Impaired social learning in patients with major depressive disorder revealed by a reinforcement learning model

Background/objective: Patients with major depressive disorder (MDD) have altered learning rates for rewards and losses in non-social learning paradigms. However, it is not well understood whether the ability to learn from social interactions is altered in MDD patients. Using reinforcement learning during the repeated Trust Game (rTG), we investigated how MDD patients learn to trust newly-met partners in MDD patients. Method: Sixty-eight MDD patients and fifty-four controls each played as ‘investor’ and interacted with ten different partners. We manipulated both the level of trustworthiness by varying the chance of reciprocity (10, 30, 50, 70 and 90%) and reputation disclosure, where partners’ reputation was either pre-disclosed or hidden. Results: Our reinforcement learning model revealed that MDD patients had significantly higher learning rates for losses than the controls in both the reputation disclosure and non-disclosure condition. The difference was larger when reputation was not disclosed than disclosed. We observed no difference in learning rates for gains in either condition. Conclusions: Our findings highlight that abnormal learning for losses underlies the social learning process in MDD patients. This abnormality is higher when situational unpredictability is high versus low. Our findings provide novel insights into social rehabilitation of MDD. (AU)

Impaired social learning in patients with major depressive disorder revealed by a reinforcement learning model.

Background/objective: Patients with major depressive disorder (MDD) have altered learning rates for rewards and losses in non-social learning paradigms. However, it is not well understood whether the ability to learn from social interactions is altered in MDD patients. Using reinforcement learning during the repeated Trust Game (rTG), we investigated how MDD patients learn to trust newly-met partners in MDD patients. Method: Sixty-eight MDD patients and fifty-four controls each played as 'investor' and interacted with ten different partners. We manipulated both the level of trustworthiness by varying the chance of reciprocity (10, 30, 50, 70 and 90%) and reputation disclosure, where partners' reputation was either pre-disclosed or hidden. Results: Our reinforcement learning model revealed that MDD patients had significantly higher learning rates for losses than the controls in both the reputation disclosure and non-disclosure condition. The difference was larger when reputation was not disclosed than disclosed. We observed no difference in learning rates for gains in either condition. Conclusions: Our findings highlight that abnormal learning for losses underlies the social learning process in MDD patients. This abnormality is higher when situational unpredictability is high versus low. Our findings provide novel insights into social rehabilitation of MDD.

A Multivariate Method for Dynamic System Analysis: Multivariate Detrended Fluctuation Analysis Using Generalized Variance.

Fractal fluctuations are a core concept for inquiries into human behavior and cognition from a dynamic systems perspective. Here, we present a generalized variance method for multivariate detrended fluctuation analysis (mvDFA). The advantage of this extension is that it can be applied to multivariate time series and considers intercorrelation between these time series when estimating fractal properties. First, we briefly describe how fractal fluctuations have advanced a dynamic system understanding of cognition. Then, we describe mvDFA in detail and highlight some of the advantages of the approach for simulated data. Furthermore, we show how mvDFA can be used to investigate empirical multivariate data using electroencephalographic recordings during a time-estimation task. We discuss this methodological development within the framework of interaction-dominant dynamics. Moreover, we outline how the availability of multivariate analyses can inform theoretical developments in the area of dynamic systems in human behavior.

The 40-Hz auditory steady-state response in bipolar disorder: A meta-analysis.

OBJECTIVE: Bipolar disorder is characterized by aberrant neurophysiological responses as measured with electroencephalography (EEG) and magnetoencephalography (MEG), including the 40-Hz auditory steady-state response (ASSR). 40-Hz ASSR deficits are also found in patients with schizophrenia and may represent a transdiagnostic biomarker of neuronal circuit dysfunction. In this systematic review and meta-analysis, we summarize and evaluate the evidence for 40-Hz ASSR deficits in patients with bipolar disorder. METHODS: We identified studies from PubMed, EMBASE, and SCOPUS. We assessed the risk of bias, calculated Hedges' g meta-level effect sizes, and investigated small-study effects using funnel plots and Egger regression. RESULTS: Seven studies, comprising 396 patients with bipolar disorder and 404 healthy controls, were included in the meta-analysis. Studies displayed methodological heterogeneity and an overall high risk of bias. Patients with bipolar disorder showed consistent reductions in 40-Hz ASSR evoked power (Hedges' g = -0.49; 95% confidence intervals [-0.67, -0.31]) and inter-trial phase coherence (ITPC) (Hedges' g = -0.43; 95 %CI [-0.58, -0.29]) compared with healthy controls. CONCLUSIONS: Our meta-analysis provides evidence that 40-Hz ASSRs are reduced in patients with bipolar disorder compared with healthy controls. SIGNIFICANCE: Future large-scale studies are warranted to link 40-Hz ASSR deficits to clinical features and developmental trajectories.

The Danish High-Risk and Resilience Study-VIA 15 - A Study Protocol for the Third Clinical Assessment of a Cohort of 522 Children Born to Parents Diagnosed With Schizophrenia or Bipolar Disorder and Population-Based Controls.

Background: Children born to parents with severe mental illness have gained more attention during the last decades because of increasing evidence documenting that these children constitute a population with an increased risk of developing mental illness and other negative life outcomes. Because of high-quality research with cohorts of offspring with familial risk and increased knowledge about gene-environment interactions, early interventions and preventive strategies are now being developed all over the world. Adolescence is a period characterized by massive changes, both in terms of physical, neurologic, psychological, social, and behavioral aspects. It is also the period of life with the highest risk of experiencing onset of a mental disorder. Therefore, investigating the impact of various risk and resilience factors in adolescence is important. Methods: The Danish High-Risk and Resilience Study started data collection in 2012, where 522 7-year-old children were enrolled in the first wave of the study, the VIA 7 study. The cohort was identified through Danish registers based on diagnoses of the parents. A total of 202 children had a parent diagnosed with schizophrenia, 120 children had a parent diagnosed with bipolar disorder, and 200 children had parents without these diagnoses. At age 11 years, all children were assessed for the second time in the VIA 11 study, with a follow-up retention rate of 89%. A comprehensive assessment battery covering domains of psychopathology, neurocognition, social cognition and behavior, motor development and physical health, genetic analyses, attachment, stress, parental functioning, and home environment was carried out at each wave. Magnetic resonance imaging scans of the brain and electroencephalograms were included from age 11 years. This study protocol describes the third wave of assessment, the VIA 15 study, participants being 15 years of age and the full, 3-day-long assessment battery this time including also risk behavior, magnetoencephalography, sleep, and a white noise paradigm. Data collection started on May 1, 2021. Discussion: We will discuss the importance of longitudinal studies and cross-sectional data collection and how studies like this may inform us about unmet needs and windows of opportunity for future preventive interventions, early illness identification, and treatment in the future.

Activated N-methyl-D-aspartate receptor ion channels detected in focal epilepsy with [18 F]GE-179 positron emission tomography.

OBJECTIVE: Imaging activated glutamate N-methyl-D-aspartate receptor ion channels (NMDAR-ICs) using positron emission tomography (PET) has proved challenging due to low brain uptake, poor affinity and selectivity, and high metabolism and dissociation rates of candidate radioligands. The radioligand [18 F]GE-179 is a known use-dependent marker of NMDAR-ICs. We studied whether interictal [18 F]GE-179 PET would detect foci of abnormal NMDAR-IC activation in patients with refractory focal epilepsy. METHODS: Ten patients with refractory focal epilepsy and 18 healthy controls had structural magnetic resonance imaging (MRI) followed by a 90-min dynamic [18 F]GE-179 PET scan with simultaneous electroencephalography (EEG). PET and EEG findings were compared with MRI and previous EEGs. Standard uptake value (SUV) images of [18 F]GE-179 were generated and global gray matter uptake was measured for each individual. To localize focal increases in uptake of [18 F]GE-179, the individual SUV images were interrogated with statistical parametric mapping in comparison to a normal database. Additionally, individual healthy control SUV images were compared with the rest of the control database to determine their prevalence of increased focal [18 F]GE-179 uptake. RESULTS: Interictal [18 F]GE-179 PET detected clusters of significantly increased binding in eight of 10 patients with focal epilepsy but none of the controls. The number of clusters of raised [18 F]GE-179 uptake in the patients with epilepsy exceeded the focal abnormalities revealed by the simultaneously recorded EEG. Patients with extensive clusters of raised [18 F]GE-179 uptake showed the most abnormal EEGs. SIGNIFICANCE: Detection of multiple foci of abnormal NMDAR-IC activation in 80% of our patients with refractory focal epilepsy using interictal [18 F]GE-179 PET could reflect enhanced neuronal excitability due to chronic seizure activity. This indicates that chronic epileptic activity is associated with abnormal NMDAR ion channel activation beyond the initial irritative zones. [18 F]GE-179 PET could be a candidate marker for identifying pathological brain areas in patients with treatment-resistant focal epilepsy.

Cortical signatures of precision grip force control in children, adolescents, and adults.

Human dexterous motor control improves from childhood to adulthood, but little is known about the changes in cortico-cortical communication that support such ontogenetic refinement of motor skills. To investigate age-related differences in connectivity between cortical regions involved in dexterous control, we analyzed electroencephalographic data from 88 individuals (range 8-30 years) performing a visually guided precision grip task using dynamic causal modelling and parametric empirical Bayes. Our results demonstrate that bidirectional coupling in a canonical 'grasping network' is associated with precision grip performance across age groups. We further demonstrate greater backward coupling from higher-order to lower-order sensorimotor regions from late adolescence in addition to differential associations between connectivity strength in a premotor-prefrontal network and motor performance for different age groups. We interpret these findings as reflecting greater use of top-down and executive control processes with development. These results expand our understanding of the cortical mechanisms that support dexterous abilities through development.

Reduced effective connectivity between right parietal and inferior frontal cortex during audiospatial perception in neglect patients with a right-hemisphere lesion.

A lesion to the right hemisphere of the brain in humans commonly leads to perceptual neglect of the left side of the sensorium. The clinical observation that lesions to disparate cortical and subcortical areas converge upon similar behavioural symptoms points to neglect as a dysconnection syndrome that may result from the disruption of a distributed network, rather than aberrant computations in any particular brain region. To test this hypothesis, we used Bayesian analysis of effective connectivity based on electroencephalographic recordings in ten patients (6 male, 4 female; age range 41-68) with left-sided neglect following a right-hemisphere lesion. In line with previous research, age-matched healthy controls showed a contralateral increase in connection strength between parietal and frontal cortex with respect to the laterality of audiospatial oddball stimuli. Neglect patients, however, showed a dysconnection between parietal and frontal cortex in the right hemisphere when oddballs appeared on their left side, but preserved connectivity in the left hemisphere when stimuli appeared on their right. This preserved fronto-parietal connectivity was associated with lower neglect severity. Moreover, we saw ipsilateral fronto-temporal connectivity increases for oddballs appearing on the neglected side, which might be a compensatory mechanism for residual left side awareness. No group differences were found in intrinsic (within-region) connectivity. While further validation is required in a bigger sample, our findings are in keeping with the idea that neglect results from the disruption of a distributed network, rather than a lesion to any single brain region. SIGNIFICANCE STATEMENT: Lesions to the right hemisphere of the brain commonly lead to neglect syndrome, characterized by perceptual deficits where patients are unaware of the left side of their body and environment. Using analysis of non-invasive electrophysiological recordings, we provide evidence that patients with left-sided neglect have reduced connectivity between the right parietal and frontal cortex during audiospatial stimuli, but preserved connectivity between regions in the non-lesioned left hemisphere. Moreover, for these intact connections we observed an ipsilateral fronto-temporal increase in connectivity during oddballs appearing on the neglected side, which might be a compensatory mechanism for residual perception. Crucially, we found that patients with more severe neglect symptoms had reduced connectivity between parietal and frontal cortex in the left hemisphere. This suggests that neglect may be caused by the disruption of a distributed network in the brain, rather than a lesion to any particular brain region.

Perceptual learning of tone patterns changes the effective connectivity between Heschl's gyrus and planum temporale.

Learning of complex auditory sequences such as music can be thought of as optimizing an internal model of regularities through unpredicted events (or "prediction errors"). We used dynamic causal modeling (DCM) and parametric empirical Bayes on functional magnetic resonance imaging (fMRI) data to identify modulation of effective brain connectivity that takes place during perceptual learning of complex tone patterns. Our approach differs from previous studies in two aspects. First, we used a complex oddball paradigm based on tone patterns as opposed to simple deviant tones. Second, the use of fMRI allowed us to identify cortical regions with high spatial accuracy. These regions served as empirical regions-of-interest for the analysis of effective connectivity. Deviant patterns induced an increased blood oxygenation level-dependent response, compared to standards, in early auditory (Heschl's gyrus [HG]) and association auditory areas (planum temporale [PT]) bilaterally. Within this network, we found a left-lateralized increase in feedforward connectivity from HG to PT during deviant responses and an increase in excitation within left HG. In contrast to previous findings, we did not find frontal activity, nor did we find modulations of backward connections in response to oddball sounds. Our results suggest that complex auditory prediction errors are encoded by changes in feedforward and intrinsic connections, confined to superior temporal gyrus.

Aberrant effective connectivity is associated with positive symptoms in first-episode schizophrenia.

Schizophrenia is a neurodevelopmental psychiatric disorder thought to result from synaptic dysfunction that affects distributed brain connectivity, rather than any particular brain region. While symptomatology is traditionally divided into positive and negative symptoms, abnormal social cognition is now recognized a key component of schizophrenia. Nonetheless, we are still lacking a mechanistic understanding of effective brain connectivity in schizophrenia during social cognition and how it relates to clinical symptomatology. To address this question, we used fMRI and dynamic causal modelling (DCM) to test for abnormal brain connectivity in twenty-four patients with first-episode schizophrenia (FES) compared to twenty-five matched controls performing the Human Connectome Project (HCP) social cognition paradigm. Patients had not received regular therapeutic antipsychotics, but were not completely drug naïve. Whilst patients were less accurate than controls in judging social stimuli from non-social stimuli, our results revealed an increase in feedforward connectivity from motion-sensitive V5 to posterior superior temporal sulcus (pSTS) in patients compared to matched controls. At the same time, patients with a higher degree of positive symptoms had more disinhibition within pSTS, a region computationally involved in social cognition. We interpret these findings the framework of active inference, where increased feedforward connectivity may encode aberrant prediction errors from V5 to pSTS and local disinhibition within pSTS may reflect aberrant encoding of the precision of cortical representations about social stimuli.

Activation of NMDA receptor ion channels by deep brain stimulation in the pig visualised with [18F]GE-179 PET.

BACKGROUND: No PET radioligand has yet demonstrated the capacity to map glutamate N-methyl-d-aspartate receptor ion channel (NMDAR-IC) function. [18F]GE-179 binds to the phencyclidine (PCP) site in open NMDAR-ICs and potentially provides a use-dependent PET biomarker of these ion channels. OBJECTIVE: To show [18F]GE-179 PET can detect increased NMDAR-IC activation during electrical deep brain stimulation (DBS) of pig hippocampus. METHODS: Six minipigs had an electrode implanted into their right hippocampus. They then had a baseline [18F]GE-179 PET scan with DBS turned off followed by a second scan with DBS turned on. Brain [18F]GE-179 uptake at baseline and then during DBS was measured with PET. Cerebral blood flow (CBF) was measured with [15O]H2O PET at baseline and during DBS and parametric CBF images were generated to evaluate DBS induced CBF changes. Functional effects of injecting the PCP blocker MK-801 were also evaluated. Electrode positions were later histologically verified. RESULTS: DBS induced a 47.75% global increase in brain [18F]GE-179 uptake (p = 0.048) compared to baseline. Global CBF was unchanged by hippocampal DBS. [18F]GE-179 PET detected a 5% higher uptake in the implanted compared with the non-implanted temporo-parietal cortex at baseline (p = 0.012) and during stimulation (p = 0.022). Administration of MK-801 before DBS failed to block [18F]GE-179 uptake during stimulation. CONCLUSION: PET detected an increase in global brain [18F]GE-179 uptake during unilateral hippocampal DBS while CBF remained unchanged. These findings support that [18F]GE-179 PET provides a use-dependent marker of abnormal NMDAR-IC activation.

Directed connectivity between primary and premotor areas underlying ankle force control in young and older adults.

The control of ankle muscle force is an integral component of walking and postural control. Aging impairs the ability to produce force steadily and accurately, which can compromise functional capacity and quality of life. Here, we hypothesized that reduced force control in older adults would be associated with altered cortico-cortical communication within a network comprising the primary motor area (M1), the premotor cortex (PMC), parietal, and prefrontal regions. We examined electroencephalographic (EEG) responses from fifteen younger (20-26 â€‹yr) and fifteen older (65-73 â€‹yr) participants during a unilateral dorsiflexion force-tracing task. Dynamic Causal Modelling (DCM) and Parametric Empirical Bayes (PEB) were used to investigate how directed connectivity between contralateral M1, PMC, parietal, and prefrontal regions was related to age group and precision in force production. DCM and PEB analyses revealed that the strength of connections between PMC and M1 were related to ankle force precision and differed by age group. For young adults, bidirectional PMC-M1 coupling was negatively related to task performance: stronger backward M1-PMC and forward PMC-M1 coupling was associated with worse force precision. The older group exhibited deviations from this pattern. For the PMC to M1 coupling, there were no age-group differences in coupling strength; however, within the older group, stronger coupling was associated with better performance. For the M1 to PMC coupling, older adults followed the same pattern as young adults - with stronger coupling accompanied by worse performance - but coupling strength was lower than in the young group. Our results suggest that bidirectional M1-PMC communication is related to precision in ankle force production and that this relationship changes with aging. We argue that the observed differences reflect compensatory reorganization that counteracts age-related sensorimotor declines and contributes to maintaining performance.

The CI MuMuFe - A New MMN Paradigm for Measuring Music Discrimination in Electric Hearing.

Cochlear implants (CIs) allow good perception of speech while music listening is unsatisfactory, leading to reduced music enjoyment. Hence, a number of ongoing efforts aim to improve music perception with a CI. Regardless of the nature of these efforts, effect measurements must be valid and reliable. While auditory skills are typically examined by behavioral methods, recording of the mismatch negativity (MMN) response, using electroencephalography (EEG), has recently been applied successfully as a supplementary objective measure. Eleven adult CI users and 14 normally hearing (NH) controls took part in the present study. To measure their detailed discrimination of fundamental features of music we applied a new multifeature MMN-paradigm which presented four music deviants at four levels of magnitude, incorporating a novel "no-standard" approach to be tested with CI users for the first time. A supplementary test measured behavioral discrimination of the same deviants and levels. The MMN-paradigm elicited significant MMN responses to all levels of deviants in both groups. Furthermore, the CI-users' MMN amplitudes and latencies were not significantly different from those of NH controls. Both groups showed MMN strength that was in overall alignment with the deviation magnitude. In CI users, however, discrimination of pitch levels remained undifferentiated. On average, CI users' behavioral performance was significantly below that of the NH group, mainly due to poor pitch discrimination. Although no significant effects were found, CI users' behavioral results tended to be in accordance with deviation magnitude, most prominently manifested in discrimination of the rhythm deviant. In summary, the study indicates that CI users may be able to discriminate subtle changes in basic musical features both in terms of automatic neural responses and of attended behavioral detection. Despite high complexity, the new CI MuMuFe paradigm and the "no-standard" approach provided reliable results, suggesting that it may serve as a relevant tool in future CI research. For clinical use, future studies should investigate the possibility of applying the paradigm with the purpose of assessing discrimination skills not only at the group level but also at the individual level.

Now you hear it: a predictive coding model for understanding rhythmic incongruity.

Rhythmic incongruity in the form of syncopation is a prominent feature of many contemporary musical styles. Syncopations afford incongruity between rhythmic patterns and the meter, giving rise to mental models of differently accented isochronous beats. Syncopations occur either in isolation or as part of rhythmic patterns, so-called grooves. On the basis of the predictive coding framework, we discuss how brain processing of rhythm can be seen as a special case of predictive coding. We present a simple, yet powerful model for how the brain processes rhythmic incongruity: the model for predictive coding of rhythmic incongruity. Our model proposes that a given rhythm's syncopation and its metrical uncertainty (precision) is at the heart of how the brain models rhythm and meter based on priors, predictions, and prediction error. Our minimal model can explain prominent features of brain processing of syncopation: why isolated syncopations lead to stronger prediction error in the brains of musicians, as evidenced by larger event-related potentials to rhythmic incongruity, and why we all experience a stronger urge to move to grooves with a medium level of syncopation compared with low and high levels of syncopation.

Reduced Pain Sensation and Reduced BOLD Signal in Parietofrontal Networks during Religious Prayer.

Previous studies suggest that religious prayer can alter the experience of pain via expectation mechanisms. While brain processes related to other types of top-down modulation of pain have been studied extensively, no research has been conducted on the potential effects of active religious coping. Here, we aimed at investigating the neural mechanisms during pain modulation by prayer and their dependency on the opioidergic system. Twenty-eight devout Protestants performed religious prayer and a secular contrast prayer during painful electrical stimulation in two fMRI sessions. Naloxone or saline was administered prior to scanning. Results show that pain intensity was reduced by 11% and pain unpleasantness by 26% during religious prayer compared to secular prayer. Expectancy predicted large amounts (70-89%) of the variance in pain intensity. Neuroimaging results revealed reduced neural activity during religious prayer in a large parietofrontal network relative to the secular condition. Naloxone had no significant effect on ratings or neural activity. Our results thus indicate that, under these conditions, pain modulation by prayer is not opioid-dependent. Further studies should employ an optimized design to explore whether reduced engagement of the frontoparietal system could indicate that prayer may attenuate pain through a reduction in processing of pain stimulus saliency and prefrontal control rather than through known descending pain inhibitory systems.

Expectation violation and attention to pain jointly modulate neural gain in somatosensory cortex.

The neural processing and experience of pain are influenced by both expectations and attention. For example, the amplitude of event-related pain responses is enhanced by both novel and unexpected pain, and by moving the focus of attention towards a painful stimulus. Under predictive coding, this congruence can be explained by appeal to a precision-weighting mechanism, which mediates bottom-up and top-down attentional processes by modulating the influence of feedforward and feedback signals throughout the cortical hierarchy. The influence of expectation and attention on pain processing can be mapped onto changes in effective connectivity between or within specific neuronal populations, using a canonical microcircuit (CMC) model of hierarchical processing. We thus implemented a CMC within dynamic causal modelling for magnetoencephalography in human subjects, to investigate how expectation violation and attention to pain modulate intrinsic (within-source) and extrinsic (between-source) connectivity in the somatosensory hierarchy. This enabled us to establish whether both expectancy and attentional processes are mediated by a similar precision-encoding mechanism within a network of somatosensory, frontal and parietal sources. We found that both unexpected and attended pain modulated the gain of superficial pyramidal cells in primary and secondary somatosensory cortex. This modulation occurred in the context of increased lateralized recurrent connectivity between somatosensory and fronto-parietal sources, driven by unexpected painful occurrences. Finally, the strength of effective connectivity parameters in S1, S2 and IFG predicted individual differences in subjective pain modulation ratings. Our findings suggest that neuromodulatory gain control in the somatosensory hierarchy underlies the influence of both expectation violation and attention on cortical processing and pain perception.

Anterior insula coordinates hierarchical processing of tactile mismatch responses.

The body underlies our sense of self, emotion, and agency. Signals arising from the skin convey warmth, social touch, and the physical characteristics of external stimuli. Surprising or unexpected tactile sensations can herald events of motivational salience, including imminent threats (e.g., an insect bite) and hedonic rewards (e.g., a caressing touch). Awareness of such events is thought to depend upon the hierarchical integration of body-related mismatch responses by the anterior insula. To investigate this possibility, we measured brain activity using functional magnetic resonance imaging, while healthy participants performed a roving tactile oddball task. Mass-univariate analysis demonstrated robust activations in limbic, somatosensory, and prefrontal cortical areas previously implicated in tactile deviancy, body awareness, and cognitive control. Dynamic Causal Modelling revealed that unexpected stimuli increased the strength of forward connections along a caudal to rostral hierarchy-projecting from thalamic and somatosensory regions towards insula, cingulate and prefrontal cortices. Within this ascending flow of sensory information, the AIC was the only region to show increased backwards connectivity to the somatosensory cortex, augmenting a reciprocal exchange of neuronal signals. Further, participants who rated stimulus changes as easier to detect showed stronger modulation of descending PFC to AIC connections by deviance. These results suggest that the AIC coordinates hierarchical processing of tactile prediction error. They are interpreted in support of an embodied predictive coding model where AIC mediated body awareness is involved in anchoring a global neuronal workspace.

Being asked to tell an unpleasant truth about another person activates anterior insula and medial prefrontal cortex.

"Truth" has been used as a baseline condition in several functional magnetic resonance imaging (fMRI) studies of deception. However, like deception, telling the truth is an inherently social construct, which requires consideration of another person's mental state, a phenomenon known as Theory of Mind. Using a novel ecological paradigm, we examined blood oxygenation level dependent (BOLD) responses during social and simple truth telling. Participants (n = 27) were randomly divided into two competing teams. Post-competition, each participant was scanned while evaluating performances from in-group and out-group members. Participants were asked to be honest and were told that their evaluations would be made public. We found increased BOLD responses in the medial prefrontal cortex, bilateral anterior insula and precuneus when participants were asked to tell social truths compared to simple truths about another person. At the behavioral level, participants were slower at responding to social compared to simple questions about another person. These findings suggest that telling the truth is a nuanced cognitive operation that is dependent on the degree of mentalizing. Importantly, we show that the cortical regions engaged by truth telling show a distinct pattern when the task requires social reasoning.

Ambivalence, equivocation and the politics of experimental knowledge: a transdisciplinary neuroscience encounter.

This article is about a transdisciplinary project between the social, human and life sciences, and the felt experiences of the researchers involved. 'Transdisciplinary' and 'interdisciplinary' research-modes have been the subject of much attention lately--especially as they cross boundaries between the social/humanistic and natural sciences. However, there has been less attention, from within science and technology studies, to what it is actually like to participate in such a research-space. This article contributes to that literature through an empirical reflection on the progress of one collaborative and transdisciplinary project: a novel experiment in neuroscientific lie detection, entangling science and technology studies, literary studies, sociology, anthropology, clinical psychology and cognitive neuroscience. Its central argument is twofold: (1) that, in addition to ideal-type tropes of transdisciplinary conciliation or integration, such projects may also be organized around some more subterranean logics of ambivalence, reserve and critique; (2) that an account of the mundane ressentiment of collaboration allows for a more careful attention to the awkward forms of 'experimental politics' that may flow through, and indeed propel, collaborative work more broadly. Building on these claims, the article concludes with a suggestion that such subterranean logics may be indissociable from some forms of collaboration, and it proposes an ethic of 'equivocal speech' as a way to live with and through these kinds of transdisciplinary experiences.