Facial aesthetic medicine has traditionally emphasized proportion, symmetry, and structural harmony based on anatomic and cultural ideals. However, rigid adherence to these principles may contribute to overcorrected, unnatural outcomes, challenging perceptions of authenticity. Although patients frequently request to "look natural," this concept remains poorly defined and is not systematically addressed in training. To distinguish beauty, attractiveness, and naturalness and to propose neuroaesthetics as a framework for improving patient-centered outcomes in aesthetic medicine. Narrative synthesis of interdisciplinary literature integrating neuroscience, evolutionary psychology, and aesthetic medicine, with a focus on neural mechanisms underlying attractiveness, reward processing, and social perception. Perceptions of attractiveness and naturalness are mediated by neural systems involved in reward valuation, rapid first-impression formation, and embodied simulation. Overreliance on static structural ideals may overlook dynamic cues critical to social and emotional evaluation. Neuroaesthetic principles provide a biologically informed framework for aligning aesthetic interventions with perceptual and psychosocial responses. Incorporating neuroaesthetics represents a shift from structural optimization toward outcomes that prioritize authenticity, emotional resonance, and social perception. As patient expectations evolve, aesthetic providers should integrate these principles to achieve more natural and meaningful results.

Oxytocin and direct reciprocity in rats.

The neural basis of reward magnitude, effort level, and subjective value: An activation likelihood estimation meta-analysis of effort-based reward tasks in healthy cohorts.

Subjective valuation of food rewards guides our dietary choices and is fundamental to human health and well-being. Extensive literature in human functional magnetic resonance imaging (fMRI) studies has consistently shown that a network of reward-processing brain regions, including the ventromedial prefrontal cortex (vmPFC) and ventral striatum, encodes the subjective values of food rewards. However, the representational geometry of value signals and the mechanisms by which they are constructed in the brain remain poorly understood. This is partly because most fMRI studies on food valuation rely on small stimulus sets, yielding datasets too shallow for advanced analyses such as multi-voxel pattern analysis, and deep neural network modeling. Here, we present a densely sampled fMRI dataset wherein 31 participants provided subjective value ratings for over 500 food images across three separate days. We validate the dataset by replicating the well-established findings regarding the neural encoding of subjective value in the vmPFC and ventral striatum. We anticipate this resource will facilitate diverse studies on neural food valuation using advanced analytical methods.

Temporal-orbitofrontal pathway regulates choices across physical reward and visual novelty.

ABSTRACTIntroductionA family history of alcohol use disorder (AUD) is associated with increased personal risk for alcohol misuse and AUD. Family history of AUD is also related to increased impulsivity as measured by delay discounting tasks, representing a potential mechanistic link between family history and alcohol misuse. Delay discounting tasks assess individual differences in preferences for smaller, immediate versus larger, delayed rewards, the former being linked to substance misuse. Decision‐making on such tasks is underpinned by multiple neural systems, including those supporting reward valuation, cognitive control, and future‐oriented thinking. We hypothesized that family history of AUD would be associated with differences in one or more neural systems related to delay discounting, with differences relating to increases in alcohol misuse in young adulthood.MethodsWe tested 163 first‐year college students (105 females, ages 18–19) with varying levels of familial risk for AUD on a functional magnetic resonance imaging (fMRI) delay discounting task. Alcohol misuse was self‐reported at baseline and in 3‐yearly follow‐up surveys using the Alcohol Use Disorders Identification Test (AUDIT). Change in alcohol misuse was modeled using a latent growth model, and we examined mediation between family history and alcohol misuse trajectory (AUDIT intercept and slope) through functional activation of brain regions implicated in reward valuation (nucleus accumbens), cognitive control (middle frontal gyrus), and future‐oriented thinking (hippocampus).ResultsFamily history of AUD was associated with greater nucleus accumbens activation (β = 0.286, SE = 0.117, p = 0.014), which in turn predicted a steeper AUDIT slope (β = 0.513, SE = 0.162, p = 0.002). No other mediators were significant.DiscussionOur results demonstrate that nucleus accumbens function may be a key mechanism by which family history increases risk for alcohol misuse and AUD.

Cigarette smoking poses a pervasive health risk increasingly recognized for its impact on the nervous system, yet its effects on brain structure and organization remain incompletely understood. This study examined how smoking addiction influences white matter microstructure and the architecture of structural brain networks in adults. We used diffusion tensor imaging to compare fractional anisotropy between participants who smoke (n = 122) and non-smoking control participants (n = 55) to detect white matter abnormalities. Whole-brain structural connectomes were constructed, with connections categorized by fiber length. Network features quantified included degree centrality and hemispheric asymmetry. Adaptive Best-Subset Selection method was applied to identify white matter connections that may serve as biomarkers for distinguishing individuals who smoke from those who do not. Participants who smoke showed widespread white matter alterations in pathways related to reward valuation, habit formation, and craving, along with abnormalities in both short- and medium-range connections. Reduced rightward asymmetry in the cuneus indicated lateralized structural changes possibly linked to cue processing in nicotine dependence. Discriminative connections involved orbitofrontal, sensorimotor, and visual regions, underscoring how smoking reshapes brain networks supporting reward valuation, motor control, and cue reactivity. Nicotine dependence is associated with extensive alterations in white matter microstructure and network organization, including reduced hemispheric asymmetry. These findings suggest that smoking affects structural connectivity in circuits involved in emotional regulation and reward-related memory.

Early life stress (ELS) in primates alters dopamine function, contributing to addiction, hyperactivity, cognitive deficits, aggression, and social subordinance. To assess whether dopamine receptor densities are affected by ELS, male juvenile rhesus monkeys (Macaca mulatta) were either mother-reared (MR, N=6) in a semi-natural environment or nursery-reared (NR, N=6) with peers in a laboratory. At 1 ½ years of age, subjects were sacrificed and the left prefrontal cortex (PFC), striatum (caudate and putamen), nucleus accumbens (NAcc), and claustrum (CLA) were explored through quantitative autoradiographic studies of dopamine receptor-1 (DRD1) and -2 (DRD2) conducted using [125I]-(+)-SCH 23982 and 125 I-Epidepride, which have high affinity and selectivity for DRD1 and DRD2, respectively. No group differences emerged in striatal or NAcc receptor binding. However, MR monkeys exhibited significantly greater DRD1 binding in the left orbital PFC and significantly greater DRD2 binding in both the left medial PFC and right CLA compared to NR. These findings implicate the medial PFC (stress vulnerability, cognition), orbital PFC (reward valuation), and CLA (anxiety modulation) as critical sites disrupted by maternal deprivation. Therefore, we propose that nursery-rearing induces a hypodopaminergic prefrontal-claustral ecophenotype, underlying the cognitive, affective, and social impairments observed in NR monkeys.

Neurodevelopmental disorders such as attention-deficit/hyperactivity disorder, autism spectrum disorder, and schizophrenia are classically defined by cognitive and sensorimotor impairments. However, dysregulated motivation is a core but underrecognized feature of these conditions with significant implications for quality of life. We present a heuristic hypothesis-generating framework that distinguishes two interacting and partially dissociable subdomains of motivation: self-initiated motivation, defined as goal-directed behavior that arises in the absence of immediate external prompting, and stimulus-driven motivation, defined as responses elicited by environmental cues or physiological states. Unlike traditional distinctions such as intrinsic versus extrinsic motivation or the liking-wanting dichotomy, this framework emphasizes the initiation of motivated action as its organizing axis, focusing on whether behaviors are generated internally or triggered by external stimuli rather than on reward valuation or hedonic impact. These subdomains are implemented by overlapping, dynamically interacting neural circuits that follow relatively distinct developmental trajectories and may exhibit differential sensitivity to early-life adversity. Our model provides a transdiagnostic conceptual scaffold that bridges categorical diagnoses and aligns with the Research Domain Criteria Motivation Systems framework. We focus on disorders with early-emerging circuit vulnerability and developmental onset, while recognizing that the framework is applicable more broadly across psychiatric conditions. Rather than offering a definitive nosology, the model supports mechanistic phenotyping, hypothesis-driven experimental design, and translational inference across neurodevelopmental disorders. To illustrate its translational utility, we highlight behavioral assays in animal models that differentially engage each subdomain and propose circuit-informed, testable strategies to guide future intervention development.

Monotonous tasks are common in academic and professional settings, yet sustaining motivation and effort in such contexts remains a persistent challenge. This research examined whether inserting a brief episode of interest into an otherwise boring, incentivized task could replenish cognitive and motivational resources and sustain effort. Two competing accounts were tested. The contrast-effect hypothesis predicted that once interest was withdrawn, the remaining rewards would lose their impact, and effort would diminish. In contrast, the transfer-effect hypothesis proposed that prior interest would leave a motivational trace that preserves the effectiveness of the rewards. Study 1 (behavioral study) employed a typing task, while Study 2 (fMRI study) used a social preference guessing task, both with performance-contingent monetary incentives. In both studies, participants in the experimental group completed a boring-interesting-boring sequence, whereas those in the control group experienced a boring-neutral-boring sequence. Across two studies, results consistently supported the transfer-effect hypothesis, demonstrating that prior interest enhanced subsequent engagement, effort, and reward sensitivity, even when monetary incentives were reduced. Neuroimaging results further revealed activity in regions involved in reward processing (e.g., anterior cingulate cortex, anterior insula) and attentional control (e.g., lateral occipital cortex, inferior parietal lobule) even after interest was removed, suggesting a lingering motivational effect of interest. These findings integrate reinforcement learning and interest theories and suggest a practical strategy: sandwiching brief, interest-enhancing episodes between boring rewarded tasks can serve as a motivational reset, enabling effort and persistence in low-stimulation environments.

ABSTRACT Delay of gratification tasks typically offer children a choice between a smaller immediate versus a larger delayed reward, assuming waiting is motivated by maximizing material gain. However, the offer itself may act as a social signal inviting pragmatic inference. Children may interpret the act of offering a delayed reward as a communicative act, prompting them to consider why it is being made and to infer that the experimenter wants them to wait. The present research tested this pragmatic account by manipulating whether a delayed reward (of equal value to the immediate one) was presented as having been intentionally selected or randomly offered by the experimenter. Across four preregistered studies (total N = 266), conducted with 3- to 5-year-old children in China, participants were told that if they waited, a sticker they had already earned would be replaced with another that was either identical or equivalent in value. As predicted, children waited significantly longer when the replacement reward appeared to be intentionally selected (about 10 minutes) than when it did not (about 6 minutes) or when no reward was offered for waiting (about 5 minutes). These findings show that Chinese young children will wait in delay of gratification tasks even when they have nothing material to gain, as long as the reward appears to have been intentionally chosen. More broadly, the results highlight the role of pragmatic reasoning in shaping behavior in classic self-regulation tasks and suggest that such reasoning may contribute to the development of self-regulation over time.

Effort discounting, or the devaluation of rewards requiring effort, depends on underlying neural computations of reward valuation and cognitive control. Although much is known about effort discounting, its temporal dynamics-how effort valuation changes when required effort is delayed-remain underexplored. Furthermore, although depression has been linked to altered effort and reward discounting, its role in the temporal dynamics of effort valuation remains unclear. In this study, we conducted three experiments to examine how temporal delays alter effort aversion, with a focus on cognitive load and individual differences in depression. In Experiment 1, we evaluated effort valuation by using the Cognitive Effort Discounting (COG-ED) paradigm together with a backward-typing task and found that effort discounting decreases over time for tasks that require high effort. Experiment 2 replicated this pattern by using a working memory (n-back) task, confirming that effort demand modulates temporal effort discounting for high cognitive loads. Experiment 3 investigated whether depressive traits modulate temporal effort discounting. Nondepressed participants showed strong effects of delay at higher effort levels, with effort discounting decreasing over time. In contrast, depressed participants exhibited reduced sensitivity to delay. Hierarchical drift diffusion modeling (HDDM) revealed that nondepressed individuals flexibly adjusted their decision-making by shifting from positive (high-effort) to negative (low-effort) drift rates as effort increased. In contrast, depressed individuals exhibited consistently negative drift rates across all effort levels, indicating a persistent bias toward effort avoidance. Taken together, these findings highlight how cognitive load influences effort valuation over time and suggest that depression blunts temporal sensitivity in effort-based decisions.

Robust autonomous driving under adversarial disturbances remains a fundamental challenge, as conventional deep reinforcement learning (DRL) frameworks exhibit fragile convergence and limited resilience to distributional shifts. This study presents the Adversarially Adaptive Reward-Enhanced Soft Actor – Critic (AARE-SAC), which reconceptualizes SAC as a hierarchically self-regulating control system. Within this paradigm, the temporal-difference error functions as a meta-feedback variable that adaptively modulates learning dynamics, reward valuation, and adversarial response, forming a self-stabilizing loop that internalizes robustness. Experiments in diverse CARLA urban environments demonstrate that AARE-SAC achieves faster and smoother convergence with markedly improved stability and safety. Ablation analyses confirm that its advantage arises from the synergistic coupling between adaptive regulation and adversarial exposure, transforming robustness from a reactive safeguard into an intrinsic property of learning. These findings establish AARE-SAC as a unified framework for achieving stability, efficiency, and resilience in safety-critical autonomous driving.

Interventions for major depressive disorder (MDD) using noninvasive brain stimulation often target the left lateral prefrontal cortex to reduce symptoms of anhedonia. However, the electrophysiological mechanism by which symptoms of anhedonia arise from dysfunction of the lateral prefrontal cortex is poorly understood. Furthermore, multiple constructs related to reward processing within the positive valence systems have been found to be blunted with anhedonia. To disentangle components of the positive valence systems, human participants with an active episode of MDD performed an adaptive version of the expenditure of effort for reward task (Adaptive-EEfRT) and three constructs of reward processing were investigated: effort motivation, reward valuation, and reward-responsive goal-directed behavior. Individual differences analysis revealed that symptoms of anhedonia were most strongly related to blunted reward-responsive goal-directed behavior. By recording electroencephalography (EEG), spectral analysis revealed that the amplitude of left prefrontal delta oscillations (2-3 Hz) increased with each reward construct and beta oscillations decreased over the motor cortex contralateral to the hand used for effort exertion. Phase-amplitude delta-beta coupling between the left prefrontal cortex and contralateral motor cortex was significantly increased for each reward construct. When cross-frequency transcranial alternating current stimulation (tACS) was delivered to 26 females and 9 males to mimic prefrontal-motor delta-beta coupling, only reward-responsive goal-directed behavior was improved relative to placebo and active-control tACS. These findings provide causal evidence that the left prefrontal cortex supports reward-responsive goal-directed behavior via cross-frequency coupling. Interventions for anhedonia that target the left prefrontal cortex might be improved by frequency-specific targeting of delta-beta coupling.

Understanding the role of a partner is key to effective human cooperation. While we know that non-human animals extensively cooperate with each other, how well they understand the role of their partner is unclear. This has been explored using economic games, yielding mixed results. A previous study showed that dogs understand the role of their human partner in an economic game setting, adjusting their behavior according to the partner's choices, but there are no clear results when it comes to dog conspecific cooperation. In this study, we tested pairs of pet dogs in the stag hunt game. In the typical payoff group, dogs had the option to perform a more challenging, cooperative action for a higher reward or work individually for a lower one. To test for a potential effect of motivation for the high value reward, we had a same reward group where cooperation or individual work led to the same reward. Dogs had minimal training and exposure to the contingencies of the game. Dog pairs from both groups only coordinated their choice on the cooperative action in 5% of the trials. Accordingly, we found that dogs were generally more likely to work individually, regardless of their partner's actions and obtainable rewards. In the typical payoff group, dogs initially showed a greater tendency to cooperate during the first session, but this declined quickly, with dogs from pairs ultimately working alone. The low success on the cooperative apparatus was likely due to dogs not investing sufficient effort to find the solution by trial-and-error. This could be due to the fact that the high-quality reward was not good enough to invest that extra effort or a preference of dogs to work alone if given the choice. Overall, our results showed that dogs did not choose to cooperate with conspecifics, in contrast to their demonstrated success in interspecific contexts. We discuss how cooperation is potentially sensitive to contextual and social constraints rather than widespread.

Lysergic acid diethylamide (LSD) has been considered as a potential treatment for depression for over 75 years, but its therapeutic potential has only recently been considered in mainstream psychiatry. Repeated ingestion of low doses of LSD ("microdoses") is thought to reduce depression, but the neurobiology underlying this effect is unknown. We previously reported that low doses of LSD increased event-related potentials (ERPs) during receipt of monetary rewards in healthy adults. LSD also produced more positive subjective effects in participants with mild-to-moderate baseline symptoms of depressed mood, compared to controls. In this report, we examined the effects of LSD on reward ERPs in participants with mild-to-moderate depressed mood and in non-depressed controls. Participants with subclinical mild-to-moderate depression (N = 20) or controls with minimal symptoms (N = 19) received LSD (26 μg tartrate) or placebo on two sessions. Primary measures were ERPs during a reward task, and secondary measures included self-reported mood during and 48 hours after the sessions. LSD (vs placebo) increased late positive potential (LPP) amplitude to loss (vs win) reward feedback only in participants with higher baseline depressed mood, suggesting enhanced affective processing given the role of LPP in emotional valuation of reward. This effect of LSD on LPP was associated with its acute positive mood effects, and with lower depressed mood 48-hour after the LSD (vs placebo) session. In the full sample, LSD (vs placebo) decreased feedback-P3 and LPP amplitude to reward (vs neutral) feedback. Although findings must be interpreted with caution, results support the idea that low doses of LSD have potential anti-depressant effects.

Introduction: Late-life depression (LLD) is a significant risk factor for suicide in older adults, yet clinical assessments for suicidality are often limited by subjective reporting and lack of predictive validity. Functional neuroimaging has highlighted overlapping alterations in neurocircuitry underlying emotional processing, decision-making and cognitive control between LLD and suicidality, potentially serving as predictors of suicide risk. However, no review to date has synthesized this evidence in the context of LLD. Methods: A systematic search was conducted in Ovid MEDLINE, Embase and APA PsycInfo databases, following PRISMA guidelines. Eligible studies included older adults (≥55 years) with clinically defined LLD, validated measures of suicidality, and fMRI data. Of 1829 articles identified, eight studies met the inclusion criteria. Study quality was assessed using the Newcastle-Ottawa Quality Assessment Scale. Results: Functional alterations were observed in frontostriatal and limbic circuits. Resting-state studies reported disrupted connectivity within/between the dorsolateral prefrontal cortex (DLPFC), ventrolateral prefrontal cortex (VLPFC), orbitofrontal cortex (OFC), caudate nucleus, and amygdala. Task-based studies revealed blunted ventromedial prefrontal responses to reward and heightened frontal operculum activation during socioemotional tasks among suicide attempters compared to depressed non-suicidal and healthy individuals. Discussion: Disruptions in functional brain activity in LLD that contribute to suicide risk may reflect impaired decisionmaking, reward valuation, cognitive control, and affective dysregulation. Differences in functional activation and connectivity may distinguish suicidal ideation from suicide attempts, though further studies with larger, more diverse samples and longitudinal designs are needed to clarify this. Conclusion: Functional neuroimaging reveals convergent patterns of dysregulation in key brain networks associated with suicide risk in LLD. These findings highlight the potential for imaging-informed models of suicide risk stratification and targeted neuromodulation. Longitudinal and interventional studies are needed to refine predictive biomarkers and improve clinical utility.

The positive valence systems (PVS) domain, a key focus of the Research Domains Criteria framework, divides reward-related processes into three constructs: reward responsiveness, reward learning, and reward valuation. Difficulties with several of these reward constructs have been reported in people with mood-psychosis spectrum disorders. This study aims to examine how performance on tasks corresponding to these three constructs covaries, and how performance relates to mood and psychotic symptoms in adults with mood-psychosis spectrum disorders, those at familial risk, and controls. Data from two studies (N=278 and N=332) were analyzed, which both included people with a psychotic disorder or bipolar disorder (patients), their first-degree relatives (FDRs), and controls. PVS constructs were measured using the Multi-Armed Bandit Task, Effort-Expenditure for Rewards Task, and Monetary Incentive Delay Task. Depression, mania, and psychosis symptoms were measured with self-report and interview instruments. Confirmatory factor analysis was used to examine covariation, and path analysis to test associations with symptoms. The three reward constructs showed weak (nonsignificant) covariance in all groups. There were a few impairments in reward-related performance in patients or FDRs, none that survived multiple-comparison correction. There were no associations between symptoms and performance on the PVS constructs after multiple comparisons correction. The findings showed no evidence that performance on any of the three PVS constructs could constitute an endophenotype of mood-psychosis spectrum disorders. We recommend future research examining the contribution of specific cognitive skills to reward-related behavior, and to sources of heterogeneity in reward functioning within the patient group.

With approximately 4% of the world's population using cannabis, there is a need to better understand its physiological effects. Cannabis consumption acutely promotes food intake ("the munchies") via delta-9-tetrahydrocannabinol-mediated activation of cannabinoid 1 receptors (CB1R); however, these appetitive effects have not been well characterized. We examined effects of cannabis vapor inhalation on energy and macronutrient intake patterns in human participants and then validated these findings in a translational rat model through which we explored behavioral and physiological mechanisms subserving this response. Vaporized cannabis acutely and robustly increased energy intake. In humans, this occurred in the first 30 min of snack and beverage access, irrespective of dose or gender. In rats, these effects were observed in the first 60 min of food access, irrespective of macronutrient content, satiation, or sex, and were a result of cannabis vapor reducing latency to eat and increasing feeding bout number. Also, cannabis vapor did not change the proportion of macronutrients consumed by human participants and abolished preexisting macronutrient-specific food preferences in rats. Our rat data indicate that cannabis vapor may override homeostatic appetite regulation by increasing motivation to eat and reducing food reward devaluation to promote energy intake. Finally, cannabis vapor did not alter circulating appetite-associated hormones, and these feeding effects were mediated by central, but not peripheral, CB1Rs. This study complements and builds upon previous literature to characterize the appetitive effects of vaporized cannabis and uses a translational approach to examine cannabis-driven energy and macronutrient intake patterns in humans and rodents.

Diet-related chronic illnesses, such as obesity and diabetes, pose major global health challenges. To promote healthier choices, policymakers have introduced nudges like front-of-package labels such as the Nutri-Score, which simplify nutritional information. While previous research has examined the impact of front-of-package labels on product valuation via reward and cognitive control pathways, the neural mechanisms underlying attribute-specific changes in food perception (e.g., healthiness, tastiness) remain unclear. In this study, the impact of a Nutri-Score derived color-coded frame on the decision domains , perceived healthiness, perceived tastiness, and willingness-to-pay as a proxy for subjective value, was investigated. Forty healthy participants (28 females, age: M = 23.8 years, SD = 3.1 years) rated 63 food products in two conditions: without (control) and with (treatment) a color-coded frame while undergoing functional magnetic resonance imaging. The investigation focused on how the color-coded frame alters all three decision domains on a behavioral but also on the neural level. Additionally, the variation in neural and behavioral responses depending on the frame color was investigated. Overall, our results show that the color-coded frame significantly influenced WTP, healthiness, and tastiness ratings, with corresponding increases in neural activation in reward-related (ventromedial prefrontal cortex), cognitive control (dorsolateral prefrontal cortex), and homeostatic (thalamus) regions. Healthiness perception involved regions associated with value-based processing (ventromedial prefrontal cortex), as well as cognitive control (dorsolateral prefrontal cortex) when the color-coded frame was present, whereas tastiness perception engaged a network including the insula, brain regions related to reward valuation (ventromedial prefrontal cortex), and regions associated with cognitive control. These findings suggest that the color-coded frame, used here as a proxy for the Nutri-Score, influences food choices by modulating attribute-specific valuation and interacting with homeostatic mechanisms, rather than directly altering overall value computation. Understanding how external cues integrate with internal physiological signals to guide food choices may inform interventions aimed at improving dietary behavior and public health outcomes.