physical activity.

Neuromodulation of Eating Disorders: A Review of Underlying Neural Network Activity and Neuromodulatory Treatments.

Eating disorders are a group of psychiatric conditions that involve pathological relationships between patients and food. The most prolific of these disorders are anorexia nervosa, bulimia nervosa, and binge eating disorder. The current standard of care involves psychotherapy, pharmacotherapy, and the management of comorbid conditions, with nutritional rehabilitation reserved for severe cases of anorexia nervosa. Unfortunately, many patients often fail to respond, leaving a concerning treatment gap between the current and requisite treatments for eating disorders. To better understand the neurobiology underlying these eating disorders, investigations have been undertaken to characterize the activity of various neural networks, primarily those activated during tasks of executive inhibition, reward processing, and self-reference. Various neuromodulatory techniques have been proposed to stimulate these networks with the goal of improving patients' BMI and mental health. The aim of this review is to compile a comprehensive summarization of the current literature regarding the underlying neural connectivity of anorexia nervosa, bulimia nervosa, and binge eating disorder as well as the numerous neuromodulatory modalities that have been investigated. Importantly, we aimed to summarize the most significant clinical trials to date as well as to provide an updated assessment of the role of deep brain stimulation, summarizing numerous recently published clinical studies that have greatly contributed to the literature. In this review, we found therapeutic evidence for transcranial magnetic stimulation and transcranial direct current stimulation in treating individuals suffering from anorexia nervosa, bulimia nervosa, and binge eating disorder. We also found significant evidence for the role of deep brain stimulation, particularly as an escalatory therapy option for the those who failed standard therapy. Finally, we hope to provide promising directions for future clinical investigations.

Evaluating cyber loss in star-ring and star-bus hybrid networks based on the bond percolation model

The rise of cyber risk as a significant concern for businesses and companies has prompted increased attention towards evaluating the loss of cyber risk in networks vulnerable to contagious cyber attacks. Expanding on recent research focusing on standard network topologies, this study investigates two hybrid topologies: star-ring and star-bus. We propose random star-ring and star-bus hybrid network models that incorporate heterogeneous node types and a contagion model based on the bond percolation model to describe the contagion of a cyber attack on them. We derive exact expressions for the mean, variance, and covariance of compromise sizes for different node types. Utilizing these expressions, we further compute the mean and variance of the aggregate cyber loss of the networks, employing a dynamic framework of loss based on the renewal reward process. Moreover, through a numerical study and analysis of mathematical properties, we gain valuable insights into the impact of parameters on the mean, variance, and correlation of compromise sizes.

Neural correlates of willingness to pay for items: A meta-analysis of functional magnetic resonance imaging studies

Willingness to pay (WTP) pervades every marketplace transaction, therefore, understanding how the brain makes bidding decisions is essential in consumer neuroscience. Although some neuroimaging studies have investigated the neural networks of WTP, systematic understanding remains limited. This study identified reliable neural networks activated by the WTP across different reward types and assessed common and distinct neural networks for different reward types (food and other) bids. We conducted an activation likelihood estimation (ALE) meta-analysis on WTP across different reward types (25 studies; 254 foci; 705 participants), and to compared neural representations of WTP for food reward (22 studies; 232 foci; 628 participants) and other rewards (7 studies, 61 foci; 177 participants). The ALE results revealed that the brain centers of WTP for different rewards mainly consist of the bilateral inferior frontal gyrus (IFG), bilateral insula, bilateral anterior cingulate cortex (ACC), along with the left caudate. This suggests that neural networks encoding WTP for different rewards consist of brain regions associated with reward processing, cost-benefit calculations, and goal-directed action activities. In addition, consistent activation of the bilateral IFG and bilateral insula for food but no other rewards bids suggest their involvement in the neural network of appetite. WTP for food and other rewards commonly activated ACC, suggesting a common region encoding bids for different rewards. Our findings provide novel insights into neural networks associated with WTP for food and other rewards bids and the mechanisms underlying WTP across different reward types.

Social support mediates the effects of childhood unpredictability on anhedonia: A retrospective investigation in an online adult community sample

Increasingly, research is highlighting the implications of exposure to unpredictable environments during childhood (i.e., “childhood unpredictability”) on outcomes in adulthood. Converging evidence from preclinical and clinical studies has implicated childhood unpredictability in disrupted reward processing and anhedonia. From the stress generation literature, altered social support has emerged as a possible mechanism by which this effect may occur. In the current study, our goal was to understand whether the pathway from childhood unpredictability to anhedonia occurs through reduced perceptions of social support. Toward this end, we recruited an online community sample of adults in the US (N = 242) to complete surveys assessing childhood unpredictability, depressive symptoms, anhedonia, and social support, as well as a novel online version of the Probabilistic Reward Task. We found that childhood unpredictability was associated with increased depressive symptoms and anhedonia (but not objective measure of anhedonia), and reduced perceptions of social support in adulthood. Mediation analyses revealed a significant indirect effect of perceived social support on the association between childhood unpredictability and anhedonia, controlling for age, sex, and non-anhedonic depressive symptoms. Unexpectedly, measures of reward responsiveness from the behavioral task were not related to childhood unpredictability. The current findings replicate previous reports linking childhood unpredictability and self-reported anhedonia, and extend them to incorporate the potential mediating pathway of reduced social support. Implications for treatment for anhedonia are discussed.

Neurophysiological correlates of interpersonal discrepancy and social adjustment in an interactive decision-making task in dyads.

The pursuit of convergence and the social behavioral adjustment of conformity are fundamental cooperative behaviors that help people adjust their mental frameworks to reach a common goal. However, while social psychology has extensively studied conformity by its influence context, there is still plenty to investigate about the neural cognitive mechanisms involved in this behavior. We proposed a paradigm with two phases, a pre-activation phase to enhance cooperative tendencies and, later, a social decision-making phase in which dyads had to make a perceptual estimation in three consecutive trials and could converge in their decisions without an explicit request or reward to do so. In Study 1, 80 participants were divided in two conditions. In one condition participants did the pre-activation phase alone, while in the other condition the two participants did it with their partners and could interact freely. In Study 2, we registered the electroencephalographical (EEG) activity of 36 participants in the social decision-making phase. Study 1 showed behavioral evidence of higher spontaneous convergence in participants who interacted in the pre-activation phase. Event related Potentials (ERP) recorded in Study 2 revealed signal differences in response divergence in different time intervals. Time-frequency analysis showed theta, alpha, and beta evidence related to cognitive control, attention, and reward processing associated with social convergence. Current results support the spontaneous convergence of behavior in dyads, with increased behavioral adjustment in those participants who have previously cooperated. In addition, neurophysiological components were associated with discrepancy levels between participants, and supported the validity of the experimental paradigm to study spontaneous social behavioral adaptation in experimental settings.

The central renin–angiotensin system: A genetic pathway, functional decoding, and selective target engagement characterization in humans

Accumulating evidence suggests that the brain renin angiotensin system (RAS) plays a pivotal role in the regulation of cognition and behavior as well as in the neuropathology of neurological and mental disorders. The angiotensin II type 1 receptor (AT1R) mediates most functional and neuropathology-relevant actions associated with the central RAS. However, an overarching comprehension to guide translation and utilize the therapeutic potential of the central RAS in humans is currently lacking. We conducted a comprehensive characterization of the RAS using an innovative combination of transcriptomic gene expression mapping, image-based behavioral decoding, and pre-registered randomized controlled discovery-replication pharmacological resting-state functional magnetic resonance imaging (fMRI) trials (N = 132) with a selective AT1R antagonist. The AT1R exhibited a particular dense expression in a subcortical network encompassing the thalamus, striatum, and amygdalo-hippocampal formation. Behavioral decoding of the AT1R gene expression brain map showed an association with memory, stress, reward, and motivational processes. Transient pharmacological blockade of the AT1R further decreased neural activity in subcortical systems characterized by a high AT1R expression, while increasing functional connectivity in the cortico-basal ganglia-thalamo-cortical circuitry. Effects of AT1R blockade on the network level were specifically associated with the transcriptomic signatures of the dopaminergic, opioid, acetylcholine, and corticotropin-releasing hormone signaling systems. The robustness of the results was supported in an independent pharmacological fMRI trial. These findings present a biologically informed comprehensive characterization of the central AT1R pathways and their functional relevance on the neural and behavioral level in humans.

Altered hierarchical auditory predictive processing after lesions to the orbitofrontal cortex.

Orbitofrontal cortex (OFC) is classically linked to inhibitory control, emotion regulation, and reward processing. Recent perspectives propose that the OFC also generates predictions about perceptual events, actions, and their outcomes. We tested the role of the OFC in detecting violations of prediction at two levels of abstraction (i.e., hierarchical predictive processing) by studying the event-related potentials (ERPs) of patients with focal OFC lesions (n = 12) and healthy controls (n = 14) while they detected deviant sequences of tones in a local-global paradigm. The structural regularities of the tones were controlled at two hierarchical levels by rules defined at a local (i.e., between tones within sequences) and at a global (i.e., between sequences) level. In OFC patients, ERPs elicited by standard tones were unaffected at both local and global levels compared to controls. However, patients showed an attenuated mismatch negativity (MMN) and P3a to local prediction violation, as well as a diminished MMN followed by a delayed P3a to the combined local and global level prediction violation. The subsequent P3b component to conditions involving violations of prediction at the level of global rules was preserved in the OFC group. Comparable effects were absent in patients with lesions restricted to the lateral PFC, which lends a degree of anatomical specificity to the altered predictive processing resulting from OFC lesion. Overall, the altered magnitudes and time courses of MMN/P3a responses after lesions to the OFC indicate that the neural correlates of detection of auditory regularity violation are impacted at two hierarchical levels of rule abstraction.

Intact modulation of response vigor in major depressive disorder

Blunted motivation is a core symptom of Major Depressive Disorder (MDD). Although the empirical picture is mixed, cognitive processes that can be collectively referred to as reward processing have been found to be consistently muted in MDD; most notably, reward sensitivity and reinforcement learning. Works on the modulation of response vigor in individuals with MDD have examined various types of reward, but recent research has shown that in the general population, response vigor is not modulated by type of reward on tasks that are highly similar to those used in these experiments. The present study implemented a form of non-reward related reinforcement which has repeatedly been shown to modulate response vigor in the general population. It investigated whether modulation of response vigor by this type of reinforcement would be effective in individuals with MDD. Clinically depressed individuals (N = 121; 76 post-exclusion) engaged in a task in which their responses led to predictable and immediate sensorimotor effects, or no such effects. Response vigor increased when responses led to sensorimotor effects, which was comparable to the increase found in the general population. These findings support the utility of isolating the computations leading to different reinforcement types and suggest that motivational deficits in MDD may be specific to the type of reward (i.e., hedonically or otherwise explicitly desired stimuli). These results contribute to the literature by suggesting that the reinforcement from sensorimotor predictability stems from processes devolved to motor control, whereas reinforcement from rewards may depend on more general-purpose processes.

TRNA epitranscriptomic alterations associated with opioid-induced reward-seeking and long-term opioid withdrawal in male mice

DNA cytosine methylation has been documented as a potential epigenetic mechanism of transcriptional regulation underlying opioid use disorder. However, methylation of RNA cytosine residues, which would drive another level of biological influence as an epitranscriptomic mechanism of gene and protein regulation has not been studied in the context of addiction. Here, we probed whether chronic morphine exposure could alter tRNA cytosine methylation (m5C) and resulting expression levels in the medial prefrontal cortex (mPFC), a brain region crucial for reward processing and executive function that exhibits opioid-induced molecular restructuring. We identified dynamic changes in glycine tRNA (tRNAGlyGCC) cytosine methylation, corresponding to altered expression levels of this tRNA at multiple timepoints following 15 days of daily morphine. Additionally, a robust increase in methylation, coupled with decreased expression, was present after 30 days of withdrawal, suggesting that repeated opioid administration produces changes to the tRNA regulome long after discontinuation. Furthermore, forebrain-wide knockout of neuronal Nsun2, a tRNA methyltransferase, was associated with disruption of opioid conditioned place preference, and this effect was recapitulated by regional mPFC Nsun2 knockout. Taken together, these studies provide a foundational link between the regulation of tRNA cytosine methylation and opioid reward and highlight the tRNA machinery as a potential therapeutic target in addiction.

Brain reward function in people who use cannabis: a systematic review.

Cannabis is one of the most widely used psychoactive substances globally. Cannabis use can be associated with alterations of reward processing, including affective flattening, apathy, anhedonia, and lower sensitivity to natural rewards in conjunction with higher sensitivity to cannabis-related rewards. Such alterations have been posited to be driven by changes in underlying brain reward pathways, as per prominent neuroscientific theories of addiction. Functional neuroimaging (fMRI) studies have examined brain reward function in cannabis users via the monetary incentive delay (MID) fMRI task; however, this evidence is yet to be systematically synthesised. We aimed to systematically integrate the evidence on brain reward function in cannabis users examined by the MID fMRI task; and in relation to metrics of cannabis exposure (e.g., dosage, frequency) and other behavioural variables. We pre-registered the review in PROSPERO and reported it using PRISMA guidelines. Literature searches were conducted in PsycINFO, PubMed, Medline, CINAHL, and Scopus. Nine studies were included, comprising 534 people with mean ages 16-to-28 years, of which 255 were people who use cannabis daily or almost daily, and 279 were controls. The fMRI literature to date led to largely non-significant group differences. A few studies reported group differences in the ventral striatum while participants anticipated rewards and losses; and in the caudate while participants received neutral outcomes. A few studies examined correlations between brain function and withdrawal, dosage, and age of onset; and reported inconsistent findings. There is emerging but inconsistent evidence of altered brain reward function in cannabis users examined with the MID fMRI task. Future fMRI studies are required to confirm if the brain reward system is altered in vulnerable cannabis users who experience a Cannabis Use Disorder, as postulated by prominent neuroscientific theories of addiction.

Unlocking the neural mechanisms of consumer loan evaluations: an fNIRS and ML-based consumer neuroscience study.

This study conducts a comprehensive exploration of the neurocognitive processes underlying consumer credit decision-making using cutting-edge techniques from neuroscience and machine learning (ML). Employing functional Near-Infrared Spectroscopy (fNIRS), the research examines the hemodynamic responses of participants while evaluating diverse credit offers. The experimental phase of this study investigates the hemodynamic responses collected from 39 healthy participants with respect to different loan offers. This study integrates fNIRS data with advanced ML algorithms, specifically Extreme Gradient Boosting, CatBoost, Extra Tree Classifier, and Light Gradient Boosted Machine, to predict participants' credit decisions based on prefrontal cortex (PFC) activation patterns. Findings reveal distinctive PFC regions correlating with credit behaviors, including the dorsolateral prefrontal cortex (dlPFC) associated with strategic decision-making, the orbitofrontal cortex (OFC) linked to emotional valuations, and the ventromedial prefrontal cortex (vmPFC) reflecting brand integration and reward processing. Notably, the right dorsomedial prefrontal cortex (dmPFC) and the right vmPFC contribute to positive credit preferences. This interdisciplinary approach bridges neuroscience, machine learning and finance, offering unprecedented insights into the neural mechanisms guiding financial choices regarding different loan offers. The study's predictive model holds promise for refining financial services and illuminating human financial behavior within the burgeoning field of neurofinance. The work exemplifies the potential of interdisciplinary research to enhance our understanding of human financial decision-making.

Stressful Life Events and Reward Processing in Adults: Moderation by Depression and Anhedonia

Background. Exposure to acute stress is associated with reduced reward processing in laboratory studies in animals and humans. However, less clear is the association between reward processing and exposure to naturalistic stressful life events. The goal of the current study was to provide a novel investigation of the relation between past 6-month stressful life events and reward processing, and the extent to which this relation was moderated by depression diagnostic status and state symptoms of anhedonia. Methods. The current study included a secondary analysis of data from 107 adults (37 current-depressed, 25 past-depressed, 45 never-depressed; 75% women) drawn from two previous community studies. Past 6-month stressful life events were assessed with a rigorous contextual interview with independent ratings. Response to monetary reward was assessed with a probabilistic reward task. Results. Among current-depressed participants, and among both current- and past-depressed participants with high levels of anhedonia, greater exposure to independent life events outside of individuals’ control was significantly associated with poorer reward learning. In direct contrast, among those with low levels of anhedonia, greater exposure to independent life events was significantly associated with a greater overall bias toward the more frequently rewarded stimulus. Conclusions. Results suggest that depression and anhedonia are uniquely associated with vulnerability to blunted reward learning in the face of uncontrollable stressors. In contrast, in the absence of anhedonia symptoms, heightened reward processing during or following independent stressful life event exposure may represent an adaptive response.

Microglia activity in the human basal ganglia is altered in alcohol use disorder and reversed with remission from alcohol.

Alcohol use disorder (AUD) is characterized by cycles of abuse, withdrawal, and relapse. Neuroadaptations in the basal ganglia are observed in AUD; specifically in the putamen, globus pallidus (GP), and ventral pallidum (VP). These regions are associated with habit formation, drug-seeking behaviors, and reward processing. While previous studies have shown the crucial role of glial cells in drug seeking, it remains unknown whether glial cells in the basal ganglia are altered in AUD. Glial cells in the putamen, GP, and VP were examined in human post-mortem tissue of AUD and alcohol remission cases. Immunohistochemistry was performed to analyze cell count, staining intensity, and morphology of microglia and astrocytes, using markers Iba-1 and GFAP. Morphological analysis revealed a significant decrease in microglia cell size and process retraction, indicating activation or a dystrophic microglia phenotype in individuals with AUD compared to controls. Microglia staining intensity was also higher in the GP and VP in AUD cases, whereas microglia staining intensity and cell size in remission cases were not different to control cases. In contrast, no astrocyte changes were observed in examined brain regions for both AUD and remission cases compared to controls. These results suggest alcohol exposure alters microglia, potentially contributing to dysfunctions in the basal ganglia that maintain addiction, and abstinence from alcohol may reverse microglia changes and associated dysfunctions. Overall, this study further characterizes AUD neuropathology and implicates microglia in the putamen, GP, and VP as a potential target for therapy.