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The feedback people receive on their behavior shapes the process of belief formation and self-efficacy in mastering a particular task. However, the neural and computational mechanisms of how the subjective value of self-efficacy beliefs, and the corresponding affect, influence the learning process remain unclear. We investigated these mechanisms during self-efficacy belief formation using fMRI, pupillometry, and computational modeling, and by analyzing individual differences in affective experience. Biases in the formation of self-efficacy beliefs were associated with affect, pupil dilation, and neural activity within the anterior insula, amygdala, ventral tegmental area/ substantia nigra, and mPFC. Specifically, neural and pupil responses mapped the valence of the prediction errors in correspondence with individuals' experienced affective states and learning biases during self-efficacy belief formation. Together with the functional connectivity dynamics of the anterior insula within this network, our results provide evidence for neural and computational mechanisms of how we arrive at affected beliefs., (© 2022. The Author(s).)

Autism spectrum disorder (ASD) is characterized by substantial social deficits. The notion that dysfunctions in neural circuits involved in sharing another's affect explain these deficits is appealing, but has received only modest experimental support. Here we evaluated a complex paradigm on the vicarious social pain of embarrassment to probe social deficits in ASD as to whether it is more potent than paradigms currently in use. To do so we acquired pupillometry and fMRI in young adults with ASD and matched healthy controls. During a simple vicarious physical pain task no differences emerged between groups in behavior, pupillometry, and neural activation of the anterior insula (AIC) and anterior cingulate cortex (ACC). In contrast, processing complex vicarious social pain yielded reduced responses in ASD on all physiological measures of sharing another's affect. The reduced activity within the AIC was thereby explained by the severity of autistic symptoms in the social and affective domain. Additionally, behavioral responses lacked correspondence with the anterior cingulate and anterior insula cortex activity found in controls. Instead, behavioral responses in ASD were associated with hippocampal activity. The observed dissociation echoes the clinical observations that deficits in ASD are most pronounced in complex social situations and simple tasks may not probe the dysfunctions in neural pathways involved in sharing affect. Our results are highly relevant because individuals with ASD may have preserved abilities to share another's physical pain but still have problems with the vicarious representation of more complex emotions that matter in life., (© 2015 Wiley Periodicals, Inc.)

Dynamic causal modeling (DCM) is a Bayesian framework for inferring effective connectivity among brain regions from neuroimaging data. While the validity of DCM has been investigated in various previous studies, the reliability of DCM parameter estimates across sessions has been examined less systematically. Here, we report results of a software comparison with regard to test-retest reliability of DCM for fMRI, using a challenging scenario where complex models with many parameters were applied to relatively few data points. Specifically, we examined the reliability of different DCM implementations (in terms of the intra-class correlation coefficient, ICC) based on fMRI data from 35 human subjects performing a simple motor task in two separate sessions, one month apart. We constructed DCMs of motor regions with fair to excellent reliability of conventional activation measures. Using classical DCM (cDCM) in SPM5, we found that the test-retest reliability of DCM results was high, both concerning the model evidence (ICC=0.94) and the model parameter estimates (median ICC=0.47). However, when using a more recent DCM version (DCM10 in SPM8), test-retest reliability was reduced notably. Analyses indicated that, in our particular case, the prior distributions played a crucial role in this change in reliability across software versions. Specifically, when using cDCM priors for model inversion in DCM10, this not only restored reliability but yielded even better results than in cDCM. Analyzing each component of the objective function in DCM, we found a selective change in the reliability of posterior mean estimates. This suggests that tighter regularization afforded by cDCM priors reduces the possibility of local extrema in the objective function. We conclude this paper with an outlook to ongoing developments for overcoming the software-dependency of reliability observed in this study, including global optimization and empirical Bayesian procedures., (Copyright © 2014 Elsevier Inc. All rights reserved.)

Emotional instability, difficulties in social adjustment, and disinhibited behavior are the most common symptoms of the psychiatric comorbidities in juvenile myoclonic epilepsy (JME). This psychopathology has been associated with dysfunctions of mesial-frontal brain circuits. The present work is a first direct test of this link and adapted a paradigm for probing frontal circuits during empathy for pain. Neural and psychophysiological parameters of pain empathy were assessed by combining functional magnetic resonance imaging (fMRI) with simultaneous pupillometry in 15 JME patients and 15 matched healthy controls. In JME patients, we observed reduced neural activation of the anterior cingulate cortex (ACC), the anterior insula (AI), and the ventrolateral prefrontal cortex (VLPFC). This modulation was paralleled by reduced pupil dilation during empathy for pain in patients. At the same time, pupil dilation was positively related to neural activity of the ACC, AI, and VLPFC. In JME patients, the ACC additionally showed reduced functional connectivity with the primary and secondary somatosensory cortex, areas fundamentally implicated in processing the somatic cause of another's pain. Our results provide first evidence that alterations of mesial-frontal circuits directly affect psychosocial functioning in JME patients and draw a link of pupil dynamics with brain activity during emotional processing. The findings of reduced pain empathy related activation of the ACC and AI and aberrant functional integration of the ACC with somatosensory cortex areas provide further evidence for this network's role in social behavior and helps explaining the JME psychopathology and patients' difficulties in social adjustment., (Copyright © 2015 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Previous studies have shown overlapping neural activations for observation and execution or imitation of emotional facial expressions. These shared representations have been assumed to provide indirect evidence for a human mirror neuron system, which is suggested to be a prerequisite of action comprehension. We aimed at clarifying whether shared representations in and beyond human mirror areas are specifically activated by affective facial expressions or whether they are activated by facial expressions independent of the emotional meaning. During neuroimaging, participants observed and executed happy and non-emotional facial expressions. Shared representations were revealed for happy facial expressions in the pars opercularis, the precentral gyrus, in the superior temporal gyrus/medial temporal gyrus (MTG), in the pre-supplementary motor area and in the right amygdala. All areas showed less pronounced activation in the non-emotional condition. When directly compared, significant stronger neural responses emerged for happy facial expressions in the pre-supplementary motor area and in the MTG than for non-emotional stimuli. We assume that activation of shared representations depends on the affect and (social) relevance of the facial expression. The pre-supplementary motor area is a core-shared representation-structure supporting observation and execution of affective contagious facial expressions and might have a modulatory role during the preparation of executing happy facial expressions.

Rhyming words, as in songs or poems, is a universal feature of human language across all ages. In the present fMRI study a novel overt rhyming task was applied to determine the neural correlates of rhyme production. Fifteen right-handed healthy male volunteers participated in this verbal fluency study. Participants were instructed to overtly articulate as many words as possible either to a given initial letter (LVF) or to a semantic category (SVF). During the rhyming verbal fluency task (RVF), participants had to generate words that rhymed with pseudoword stimuli. On-line overt verbal responses were audiotaped in order to correct the imaging results for the number of generated words. Fewer words were generated in the rhyming compared to both the lexical and the semantic condition. On a neural level, all language tasks activated a language network encompassing the left inferior frontal gyrus, the middle and superior temporal gyri as well as the contralateral right cerebellum. Rhyming verbal fluency compared to both lexical and semantic verbal fluency demonstrated significantly stronger activation of left inferior parietal region. Generating novel rhyme words seems to be mainly mediated by the left inferior parietal lobe, a region previously found to be associated with meta-phonological as well as sub-lexical linguistic processes., (Copyright © 2011 Elsevier B.V. All rights reserved.)

The glutamatergic N-methyl-D-aspartate (NMDA) receptor has been implicated in the pathophysiology of schizophrenia. Administered to healthy volunteers, a subanesthetic dose of the non-competitive NMDA receptor antagonist ketamine leads to psychopathological symptoms similar to those observed in schizophrenia. In patients with schizophrenia, ketamine exacerbates the core symptoms of illness, supporting the hypothesis of a glutamatergic dysfunction. In a counterbalanced, placebo-controlled, double-blind study design, healthy subjects were administered a continuous subanesthetic S-ketamine infusion while differences in BOLD responses measured with fMRI were detected. During the scanning period, subjects performed continuous overt verbal fluency tasks (phonological, lexical and semantic). Ketamine-induced psychopathological symptoms were assessed with the Positive and Negative Syndrome Scale (PANSS). Ketamine elicited psychosis like psychopathology. Post-hoc t-tests revealed significant differences between placebo and ketamine for the amounts of words generated during lexical and semantic verbal fluency, while the phonological domain remained unaffected. Ketamine led to enhanced cortical activations in supramarginal and frontal brain regions for phonological and lexical verbal fluency, but not for semantic verbal fluency. Ketamine induces activation changes in healthy subjects similar to those observed in patients with schizophrenia, particularly in frontal and temporal brain regions. Our results provide further support for the hypothesis of an NMDA receptor dysfunction in the pathophysiology of schizophrenia., (Copyright © 2010 Elsevier Inc. All rights reserved.)

Introduction: Memory dysfunction is a prominent feature in schizophrenia. Impairments of declarative memory have been consistently linked to alterations especially within hippocampal-prefrontal regions. Due to the high heritability of schizophrenia, susceptibility genes and their modulatory impact on the neural correlates on memory are of major relevance. In the present study the influence of the COMT val(158)met status on the neural correlates of declarative memory was investigated in healthy subjects., Methods: From an initial behavioural sample of 522 healthy individuals (Sheldrick et al., 2008), 84 subjects underwent fMRI scanning while performing a memory encoding and a retrieval task. The COMT val(158)met status was determined for the whole sample and correlated with cortical activation within the group of n=84 individuals., Results: There were no effects of COMT status on behavioural performance. For declarative memory processing the number of met alleles predicted circumscribed bilateral insula and anterior hippocampus activations during memory encoding as well as less deactivations within the bilateral posterior parahippocampal gyri during memory retrieval., Discussion: Although declarative memory performance was unaffected, the neural correlates within hippocampal-prefrontal regions demonstrate a link between COMT val(158)met carrier status and brain areas associated with declarative memory processing. The study contributes to a better understanding of the role that susceptibility genes might play in the aetiology of schizophrenia., (Copyright 2009 Elsevier Inc. All rights reserved.)

Neuregulin 1 (NRG1) has been found to be associated with schizophrenia. Impaired performance in episodic memory tasks is an often replicated finding in this disorder. In functional neuroimaging studies, this dysfunction has been linked to signal changes in prefrontal and medial temporal areas. Therefore, it is of interest whether genes associated with the disorder, such as NRG1, modulate episodic memory performance and its neural correlates. Ninety-four healthy individuals performed an episodic memory encoding and a retrieval task while brain activation was measured with functional MRI. All subjects were genotyped for the single nucleotide polymorphism (SNP) rs35753505 in the NRG1 gene. The effect of genotype on brain activation was assessed with fMRI during the two tasks. While there were no differences in performance, brain activation in the cingulate gyrus (BA 24), the left middle frontal gyrus (BA 9), the bilateral fusiform gyrus and the left middle occipital gyrus (BA 19) was positively correlated with the number of risk alleles in NRG1 during encoding. During retrieval brain activation was positively correlated with the number of risk alleles in the left middle occipital gyrus (BA 19). NRG1 genotype does modulate brain activation during episodic memory processing in key areas for memory encoding and retrieval. The results suggest that subjects with risk alleles show hyperactivations in areas associated with elaborate encoding strategies., (Copyright 2009 Elsevier Inc. All rights reserved.)

Polymorphisms in the G72 (also named d-amino acid oxidase activator, DAOA) gene increase the vulnerability for schizophrenia and affective psychosis. Three recent genetic neuroimaging studies showed that variation in G72 influences the brain activity in the medial temporal lobe (MTL), supporting the hypothesis that G72 might play a modulatory role on brain activity in MTL structures. In the present study we therefore investigated the effect of G72 on the neural correlates of long-term memory encoding and retrieval in a large sample of healthy subjects (n=83) using functional magnetic resonance imaging. A face encoding and a face retrieval memory task were chosen because on the one hand they specifically activate MTL structures and on the other hand they tap into memory processes that are compromised in patients with schizophrenia and affective disorder. Despite a strong a-priori hypothesis of genotype group activation differences in the MTL along with a large sample size we did neither find an effect of G72 genotype status on brain activity in the MTL nor in any other brain regions. The present data therefore do not support the view of a general modulatory role of G72 on MTL brain activity, at least not in the domain of long-term memory encoding and retrieval. Our results highlight the importance of replication studies in genetic neuroimaging., (Copyright 2009 Elsevier Inc. All rights reserved.)

In our everyday life we process information from different modalities simultaneously with great ease. With the current study we had the following goals: to detect the neural correlates of (1) automatic semantic processing of associates and (2) to investigate the influence of different visual modalities on semantic processing. Stimuli were presented with a short SOA (350 ms) as subjects performed a lexical decision task. To minimize the variance and increase homogeneity within our sample, only male subjects were measured. Three experimental conditions were compared while brain activation was measured with a 3 T fMRI scanner: related word-pairs (e.g., frame-picture), unrelated word-pairs (e.g., frame-car) as well as word-nonword pairs (e.g., frame-fubber). They were presented uni- (word-word) and cross-modally (picture-word). Behavioral data revealed a priming effect for cross-modal and unimodal word-pairs. On a neural level, the unimodal condition revealed response suppression in bilateral fronto-parietal regions. Cross-modal priming led to response suppression within the right inferior frontal gyrus. Common areas of deactivation for both modalities were found in bilateral fronto-tempo-parietal regions. These results suggest that the processing of semantic associations presented in different modalities lead to modality-specific activation caused by early access routes. However, common activation for both modalities refers to a common neural network for semantic processing suggesting amodal processing., (2009 Wiley-Liss, Inc.)

Impaired performance in verbal fluency tasks is an often replicated finding in schizophrenia. In functional neuroimaging studies, this dysfunction has been linked to signal changes in prefrontal and temporal areas. Since schizophrenia has a high heritability, it is of interest whether susceptibility genes for the disorder, such as NRG1, modulate verbal fluency performance and its neural correlates. Four hundred twenty-nine healthy individuals performed a semantic and a lexical verbal fluency task. A subsample of 85 subjects performed an overt semantic verbal fluency task while brain activation was measured with functional magnetic resonance imaging (MRI). NRG1 (SNP8NRG221533; rs35753505) status was determined and correlated with verbal fluency performance and brain activation. For the behavioral measure, there was a linear effect of NRG1 status on semantic but not on lexical verbal fluency. Performance decreased with number of risk-alleles. In the fMRI experiment, decreased activation in the left inferior frontal and the right middle temporal gyri as well as the anterior cingulate gyrus was correlated with the number of risk-alleles in the semantic verbal fluency task. NRG1 genotype does influence language production on a semantic level in conjunction with the underlying neural systems. These findings are in line with results of studies in schizophrenia and may explain some of the cognitive and brain activation variation found in the disorder. More generally, NRG1 might be one of several genes that influence semantic language capacities.

Motivation for goal-directed behaviour largely depends on the expected value of the anticipated reward. The aim of the present study was to examine how different levels of reward value are coded in the brain for two common forms of human reward: money and social approval. To account for gender differences 16 male and 16 female participants performed an incentive delay task expecting to win either money or positive social feedback. fMRI recording during the anticipation phase revealed proportional activation of neural structures constituting the human reward system for increasing levels of reward, independent of incentive type. However, in men activation in the prospect of monetary rewards encompassed a wide network of mesolimbic brain regions compared to only limited activation for social rewards. In contrast, in women, anticipation of either incentive type activated identical brain regions. Our findings represent an important step towards a better understanding of motivated behaviour by taking into account individual differences in reward valuation.

For successful interpersonal communication, inferring intentions, goals or desires of others is highly advantageous. Increasingly, humans also interact with computers or robots. In this study, we sought to determine to what degree an interactive task, which involves receiving feedback from social partners that can be used to infer intent, engaged the medial prefrontal cortex, a region previously associated with Theory of Mind processes among others. Participants were scanned using fMRI as they played an adapted version of the Prisoner's Dilemma Game with alleged human and computer partners who were outside the scanner. The medial frontal cortex was activated when both human and computer partner were played, while the direct contrast revealed significantly stronger signal change during the human-human interaction. The results suggest a link between activity in the medial prefrontal cortex and the partner played in a mentalising task. This signal change was also present for to the computers partner. Implying agency or a will to non-human actors might be an innate human resource that could lead to an evolutionary advantage.