Blunted ventral striatal reactivity to social reward is associated with more severe motivation and pleasure deficits in psychosis

Among individuals living with psychotic disorders, social impairment is common, debilitating, and challenging to treat. While the roots of this impairment are undoubtedly complex, converging lines of evidence suggest that social motivation and pleasure (MAP) deficits play a key role. Yet most neuroimaging studies have focused on monetary rewards, precluding decisive inferences. Here we leveraged parallel social and monetary incentive delay fMRI paradigms to test whether blunted reactivity to social incentives in the ventral striatum–a key component of the distributed neural circuit mediating appetitive motivation and hedonic pleasure–is associated with more severe MAP symptoms in a transdiagnostic sample enriched for psychosis. To maximize ecological validity and translational relevance, we capitalized on naturalistic audiovisual clips of an established social partner expressing positive feedback. Although both paradigms robustly engaged the ventral striatum, only reactivity to social incentives was associated with clinician-rated MAP deficits. This association remained significant when controlling for other symptoms, binary diagnostic status, or ventral striatum reactivity to monetary incentives. Follow-up analyses suggested that this association predominantly reflects diminished striatal activation during the receipt of social reward. These observations provide a neurobiologically grounded framework for conceptualizing the social-anhedonia symptoms and social impairments that characterize many individuals living with psychotic disorders and underscore the need to establish targeted intervention strategies.

To date, only a handful of psychosis studies have examined potential alterations in neural reactivity to social rewards.Two modest case-control studies provide preliminary evidence of aberrant reactivity to social incentives in the ventral striatum (Supplementary Figure S1)-a key hub in the distributed neural system mediating appetitive motivation ('wanting') and hedonic pleasure ('liking') [24][25][26] -among individuals with schizophrenia (n Cases =27) 27,28 .Leveraging a much larger, transdiagnostic psychosis sample (n Cases =71), Jimenez and colleagues reported that diminished ventral striatum reactivity to social reward is associated with more severe MAP de cits and social-anhedonia symptoms 29 .Whether this association is reproducible remains unknown and whether it is speci c to social reward remains unclear, as the authors only examined social incentives.
Here we used fMRI and parallel social and monetary incentive delay (SID/MID) paradigms to test the overarching hypothesis that blunted ventral striatum reactivity to social incentives will be associated with more severe MAP symptoms, indexed using gold-standard clinician ratings (Figure 1).The inclusion of the MID paradigm enabled us to clarify the speci city of this hypothesized association for the rst time.Follow-up analyses were used to explore the relevance of other symptom dimensions, narrower reward facets (anticipation vs. presentation), and less intensively scrutinized brain regions.To ensure a broad spectrum of social impairment and MAP symptomatology, we adopted a Research Domain Criteria (RDoC) sampling strategy, focusing on a transdiagnostic community sample that was heavily enriched for psychosis (Table 1) 30,31 .Most participants were on a stable regimen of outpatient treatment, enhancing clinical relevance.To date, clinical neuroimaging studies of social reward have relied almost exclusively on static photographs of positive facial expressions posed by unfamiliar adult models (i.e., strangers).To maximize ecological validity and translational relevance, we instead capitalized on audiovisual clips of an established social partner expressing varying degrees of social reward.As shown in Figure 1, we used the Social A liation Enhancement Task (SAET) to cultivate a sense of a liation with an experimental partner just before the neuroimaging assessment 10 .Prior work by our group con rms the validity of this approach, demonstrating that the SAET signi cantly enhances a liative feelings, perceived closeness, and willingness to interact with the partner 14 .This novel naturalistic approach enabled us to manipulate the intensity of nonverbal (facial expressions and gestures), paralinguistic (vocal intonation), and verbal (praise) indicators of social reward expressed by a social partner.

Study Overview
The present study stems from a larger project focused on the nature and neurobiology of social a liative de cits in psychosis (R01-MH110462) 14,[32][33][34] .Participants completed two assessments: a baseline clinical session and a two-phase laboratory session.At the baseline clinical session, eligibility was con rmed; participants provided informed written consent; and demographic, diagnostic, symptom, and other self-report data were acquired.Participants were instructed to abstain from taking sedatives/benzodiazepines for at least 12 hours prior to the MRI assessment.None of these individuals disclosed concerns or exhibited noteworthy withdrawal or rebound effects.Latency between the two sessions was <2 weeks (M=6.5 days, SD=2.9).During the two-phase laboratory session, participants completed (a) the SAET outside the scanner, and (b) the social and monetary incentive delay (SID/MID) paradigms inside the scanner (Figure 1) as well as additional tasks not reported here 14 .Following the last scan, participants were debriefed and compensated.Procedures were approved by the University of Maryland, Baltimore Institutional Review Board.

Participants
Recruitment.To capture a broad spectrum of motivation and pleasure de cits, maximizing range and statistical power, a mixed transdiagnostic adult sample-including both clinical and community participants-was recruited 31 .A modest number of psychiatrically healthy community participants was included (19.4%;Table 1) to ensure that the full range of a liative function was captured 31 S1).The CAINS has been successfully deployed in a variety of clinical and non-clinical populations 9,14,27,29,36,37 .For hypothesis testing, MAP served as the primary index of social amotivation and anhedonia.The expanded Brief Psychiatric Rating Scale (BPRS) is a 24-item interview that was used to index Positive Symptoms (8 items; α=0.69),Depression/Anxiety (4 items; α=0.74), and Agitation (6 items; α=0.53) 38, 39 .
Self-Reported Social Function.The 7-item Interpersonal Relationships scale from the Speci c Levels of Functioning (SLOF) instrument was used to index interpersonal functioning (α=0.89)(Supplementary Table S1) 40,41 .Consistent with prior studies, in the current sample more severe MAP symptoms were associated with poorer interpersonal functioning (r = -.56,p < .001).

Social A liation Enhancement Task (SAET)
The Social A liation Enhancement Task (SAET) encompasses a validated suite of procedures for cultivating social rapport, trust, and a liation (Figure 1a) (for details, see Refs. 10,14 .Prior work by our group demonstrates that the SAET signi cantly enhances a liative feelings, perceived closeness, and willingness to interact with the partner 14 , consistent with work using similar paradigms 17 . Social and Monetary Incentive Delay (SID/MID) fMRI Paradigms Overview and Procedures.As shown in Figure 1b, paralell incentive-delay paradigms were used to probe neural reactivity to social and monetary reward 42,43 .Both paradigms took the form of balanced 3condition (Reward Level: High, Low, None) randomized, event-related, repeated-measures designs (paradigm order counterbalanced; 2 scans/paradigm; 22 trials/condition/scan).General task structure, timing, and procedures were identical across paradigms.Because we did not harbor a strong a priori hypothesis about the impact of MAP symptoms on the anticipation-versus-presentation of social reward, trial timing was optimized via simulations to maximize the detection of global differences in reward sensitivity, while remaining mindful of participant burden and tolerability (variance in ation factors < 2.55).Participants were completely informed about the task structure and contingencies prior to scanning.They were instructed that the goal of both paradigms was to maximize reward receipt and that this was contingent on the speed of their response to a brie y presented visual target.Responses were made using the rst digit of the dominant hand and an MRI-compatible response-pad (MRA, Washington, PA).To maintain a comparable level of di culty across paradigms, trials, and participants, the response-
To enhance resolution, a multi-band sequence was used to collect oblique-axial echo planar imaging (EPI) volumes (acceleration=6; TR=1,250 ms; TE=39.4 ms; ip =36.4°; slice thickness=2.2mm, number slices=66; in-plane=2.1875mm 2 ; matrix=96×96; 355 volumes × 4 scans).Images were collected in the oblique axial plane (approximately −20° relative to the AC-PC plane) to minimize potential susceptibility artifacts.The scanner automatically discarded 7 volumes prior to the rst recorded volume.To enable eldmap correction, two oblique-axial spin echo (SE) images were collected in each of two opposing phase-encoding directions (rostral-to-caudal/caudal-to-rostral) co-planar to the functional volumes (TR=7,220 ms; TE=73 ms).Respiration and pulse were acquired using a respiration belt and photoplethysmograph a xed to the rst digit of the non-dominant hand.Participants were continuously monitored using an MRI-compatible eye-tracker (Eyelink 1000; SR Research, Ottawa, Ontario, Canada) and the AFNI real-time motion plugin 46 .Eye-tracking data were not recorded.

MRI Data Processing Pipeline
Methods were optimized to minimize spatial normalization error and other potential sources of noise, and are similar to those detailed in other recent reports by our group 14,47,48 .Data were visually inspected before and after processing for quality assurance.All participants provided 4 usable scans.
Anatomical Data.T1-weighted images were inhomogeneity corrected using N4 49 and ltered using ANTS DenoiseImage 50 .Brains were extracted using BEaST 51 and brain-extracted-and-normalized referencebrains 52 .Brain-extracted T1 images were normalized to a version of the brain-extracted 1-mm T1weighted MNI152 (version 6) template modi ed to remove extracerebral tissue 53 .Normalization was performed using the diffeomorphic approach implemented in SyN (version 2.3.4) 50.T2-weighted images were rigidly co-registered with the corresponding T1 prior to normalization.The brain-extraction mask from the T1 was then applied.Tissue priors were unwarped to native space using the inverse of the diffeomorphic transformation 54 .Brain-extracted T1 and T2 images were segmented-using native-space priors generated in FAST (version 6.0.4) 55 -for subsequent use in T1-EPI co-registration (see below).
Fieldmap Data.SE images and topup were used to create eldmaps.Fieldmaps were converted to radians, median-ltered, and smoothed (2-mm).The average of the motion-and distortion-corrected SE images was inhomogeneity corrected using N4 and masked to remove extracerebral voxels using 3dSkullStrip (version 20.2.14).Functional Data.EPI les were de-spiked using 3dDespike, slice-time corrected to TR-center using 3dTshift, and motion corrected to the rst volume using ANTS (12-parameter a ne).Transformations were saved in ITK-compatible format for subsequent use 56 .The rst volume was extracted and inhomogeneity corrected for EPI-T1 co-registration.The reference EPI volume was simultaneously coregistered with the corresponding T1-weighted image in native space and corrected for geometric distortions using boundary-based registration 55 .This step incorporated the previously created eldmap, undistorted SE, T1, white matter (WM) image, and masks.To minimize potential normalization error, reference EPI volumes were spatially normalized to the MNI template using SyN, intensity standardized, and averaged to create a study-speci c EPI template [57][58][59] .Normalized EPI reference volumes were then normalized to the study-speci c.To minimize incidental spatial blurring, the operations necessary to transform each EPI volume from native space to the reference EPI, from the reference EPI to the T1, from the T1 to the MNI template, and from the MNI template to the study-speci c EPI template were concatenated and applied to the processed EPI data in a single step.Normalized EPI data were resampled (2 mm 3 ) using fth-order b-splines and spatially smoothed (6-mm) using 3DblurInMask.fMRI Data Modeling General Approach.For each participant, rst-level modeling was performed using general linear models (GLMs) implemented in SPM12 (version 7771), using the default autoregressive model and temporal band-pass lter set to the hemodynamic response function (HRF) and 128 s 60 .Consistent with past work 14,47,48 , nuisance variates included volume-to-volume displacement and its derivative, motion (6 standard parameters, global volume-to-volume displacement, and temporal derivatives), cerebrospinal uid (CSF) signal, instantaneous pulse and respiration signals, and ICA-derived nuisance signals (e.g., global motion) 61 .Volumes with excessive volume-to-volume displacement (>0.66 mm) were censored.The inter-trial interval served as the implicit baseline.
Hypothesis Testing.For hypothesis testing purposes, reward signals were modeled using variableduration rectangular ('box-car') regressors that spanned the entire trial, separately for each combination of reward level (High, Low, None) and outcome (Hit/Miss) (Figure 1b).Regressors were convolved with a canonical hemodynamic response function (HRF) and its temporal derivative.
Reward Anticipation and Presentation.To explore the relevance of ner differences in neural reward signaling, we separately modeled the anticipation and presentation phases of the trial using delta functions time-locked to the onset of the cue and outcome, respectively, for each combination of reward level and outcome (Figure 1b).Although our incentive-delay paradigms were not originally optimized for this modeling approach, collinearity proved acceptable (variance in ation factors <3.36) 62 68 .Clusters and peaks were labeled using the Harvard-Oxford atlas [69][70][71] , supplemented by descriptions of the orbitofrontal cortex, the ventral striatum, and its two major divisions: the core and shell (Supplementary Figure S1) [72][73][74][75][76][77] .
Con rmatory Testing.Whole-brain voxelwise ('second-level') repeated-measures ('random effects') general linear models (GLMs) were used to con rm that the SID and MID tasks robustly engaged the ventral striatum, as indexed by the cardinal High-versus-No-Reward contrast for hit trials.Signi cance was assessed using p<0.05,whole-brain familywise error (FWE) corrected for cluster extent, and a cluster-de ning threshold of p<0.001 78 .
Hypothesis Testing.The overarching goal of this study was to test the hypothesis that blunted ventral striatum reactivity to social incentives is associated with more severe clinician-rated MAP symptoms.To do so, we used a standard voxelwise regression, with mean-centered CAINS MAP as the predictor, meancentered biological sex and age as nuisance variates, and the High-versus-No-Reward contrast as the outcome (Figure 1d), consistent with prior work 26,28 .Signi cance was assessed using p<0.05,FWE corrected for the volume of the anatomically de ned ventral striatum (Figure 1d) 79 .The same approach was used to probe potential associations with ventral striatum reactivity to monetary incentives.
Speci city Analyses.When a signi cant association was observed, a voxelwise multiple regression was used to test whether ventral striatum reactivity to that incentive (e.g., social) continued to explain signi cant variance in MAP symptoms when statistically controlling for mean-centered reactivity to the other incentive (e.g., monetary), sex, and age (p<0.05,ventral striatum FWE corrected).For a similar voxelwise-covariate approach, see Ref. 80 .Follow-up analyses also allowed us to test whether MAP symptoms explain signi cant variance in ventral striatum reward signaling, over-and-above meancentered affective attening/alogia, positive symptoms, depression/anxiety, agitation, and binary diagnostic status (i.e., case-versus-control; p<0.05, ventral striatum FWE corrected).
Secondary Analyses.The same general approach was used to determine the relevance of disaggregating striatal responses to the anticipation-versus-presentation of reward (see above for fMRI modeling details).Here again, when a signi cant association was detected, voxelwise multiple regression was used to test whether ventral striatum reactivity to that phase of the trial (e.g., anticipation) continued to explain signi cant variance in MAP symptoms when statistically controlling for mean-centered reactivity to the other phase (e.g., presentation), sex, and age (p<0.05,ventral striatum FWE corrected).For a similar approach, see Ref. 81 .
Exploratory Analyses.Voxelwise regressions were used to explore potential associations between ventral striatum reward signaling and self-reported interpersonal functioning (SLOF; p<0.05, ventral striatum FWE corrected), and to assess associations between MAP symptoms and reward signaling in other, less intensively scrutinized brain regions (p<0.05,whole-brain FWE corrected).

Social and Monetary Incentives Robustly Engage the Ventral Striatum
As a precursor to hypothesis testing, we used whole-brain voxelwise GLMs to determine whether the SID and MID paradigms had the expected neurophysiological consequences, as indexed by the cardinal High Reward vs. No-Reward contrast (hit trials).Consistent with work in healthy 82, 83 and psychotic 21,23 samples, results con rmed that social and monetary incentives recruited an overlapping network of subcortical and cortical regions, including bilateral ventral striatum, thalamus, cingulate (subgenual, pregenual, and midcingulate), anterior insula, orbitofrontal cortex (posterior orbital gyrus), superior parietal lobule, and ventral visual cortex (p<0.05,whole-brain FWE corrected; Figure 2; Supplementary Tables S2-S5).

Accumbens Reactivity to Social Incentives is Uniquely Associated with MAP De cits
We used a standard voxelwise regression to test whether ventral striatum reactivity to social incentivesindexed by the High-versus-No-Reward contrast (hit trials)-is associated with MAP symptoms (Figure 1).As shown in Figure 3a, results revealed a signi cant cluster in the left ventral striatum where this pattern was evident (p<0.05,FWE corrected for the volume of the ventral striatum; controlling for meancentered age and sex), with the peak lying in the putative region of the medial shell of the nucleus accumbens (NACs; cf.Supplementary Figure S1).Leveraging the same analytic approach, no signi cant associations were evident for ventral striatum reactivity to monetary incentives.Consistent with this observation, a voxelwise multiple regression demonstrated that ventral striatum reactivity to social incentives continued to explain signi cant variance in MAP symptoms while statistically controlling for mean-centered reactivity to monetary incentives (p<0.05,ventral striatum FWE corrected).The association between ventral striatum reactivity to social incentives and MAPS symptoms also remained signi cant when individually controlling for other symptoms (affective attening, positive symptoms, depression/anxiety, agitation) or binary diagnostic status (i.e., case-versus-control; p<0.05, ventral striatum FWE corrected).Taken together, these ndings demonstrate that blunted ventral striatum reactivity to naturalistic social incentives (Figure 1) is uniquely associated with the severity of clinicianrated MAP de cits.
Accumbens Reactivity to the Presentation of Social Rewards is Uniquely Associated with MAP De cits Using the same general analytic approach, secondary analyses enabled us to examine the potential relevance of disaggregating ventral striatum responses to the anticipation-versus-presentation of social reward (Figure 1).We began by using a whole-brain voxelwise GLMs to determine whether the two phases of the SID paradigm, here considered separately, recruit the ventral striatum.As shown in Supplementary Figure S2, signi cant ventral striatum activation was only evident during the presentation of social rewards (p<0.05,whole-brain FWE corrected; Supplementary Tables S6-S7).The same pattern was evident using a more liberal small-volume threshold (p<0.05,ventral striatum FWE corrected).Next, we used a voxelwise regression to determine whether ventral striatum activation during the presentation of social rewards is associated with more severe MAP symptoms.As shown in Figure 3b, this pattern was again evident in the medial NACs, overlapping the ventral striatum cluster identi ed in our primary analyses (p<0.05,ventral striatum FWE corrected; Figure 3a).Ventral striatum activation during the presentation phase continued to explain signi cant variance in MAP symptoms when statistically controlling for mean-centered activation during the anticipation phase, sex, and age (p<0.05,ventral striatum FWE corrected).In short, diminished ventral striatum reactivity to the receipt of naturalistic social rewards is uniquely associated with the severity of MAP de cits.

Exploratory Analyses
Ventral striatum reactivity to social and monetary incentives was unrelated to variation in self-reported social functioning (p<0.05,ventral striatum FWE corrected).Whole-brain voxelwise analyses did not detect any signi cant associations between MAP symptoms and reactivity to either social or monetary incentives outside of the ventral striatum (p<0.05,whole-brain FWE corrected).

Discussion
The present results demonstrate that blunted ventral striatum reactivity to naturalistic social incentives (Figure 1) is associated with more severe clinician-rated MAP symptoms (Figure 3a).This association remained signi cant when controlling for a variety of other symptoms (e.g., diminished expressivity) or for diagnostic status, underscoring the utility of conceptual models-such as RDoC and the Hierarchical Taxonomy of Psychopathology (HiTOP)-centered on transdiagnostic symptom dimensions 30,31,84,85 .Although the ventral striatum was robustly engaged by both social and monetary incentives (Figure 2), reactivity to monetary incentives was unrelated to MAP de cits.Consistent with this nil result, in a simultaneous regression model, ventral striatum reactivity to social incentives was uniquely and signi cantly associated with dimensional variation in MAP symptoms, over-and-above that accounted for by monetary incentives.Secondary analyses demonstrated that diminished reactivity to the presentation of naturalistic social rewards in an overlapping region of the ventral striatum was associated with greater MAP de cits (Figure 3b), replicating and extending work focused on conventional social-reward stimuli (photographs of smiling faces) 29 .This association remained signi cant when controlling for activation during the earlier reward-anticipation phase, suggesting a unique link between striatal reactivity to positive social feedback and MAP symptoms.Taken together, these observations provide a novel neurobiologically grounded framework for conceptualizing the social de cits that characterize many individuals living with psychotic disorders.
Clinical neuroscientists have long suspected that alterations in ventral striatum function might contribute to the pathophysiology of psychosis, but the speci c mapping from brain to symptomatology has only recently begun to come into focus 29,86,87 .The present results indicate that more severe MAP symptoms are preferentially associated with blunted reactivity to the receipt of social reward in the medial NACS, a region thought to play a mechanistically critical role in opioid/cannabinoid-mediated hedonic pleasure ('liking' reward) 24,25 (Supplementary Figure S1).For example, preclinical neuroimaging research shows that acute administration of the opioid antagonist naloxone dampens both subjective pleasure and medial NACs reactivity to positive social stimuli (erotic photographs) 88 .Paralleling our results, dampening was weak-to-nonexistent for monetary stimuli or for the anticipation of social stimuli.Taken together, these observations motivate the hypothesis that, among individuals living with psychosis, more severe MAP de cits re ect aberrant opioid/cannabinoid signaling in the medial NACs during normatively rewarding social interactions, manifesting as diminished feelings of pleasure.While the molecular neurobiology remains untested, prior work by our group supports the psychological component of this hypothesis, showing that individuals with more severe MAP symptoms experienced lower levels of positive affect and social a liation and emitted fewer positive facial expressions during interactions with a social partner in the SAET, the same individual who served as the model for our naturalistic social-reward stimuli (Figure 1) 14 .Outside of the laboratory, ecological momentary assessment research shows that more severe MAP symptoms are associated with less time spent with others and diminished positive affect in unstructured social contexts 15 .A key challenge for the future will be to clarify the origins and timing of social-reward de cits in psychosis.In particular, it will be fruitful to determine if blunted ventral striatum reactivity to social reward precedes and promotes the emergence of frank psychosis or whether it re ects a consequence of the social isolation and rejection often experienced by individuals with psychotic disorders 2,[89][90][91] .
The current study elaborates on our prior results 14 from the parent research program that explored a liative de cits in psychosis spectrum disorders.Speci cally, in that prior study we found that in response to cues of threat, motivation and pleasure de cits undermine the neuroregulatory bene ts of social a liation. 14Together with the current ndings, these studies indicate that more severe motivation and pleasure symptoms are broadly related to diminished neural responses typically associated with a liation and social reward.Furthermore, our ndings across these two studies suggest that in the social sphere pleasure de cits in psychosis spectrum disorders can occur in the consummatory phase and are not limited to the anticipatory phase 92,93 .
Clearly, important challenges remain.First, our study was focused on a transdiagnostic community sample enriched for stable psychosis (Table 1).Moving forward it will be important to expand this to more nationally representative samples, and to explore ner-grained differences across diagnostic syndromes (e.g., Schizophrenia vs. Bipolar Disorder) and between clinical and community participants.
Second, most participants were on a stable regimen of outpatient treatment.While this approach enhances clinical relevance, the impact on our ndings is unknown.Since medication types and dosages were clinically determined, and as we are lacking information on actual medication adherence, we are not able to determine what impact if any medication may have.Third, while our results highlight the importance of the medial NACs, MAP de cits are complex, multi-dimensional, and likely re ect multiple distributed networks.It will be important to understand how interactions between the ventral striatum and other regions implicated in appetitive motivation and hedonic pleasure support variation in MAPS symptoms.Fourth, the absence of punishment trials precludes strong claims about valence 94 .While unlikely, similar associations might be evident for negative social feedback.Finally, given ndings that self-assessments of social functioning (as used in the current study) may show discrepancy with informant ratings 95 , 96 it will be informative to further examine neural associations with functioning by broadening functional assessments to include high-contact informants and ecological momentary assessment 97 In sum, the present study leveraged matched SID/MID fMRI paradigms and naturalistic social rewards to demonstrate that MAP symptoms are uniquely associated with blunted ventral striatum reactivity during the receipt of social reward in psychosis.These observations provide fresh neurobiological insights into the social-anhedonia symptoms and social impairment that a ict many individuals with psychotic disorders 1-6, 98, 99 .While established treatments often fail to alleviate these symptoms-making this a critical unmet need 7, 87, 100-102 -our results underscore the potential bene t of emerging interventions targeting positive affect, hedonic pleasure, and social a liation 17,[101][102][103][104][105] .From an experimental therapeutics perspective 100,101 , it will be helpful to determine whether such interventions normalize NACs reactivity to social reward.
photographs of positive facial expressions posed by unfamiliar adult models[27][28][29] .Here we capitalized on naturalistic audiovisual clips of the experimental partner from the SAET, enhancing ecological validity and translational relevance (Figure1).Building on preclinical work in university students44 , this approach enabled us to manipulate the intensity of nonverbal (facial expressions and gestures), paralinguistic (vocal intonation), and verbal (praise) indicators of social reward expressed by a psychologically meaningful social partner.High-Reward clips featured large open-mouth smiles, thumbs-up gestures, and verbal feedback indicative of exceptional performance (Amazing!, Awesome!, Fabulous!, Fantastic!, Spectacular!) and expressed in an ebullient manner (Figure1c).Low-Reward clips featured small closedmouth smiles and verbal feedback indicative of good performance (Decent, That was cool, That was ne, That was nice, That was neat), expressed in a mildly positive manner.No-Reward clips were devoid of facial expressions and gestures; instead, the partner simply instructed the participant to prepare for the next trial (Continue, Get ready, Keep going, Next one, Proceed) in a neutral monotone.

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Figure 2 Social
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Table 1 .
Sample Characteristics . Regressors were convolved with a canonical HRF.