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Kendrick, K. M.

Publications and source records attributed to Kendrick, K. M..

At least 19 recordsLinked to original sources

Oxytocin promotes advantageous inequity preference by modulating the fairness norm enforcement system

Aversion to inequity is innate in humans and constitutes a major contributor to social tension. Such aversion can be triggered either when one receives more (advantageous inequity-AI) or less (disadvantageous inequity-DI) than others. However, it remains unclear whether oxytocin can modulate how humans respond to inequity. The present pre-registered study combined behavioral measures, computational modelling, and fMRI in a novel monetary allocation evaluation paradigm to examine oxytocins modulation of behavioral and neural responses to inequity. Results showed that oxytocin increased perceived fairness and AI allocation choices via enhancing AI preference independent of gain vs. loss contexts, which was further confirmed by model-based results of oxytocin decreasing AI aversion. In parallel at the neural level, oxytocin increased fairness rating-related activity in regions within fairness-related norm enforcement systems involved in norm violation detection, salience processing, and cognitive control. Multivariate-based representational similarity analyses provided further evidence that oxytocin induced distinct representational patterns of inequity in these core regions. These results suggest that oxytocin promoted AI preference possibly by strengthening regulatory control to support the pursuit of economic self-interest, while simultaneously enhancing the salience of AI allocations. Our study provides new insights into behavioral and neural mechanisms through which oxytocin modulates fairness-related behavior.

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Connectome lateralization in autism across the first 14 years: heterogeneity related to developmental stage, hemisphere, and pathophysiology

Hemispheric lateralization is fundamental feature to neurodevelopment, yet its dynamic evolution in autism across childhood and underlying molecular mechanisms remain unknown. Thus, using a large-scale resting-state fMRI dataset (n = 1553, ages 1-14), we investigated developmental heterogeneity in connectome lateralization. At the group level, abnormalities in dynamic connectome lateralization strength (DCLS) progressed from focal patterns in early childhood ([≤] 6 years) to widespread distributions by late childhood ([≤] 14 years), independent of symptom severity. The late-stage patterns were validated using the ABIDE dataset (n=153). Late childhood also showed marked increases in inter-individual heterogeneity. These alterations were significantly associated with clinical phenotypes, transcriptomic profiles, and multiple neurotransmitter systems, with distinct patterns across childhood groups. Our findings reveal a developmentally dynamic trajectory of connectome lateralization in autism and highlight late childhood as a critical window for stage- and individual-specific interventions tailored to substantial individual heterogeneity.

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Shared and distinct default mode systems in mental time travel and affective experience over time

Overarching conceptualizations propose a critical role of the default mode network (DMN) in self-referential mental time travel, particularly in autobiographical memory retrieval and episodic future thinking, and internal (intrinsic) emotion generation and regulation. However, these conceptualizations have not been directly evaluated. Against this background, the present fMRI study aimed to identify both shared and distinct neural systems underlying autobiographical episodic processing across different temporal contexts - specifically, episodic memory retrieval (EMR) and episodic future thinking (EFT) - and to examine how these systems interact with affective experiences, including valence and arousal. Our findings demonstrated the central role of the DMN - encompassing the medial prefrontal cortex (mPFC), posterior cingulate cortex (PCC), and medial temporal lobe (MTL) - in both EMR and EFT. Importantly, we identified a functional dissociation along both valence and temporal dimensions: the ventromedial prefrontal cortex (vmPFC) was more strongly associated with positive experiences and simulations, whereas the dorsomedial prefrontal cortex (dmPFC) was consistently engaged during the processing of negative affect across past and future contexts. Moreover, representational similarity and parametric analyses indicated that the hippocampus supports differential processing of valence and arousal across temporal domains. Together, these findings provide empirical evidence for the involvement of cortical midline core DMN systems in autobiographical processing across time and suggest overlapping and distinct systems for the integration of emotional experiences across mental time travel.

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Real-time functional connectivity-based neurofeedback of the DLPFC-amygdala pathway during threat-exposure attenuates anxiety

BackgroundAdaptive regulation of negative emotion is vital for mental health and dysregulations in this domain contribute to the major mental disorders, including anxiety and depression. On the neural level, efficient emotion regulation has been linked to functional communication between the dorsolateral prefrontal cortex (DLPFC) and the amygdala. Gaining voluntary control over this pathway may present an effective strategy for potentiating emotion regulation. ObjectiveAgainst this background, we developed a novel connectivity-based real-time fMRI (rt-fMRI) neurofeedback (NF) training that enables individuals to gain volitional control over the DLPFC-amygdala pathway during exposure to threatening stimuli. MethodsThe study employed a pre-registered, randomized, sham-controlled design with the experimental group (n = 22) receiving real-time NF information on connectivity between the right DLPFC and the amygdala during threat exposure and the sham control group (n = 23) receiving connectivity NF from a circuit not related to emotion regulation. The ability to maintain regulatory control in the absence of feedback was assessed after four NF runs. Primary outcomes included functional connectivity of the target pathway, as well as anxiety scores. ResultsThe results demonstrate that successful acquisition of self-regulation of the rDLPFC-amygdala top-down regulatory circuit in the experimental NF group facilitated attenuation of anxiety. ConclusionIn summary, our findings suggest that real-time fMRI neurofeedback (rtfMRI-NF) allows to volitionally enhance rDLPFC-amygdala connectivity, and in turn reduces negative emotional states, rendering the training a promising neurotechnology intervention for mental disorders.

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Large-Scale Neural Network Compensation Underlying Camouflaging in Trait Autism and Its Potential Mental Health Costs

Social camouflaging refers to strategies to hide or compensate for social difficulties, often at a significant mental health cost, and is particularly prevalent in autism. The large-scale neural network mechanisms underlying this adaptation remain poorly understood. This study aimed to identify these neural underpinnings and their link to other potential mental health issues. Using a dimensional approach, we recruited 110 healthy young adults who completed self-report questionnaires measuring autistic traits and camouflaging as well as depression and anxiety, and underwent resting-state fMRI scans. Using the 300-node Seitzman atlas encompassing 13 functional networks, we examined the interaction between camouflaging and autistic traits on brain network connectivity. Results showed that among individuals with higher autistic traits, greater camouflaging was associated with hyperconnectivities between the Default Mode (DMN) and Cingulo-Opercular Networks (CON), and within the CON. Crucially, DMN-CON hyperconnectivity mediated the relationship between camouflaging and potential mental health cost (i.e., depression and anxiety scores) but only in individuals with higher autistic traits. These findings reveal a specific neuro-compensatory mechanism underlying autistic camouflaging involving self-referential and executive control systems and provide a neurobiological explanation for its potential mental health burden, highlighting the need for societal changes that reduce the pressure for such adaptations. Lay AbstractSocial camouflaging refers to strategies autistic people often use to hide their social differences to better adapt to everyday social contexts. While it may help in the short term, this constant effort can be mentally exhausting and is often linked to severe anxiety and depression. However, little is known about how different brain networks work together to enable social camouflaging and might contribute to a greater risk of anxiety and depression. In this study, autistic traits were measured in 110 young healthy adults in addition to questionnaire-based measures of social camouflaging, anxiety, and depression. Additionally, brain activity was recorded using magnetic resonance imaging while they were resting and not doing any task. We found that, in people with higher autistic traits, social camouflaging was linked to stronger connections between the brain network involved in thinking about oneself (self-reflection; Default Mode Network) and the one in charge of maintaining goal-directed behavior (action control; Cingulo-Opercular Network), as well as stronger connections within the latter brain network. These stronger connections between the self-reflection network and action control network partly explained why camouflaging may be associated with higher levels of anxiety and depression. In short, autistic camouflaging seems to rely on a cognitively demanding neural compensatory process, which can take a toll on mental health. Understanding this underscores the importance of creating a more accepting society to support the well-being of autistic individuals.

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Does Unfairness Evoke Anger or Disgust? A Quantitative Neurofunctional Dissection Based on 25 Years of Neuroimaging

Over the last decades, the traditional Homo economicus model has been increasingly challenged by convergent evidence underscoring the impact of emotions on decision-making. A classic example is the perception of unfairness operationalized in the Ultimatum Game where humans readily sacrifice personal gains to punish those who violate fairness norms. While the emotional mechanism underlying costly punishments has been widely acknowledged, the distinct contributions of moral emotions (anger or disgust) remain debated, partly due to methodological limitations of the conventional experiments. Here, we capitalize on a quantitative neurofunctional dissection approach by combining recent developments in neuroimaging meta-analyses, behavioral-level, network-level, and neurochemical-level decoding and data from 3,266 participants from functional neuroimaging studies to determine the common and distinct neural representations between unfairness and the two moral emotions. Experience of unfairness engaged a widespread bilateral network encompassing insular, cingulate, and frontal regions, with dorsal striatal regions mediating the decision to reject unfair offers. Disgust engaged a defensive-avoidance circuit encompassing amygdalar, occipital, and frontal regions, while anger engaged non-overlapping systems including mid-cingulate, thalamic, and frontal regions. Unfairness and anger or disgust respectively commonly engaged the anterior and mid-insula, while the latter additionally showed common recruitment of ventrolateral prefrontal and orbitofrontal cortices. Multimodal network, behavioral, and serotonergic decoding provided a more granular and convincing dissection of these results. Findings indicate a shared neuroaffective basis underlying the impact of emotions on unfairness-induced punishment behavior and suggest a common brain circuit has been evolutionarily shaped to protect individuals from personal harm and enforce societal norms.

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State and trait serotonin variations interact to shape the intrinsic connectivity and gradient architecture of the brain: a combined TPH2 genetics and tryptophan depletion study

BackgroundSerotonin (5-HT) critically regulates cognitive and emotional functions, and both stable and transient variations in 5-HT signaling have been associated with emotional dysregulations. However, findings regarding the neurofunctional effects of transient 5-HT variations have been highly inconsistent. Therefore, we examined whether individual variations in a central 5-HT-regulating genetic polymorphism (tryptophan hydroxylase 2, TPH2) represent a vulnerability or resilience factor for the effects of acute tryptophan depletion (ATD) on functional brain architecture. MethodThe current study utilized a pharmacogenetic within-subject randomized placebo-controlled resting-state fMRI design with n=53 healthy male participants in combination with spontaneous intrinsic neural activity, functional connectivity, and connectome gradient analyses to compare the neurofunctional effects of ATD-induced transient reduction in central 5-HT signaling between TPH2 genotypes (a priori genotyping for rs4570625, GG n = 25 vs. TT n = 23). ResultsATD induced significant increases in spontaneous neural activity in hippocampal CA1 irrespective of genotype and enhanced communication of this region with the bilateral amygdala and the vmPFC specifically in GG carriers. ATD sharpened the intrinsic connectome gradient architecture in several large-scale networks, including the salience, frontoparietal, and default mode network. ConclusionsOur results identify a potential genetic marker for an increased vulnerability to the neural effects of transient variations in 5-HT signaling on the functional architecture of an anxiety- and stress-related brain circuit. Connectome gradient results underscore the regulatory role of 5-HT on the intricate organization of large-scale networks involved in emotional reactivity and regulation.

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Disruption of sustained attention and orbitofrontal cortex engagement by incoming social media messages vary as a function of problematic social media use

BackgroundSmartphones and social media have become ubiquitous in our lives, and while debates about their negative impact on mental health, addictive potential, and disruptive effects on daily activities have surged, neurobiological evidence remains scarce. Here, we investigated whether the behavioral and neural effects of interference of continuous attention by incoming social media messages on WeChat varies according to its problematic use as assessed via an addiction framework. MethodsN = 60 healthy individuals were stratified based on their level of problematic WeChat usage as measured by the WeChat Addiction Scale (WAS): LOW (15 males and 15 females) and HIGH (15 males and 15 females) addictive tendencies. Participants underwent an AX-Continuous Performance Task (AX-CPT) with WeChat-associated (incoming message) and neutral auditory distractors as well as a no distractor condition. Concurrent functional Near-Infrared Spectroscopy (fNIRS) assessments of the orbitofrontal cortex (OFC) were implemented to determine the underlying neurofunctional mechanisms. ResultsOn the behavioral level the HIGH group demonstrated faster reaction times during the WeChat and no distractor condition compared to the LOW group. Exploratory analyses indicated that the WeChat distraction decreased left lateral OFC activity in the LOW but enhanced activity in this region in the HIGH group. ConclusionAgainst our hypotheses WeChat distraction enhanced behavioral performance specially in individual with a tendency for problematic WeChat use, with the neural data pointing to less suppression of the OFC in individuals with a tendency for problematic usage. Findings underscore the complexity of the potential effects of new technology on daily live and indicate that addiction models might not be simply extendable to problematic social media usage.

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Signatures of social pain empathy: general and process-specific brain-wide representations of social exclusion and separation

Empathy can be elicited by physiological pain, as well as in social contexts. Although physiological and different social contexts induce a strong subjective experience of empathy, the general and context-specific neural representations remain elusive. Here, we combine fMRI with multivariate pattern analysis to establish neurofunctional models for pain empathy triggered by social exclusion and separation. Our findings revealed both overlapping and distinct neural representations for social exclusion and separation empathy across cortical and subcortical regions. This study established an evolutionary model that traces the progression from social pain to physiological pain empathy. In conclusion, this study establishes neural decoding models for pain empathy evoked by social exclusion and social separation, revealing their neural foundations and interconnectedness of empathy induced by social and physiological stimuli. These findings deepen our understanding of the neurobiological mechanisms underlying social pain empathy and provide robust neuromarkers to precisely evaluate empathy across physiological and social domains.

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Decoding the spatiotemporal dynamic neural representation of repetitive facial expression imitation

Imitating facial emotion expressions can facilitate social interactions, although the behavioral and neural spatiotemporal dynamics is unclear. Here participants (N=100) imitated facial emotions repeatedly over one month (16 times in total) with neural activity measured on three occasions using functional near-infrared spectroscopy. Additionally, the transfer effect of repeated imitation on emotional face and scene perception was assessed by fMRI with multivariate pattern analysis. Valence specific imitation performance was facilitated by the alterations in the similarity of spatiotemporal patterns evoked in the mirror neuron system (MNS) with information flow moving progressively towards the inferior frontal gyrus as the as the number of times of imitation increase. Furthermore, MNS representation predictive patterns of processing emotional faces, but not scenes, were enhanced. Overall, these findings provide a neural changes of information flow within MNS and advance our understanding of the spatiotemporal dynamics from novice to proficient of facial emotion imitation.

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A neural signature for the subjective experience of threat anticipation under uncertainty

Uncertainty about potential future threats and the associated anxious anticipation represents a key feature of anxiety. However, the neural systems that underlie the subjective experience of threat anticipation under uncertainty remain unclear. Combining a novel uncertain shock anticipation paradigm that allows precise modulation of the level of momentary anxious arousal during functional magnetic resonance imaging (fMRI) with multivariate predictive modeling, we trained a brain model that accurately predicted the intensity of subjective experience of anxious arousal on the population and individual level. In a series of analyses utilizing available fMRI datasets, we further demonstrate that the signature specifically predicted anxious anticipation and was not sensitive in predicting pain, general anticipation or unspecific arousal. The signature was functionally and spatially distinguishable from representations of subjective fear or negative affect. We developed a sensitive, generalizable, and specific neuromarker for subjective anxious arousal experienced during uncertain threat anticipation that can facilitate model development and clinical translation.

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The right inferior frontal gyrus as pivotal node and effective regulator of the basal ganglia-thalamocortical response inhibition circuit in humans

The involvement of specific basal ganglia-thalamocortical circuits in response inhibition has been extensively mapped in the last few decades. However, the pivotal brain nodes and directed casual regulation within this inhibitory circuit in humans remains controversial. Here, we capitalize on recent progress in robust and biologically plausible directed causal modelling (DCM-PEB) and a large fMRI response inhibition dataset (n=218) to determine key nodes, their causal regulation and modulation via biological variables (sex) and inhibitory performance in the inhibitory control circuit encompassing the right inferior frontal gyrus (rIFG), caudate nucleus (rCau), globus pallidum (rGP) and thalamus (rThal).The entire neural circuit exhibited high intrinsic connectivity and an increasing rIFG inflow and its causal regulation over the rCau and rThal during response inhibition. In addition, sex and behavioral performance influenced the architecture of the regulatory circuits such that women displayed increased rThal self-inhibition and decreased rThal to GP modulation, while better inhibitory performance was associated with stronger rThal to rIFG communication. Furthermore, control analyses did not reveal a similar key communication in a left lateralized model. Together these findings indicate a pivotal role of the rIFG as input and causal regulator of subcortical response inhibition nodes.

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The central autonomic system revisited - convergent evidence for a regulatory role of the insular and midcingulate cortex from neuroimaging meta-analyses

The autonomic nervous system regulates dynamic body adaptations to internal and external environment changes. Capitalizing on two different algorithms (Analysis of Brain Coordinates and GingerALE) that differ in empirical assumptions, we scrutinized the meta-analytic convergence of human neuroimaging studies investigating the neural basis of peripheral autonomic signal processing. Among the selected studies, we identified 42 records reporting 44 different experiments and testing 792 healthy individuals. The results of the two different algorithms converge in identifying the bilateral dorsal anterior insula and midcingulate cortex as the critical areas of the central autonomic system (CAN). However, whereas the bilateral dorsal anterior insula appears to be involved in processing autonomic nervous system signals regardless of task type, activity in the midcingulate cortex appears to be primarily engaged in processing autonomic signals during cognitive tasks and task-free conditions. Applying an unbiased approach, we were able to identify a single functionally condition-independent circuit that supports CAN activity. Although partially overlapping with the salience network, this functional circuit includes, in addition to the bilateral insular cortex and midcingulate cortex, the bilateral inferior parietal lobules and small clusters in the bilateral middle frontal gyrus. Our results do not support the hypothesis of divergent pathways for the sympathetic and parasympathetic systems or a robust involvement of the default mode network, particularly during parasympathetic activity. However, these results may be due to the relatively low number of studies investigating the parasympathetic system (12%), making our results more consistent with the central processing network of sympathetic activity. Remarkably, the critical regions of the CAN observed in this meta-analysis are among the most reported co-activated areas in neuroimaging studies and have been repeatedly shown as being dysregulated across different mental and neurological disorders. This suggests that the central dynamic interaction maintaining bodily homeostasis reported in several brain imaging studies may be associated with increased autonomic nervous system engagement and that disruptions in this interplay may underpin unspecific pathological symptoms across mental and neurological disorders.

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Opposing associations of Internet Use Disorder symptom domains with structural and functional organization of the striatum: a dimensional neuroimaging approach

BackgroundAccumulating evidence suggests brain structural and functional alterations in Internet Use Disorder (IUD). However, conclusions are strongly limited due to the retrospective case-control design of the studies, small samples, and the focus on general rather than symptom-specific approaches. MethodsWe here employed a dimensional multi-methodical MRI-neuroimaging design in a final sample of n = 203 subjects to examine associations between levels of IUD and its symptom-dimensions (loss of control/time management, craving/social problems) with brain structure, resting state and task-based (pain empathy, affective go/no-go) brain function. ResultsAlthough the present sample covered the entire range of IUD, including normal, problematic as well as pathological levels, general IUD symptom load was not associated with brain structural or functional alterations. However, the symptom-dimensions exhibited opposing associations with the intrinsic and structural organization of the brain, such that loss of control/time management exhibited negative associations with intrinsic striatal networks and hippocampal volume, while craving/social problems exhibited a positive association with intrinsic striatal networks and caudate volume. ConclusionsOur findings provided the first evidence for IUD symptom-domain specific associations with progressive alterations in the intrinsic structural and functional organization of the brain, particularly of striatal systems involved in reward, habitual and cognitive control processes.

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Self-navigating the "Island of Reil": a systematic review of real-time fMRI neurofeedback training of insula activity

Real-time fMRI (rtfMRI) neurofeedback (NF) is a novel noninvasive technique that permits individuals to voluntarily control brain activity or connectivity, with demonstrated feasibility in experimental and therapeutic applications. The crucial role of the insula in emotional and salience processing makes it a popular target in rtfMRI studies although there is no systematic review of their efficacy. To promote our understanding of mechanisms underlying insula regulation and thereby facilitate therapeutic translation, the present review identified 22 preclinical and clinical studies and found that rtfMRI-based NF training is efficient for modulating insula activity (> 86%) and its associated behavioral and neural changes. Based on findings, continuous feedback for multiple training sessions, specific strategies validated before application, inclusion of a practice session, and choosing appropriate localization strategies are suggested as guidelines. We also recommend standardization of training protocol design, statistical analyses and results reports for future studies. In summary, the present review informs both fundamental research and therapeutic translation of NF training as an intervention in mental disorders, particularly those with insula dysfunction.

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Transcutaneous auricular vagus nerve stimulation increases eye-gaze on salient facial features and oxytocin release

BackgroundTranscutaneous auricular vagus nerve stimulation (taVNS) is a non-invasive neuromodulation technique with promising therapeutic potential in the context of epilepsy, pain, and depression and which may also have beneficial effects on social cognition. However, the underlying mechanisms of taVNS are unclear and evidence regarding its role in social cognition improvement is limited. ObjectiveIn order to investigate the impact of taVNS on social cognition we have studied its effects on gaze towards emotional faces using an eye-tracking task and also on release of the neuropeptide oxytocin which plays a key role in influencing social cognition and motivation. MethodsA total of fifty-four subjects were enrolled in a sham-controlled, participant-blind crossover experiment, consisting of two treatment sessions, separated by one week. In one session participants received 30-min taVNS (tragus), and in the other, they received 30-min sham (earlobe) stimulation with the treatment order counterbalanced across participants. Gaze duration towards the faces and facial features (eyes, nose, and mouth) were measured together with resting pupil size. Additionally, saliva samples were taken for the measurement of oxytocin concentrations by enzyme-linked immunoassay. ResultsSaliva oxytocin concentrations increased significantly after taVNS compared to sham stimulation, while resting pupil size did not. In addition, taVNS increased fixation time on the nose region irrespective of face emotion, and this was positively correlated with increased saliva oxytocin concentrations. ConclusionOur findings suggest that taVNS biases visual attention towards socially salient facial features across different emotions and this is associated with its effects on increasing endogenous oxytocin release.

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Losartan shifts social reward motivation and punishment feedback sensitivity via modulating midbrain-striato-frontal circuits

Social deficits and dysregulations in dopaminergic midbrain-striato-frontal circuits represent transdiagnostic symptoms across psychiatric disorders. Animal models suggest that interactions between the dopamine and renin-angiotensin system may modulate learning and reward-related processes. The present study therefore examined the behavioral and neural effects of the angiotensin II type 1 receptor (AT1R) antagonist Losartan on social reward and punishment processing in humans. A pre-registered randomized double-blind placebo-controlled between-subject pharmacological design was combined with a social incentive delay fMRI paradigm during which subjects could avoid social punishment or gain social reward. Healthy volunteers received a single-dose of Losartan (50mg, n=43) or placebo (n=44). Reaction times and emotional ratings served as behavioral outcomes, on the neural level activation and connectivity were modelled. Relative to placebo, Losartan modulated the reaction time and arousal differences between social punishment and social reward. On the neural level the Losartan-enhanced motivational salience of social rewards was accompanied by stronger ventral striatum-prefrontal connectivity during reward anticipation. Losartan increased the reward-neutral difference in the ventral tegmental area (VTA) and attenuated VTA associated connectivity with the bilateral insula in response to punishment during the outcome phase. Losartan modulated approach-avoidance motivation and emotional salience during social punishment versus social reward via modulating distinct core nodes of the midbrain-striato-frontal circuits. The findings document a modulatory role of the renin-angiotensin system in these circuits and associated social processes, suggesting a promising treatment target to alleviate social dysregulations. Significance StatementSocial deficits and anhedonia characterize several mental disoders and have been linked to the midbrain-striato-frontal circuits of the brain. Based on initial findings from animal models we here combine the pharmacological blockade of the angiotensin II type 1 receptor (AT1R) via Losartan with functional MRI to demonstrate that AT1R blockade enhances the motivational salience of social rewards and attenuates the negative impact of social punishment via modulating the communication in the midbrain-striato-frontal circuits in humans. The findings demonstrate for the first time an important role of the AT1R in social reward processing in humans and render the AT1R as promising novel treatment target for social and motivational deficits in mental disoders.

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Intranasal vasopressin like oxytocin increases social attention by influencing top-down control, but additionally enhances bottom-up control

The respective roles of the neuropeptides arginine vasopressin (AVP) and oxytocin (OXT) in modulating social cognition and for therapeutic intervention in autism spectrum disorder have not been fully established. In particular, while numerous studies have demonstrated effects of oxytocin in promoting social attention the role of AVP has not been examined. The present study employed a randomized, double-blind, placebo (PLC)-controlled between-subject design to explore the social- and emotion-specific effects of AVP on both bottom-up and topdown attention processing with a validated emotional anti-saccade eye-tracking paradigm in 80 male subjects (PLC = 40, AVP = 40). Our findings showed that AVP increased the error rate for social (angry, fearful, happy, neutral and sad faces) but not non-social (oval shapes) stimuli during the anti-saccade condition and reduced error rates in the pro-saccade condition. Comparison of these findings with a previous study (sample size: PLC = 33, OXT = 33) using intranasal oxytocin revealed similar effects of the two peptides on anti-saccade errors but a significantly greater effect of AVP on pro-saccades. Both peptides also produced a post-task anxiolytic effect by reducing state anxiety. Together these findings suggested that both AVP and OXT decrease goal-directed top-down attention control to social salient stimuli but that AVP more potently increased bottom-up social attentional processing.

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