Neural Substrates Research Articles

Different neural correlates of deception: Crafting high and low creative scams

Deception is a complex social behavior that manifests in various forms, including scams. To successfully deceive victims, liars have to continually devise novel scams. This ability to create novel scams represents one kind of malevolent creativity, referred to as lying. This study aimed to explore different neural substrates involved in the generation of high and low creative scams. A total of 40 participants were required to design several creative scams, and their cortical activity was recorded by functional near-infrared spectroscopy. The results revealed that the right frontopolar cortex (FPC) was significantly active in scam generation. This region associated with theory of mind may be a key region for creating novel and complex scams. Moreover, creativity-related regions were positively involved in creative scams, while morality-related areas showed negative involvement. This suggests that individuals might attempt to use malevolent creativity while simultaneously minimizing the influence of moral considerations. The right FPC exhibited increased coupling with the right precentral gyrus during the design of high-harmfulness scams, suggesting a diminished control over immoral thoughts in the generation of harmful scams. Additionally, the perception of the victim’s emotions (related to right pre-motor cortex) might diminish the quality of highly original scams. Furthermore, an efficient and cohesive neural coupling state appears to be a key factor in generating high-creativity scams. These findings suggest that the right FPC was crucial in scam creation, highlighting a neural basis for balancing malevolent creativity against moral considerations in high-creativity deception.

Spatially organized striatal neuromodulator release encodes trajectory errors.

Goal-directed navigation requires animals to continuously evaluate their current direction and speed of travel relative to landmarks to discern whether they are approaching or deviating from their goal. Striatal dopamine and acetylcholine are powerful modulators of goal-directed behavior, but it is unclear whether and how neuromodulator dynamics at landmarks incorporate relative motion for effective behavioral guidance. Using optical measurements in mice, we demonstrate that cue-evoked striatal dopamine release encodes bi-directional 'trajectory errors' reflecting relationships between ongoing speed and direction of locomotion and visual flow relative to optimal goal trajectories. Striatum-wide micro-fiber array recordings resolved an anatomical gradient of trajectory error signaling across the anterior-posterior axis, distinct from trajectory error independent cue signals. Dynamic regression modeling revealed that positive and negative trajectory error encoding emerges early and late respectively during learning and over different time courses in the medial and lateral striatum, enabling region specific contributions to learning. Striatal acetylcholine release also encodes trajectory errors, but encoding is more spatially restricted, opposite polarity, and delayed relative to dopamine, supporting distinct roles in modulating striatal output and behavior. Dopamine trajectory error signaling and task performance were reproduced in a reinforcement learning model incorporating a conjunctive state space representation, suggesting a potential neural substrate for trajectory error generation. Our results establish region specific neuromodulator signals positioned to guide the speed and direction of locomotion to reach goals based on environmental landmarks during navigation.

The right posterior parietal cortex mediates spatial reorienting of attentional choice bias

Attention facilitates behavior by enhancing perceptual sensitivity (sensory processing) and choice bias (decisional weighting) for attended information. Whether distinct neural substrates mediate these distinct components of attention remains unknown. We investigate the causal role of key nodes of the right posterior parietal cortex (rPPC) in the forebrain attention network in sensitivity versus bias control. Two groups of participants performed a cued attention task while we applied either inhibitory, repetitive transcranial magnetic stimulation (n = 28) or 40 Hz transcranial alternating current stimulation (n = 26) to the dorsal rPPC. We show that rPPC stimulation – with either modality – impairs task performance by selectively altering attentional modulation of bias but not sensitivity. Specifically, participants’ bias toward the uncued, but not the cued, location reduced significantly following rPPC stimulation – an effect that was consistent across both neurostimulation cohorts. In sum, the dorsal rPPC causally mediates the reorienting of choice bias, one particular component of visual spatial attention.

Aggression Unleashed: Neural Circuits from Scent to Brain.

Aggression is a fundamental behavior with essential roles in dominance assertion, resource acquisition, and self-defense across the animal kingdom. However, dysregulation of the aggression circuitry can have severe consequences in humans, leading to economic, emotional, and societal burdens. Previous inconsistencies in aggression research have been due to limitations in techniques for studying these neurons at a high spatial resolution, resulting in an incomplete understanding of the neural mechanisms underlying aggression. Recent advancements in optogenetics, pharmacogenetics, single-cell RNA sequencing, and in vivo electrophysiology have provided new insights into this complex circuitry. This review aims to explore the aggression-provoking stimuli and their detection in rodents, particularly through the olfactory systems. Additionally, we will examine the core regions associated with aggression, their interactions, and their connection with the prefrontal cortex. We will also discuss the significance of top-down cognitive control systems in regulating atypical expressions of aggressive behavior. While the focus will primarily be on rodent circuitry, we will briefly touch upon the modulation of aggression in humans through the prefrontal cortex and discuss emerging therapeutic interventions that may benefit individuals with aggression disorders. This comprehensive understanding of the neural substrates of aggression will pave the way for the development of novel therapeutic strategies and clinical interventions. This approach contrasts with the broader perspective on neural mechanisms of aggression across species, aiming for a more focused analysis of specific pathways and their implications for therapeutic interventions.

Deletion of endocannabinoid synthesizing enzyme DAGLα from cerebellar Purkinje cells decreases social preference and elevates anxiety.

ABSTRACTThe endocannabinoid (eCB) signaling system is robustly expressed in the cerebellum starting from the embryonic developmental stages to adulthood. There it plays a key role in regulating cerebellar synaptic plasticity and excitability, suggesting that impaired eCB signaling will lead to deficits in cerebellar adjustments of ongoing behaviors and cerebellar learning. Indeed, human mutations inDAGLαare associated with neurodevelopmental disorders. In this study, we show that selective deletion of the eCB synthesizing enzyme diacylglycerol lipase alpha (Daglα) from mouse cerebellar Purkinje cells (PCs) alters motor and social behaviors, disrupts short-term synaptic plasticity in both excitatory and inhibitory synapses, and reduces Purkinje cell activity during social exploration. Our results provide the first evidence for cerebellar-specific eCB regulation of social behaviors and implicate eCB regulation of synaptic plasticity and PC activity as the neural substrates contributing to these deficits.Abstract FigureGraphical abstract.Cerebellar anatomy, morphology of Purkinje cells, localization, density, and spontaneous activity of excitatory and inhibitory synapses are normal in cerebellar-Purkinje-cell-specific Daglα KOs. However, endocannabinoid-dependent short-term synaptic plasticity (DSE and DSI) and activity of Purkinje cells in lobe VI during social exploration are dramatically reduced, and the KO mice exhibit alterations in sensorimotor coordination, deceased social preference, and increased anxiety.

Nicotine reduces discrimination between threat and safety in the hippocampus, nucleus accumbens and amygdala

Nicotine intake is linked to the maintenance and development of anxiety disorders and impairs adaptive discrimination of threat and safety in rodents and humans. Yet, it is unclear if nicotine exerts a causal pharmacological effect on the affective and neural mechanisms that underlie aversive learning. We conducted a pre-registered, pseudo-randomly and double-blinded pharmacological fMRI study to investigate the effect of acute nicotine on Fear Acquisition and Extinction in non-smokers (n = 88). Our results show that nicotine administration led to decreased discrimination between threat and safety in subjective fear. Nicotine furthermore decreased differential (threat vs. safety) activation in the hippocampus, which was functionally coupled with Nucleus Accumbens and amygdala, compared to placebo controls. Additionally, nicotine led to enhanced physiological arousal to learned threats and overactivation of the ventral tegmental area. This study provides mechanistic evidence that single doses of nicotine impair neural substrates of adaptive aversive learning in line with the risk for the development of pathological anxiety.

Unraveling the Neural Landscape of Mental Disorders using Double Functional Independent Primitives (dFIPs).

Mental illnesses extract a high personal and societal cost, and thus explorations of the links between mental illness and functional connectivity in the brain are critical. Investigating major mental illnesses, believed to arise from disruptions in sophisticated neural connections, allows us to comprehend how these neural network disruptions may be linked to altered cognition, emotional regulation, and social interactions. Although neuroimaging has opened new avenues to explore neural alterations linked to mental illnesses, the field still requires precise and sensitive methodologies to inspect these neural substrates of various psychological disorders. In this study, we employ a hierarchical methodology to derive double functionally independent primitives (dFIPs) from resting state functional magnetic resonance neuroimaging data (rs-fMRI). These dFIPs encapsulate canonical overlapping patterns of functional network connectivity (FNC) within the brain. Our investigation focuses on the examination of how combinations of these dFIPs relate to different mental disorder diagnoses. The central aim is to unravel the complex patterns of FNC that correspond to the diverse manifestations of mental illnesses. To achieve this objective, we used a large brain imaging dataset from multiple sites, comprising 5805 total individuals diagnosed with schizophrenia (SCZ), autism spectrum disorder (ASD), bipolar disorder (BPD), major depressive disorder (MDD), and controls. The key revelations of our study unveil distinct patterns associated with each mental disorder through the combination of dFIPs. Notably, certain individual dFIPs exhibit disorder-specific characteristics, while others demonstrate commonalities across disorders. This approach offers a novel, data-driven synthesis of intricate neuroimaging data, thereby illuminating the functional changes intertwined with various mental illnesses. Our results show distinct signatures associated with psychiatric disorders, revealing unique connectivity patterns such as heightened cerebellar connectivity in SCZ and sensory domain hyperconnectivity in ASD, both contrasted with reduced cerebellar-subcortical connectivity. Utilizing the dFIP concept, we pinpoint specific functional connections that differentiate healthy controls from individuals with mental illness, underscoring its utility in identifying neurobiological markers. In summary, our findings delineate how dFIPs serve as unique fingerprints for different mental disorders.

Optogenetic inhibition of light-captured alcohol-taking striatal engrams facilitates extinction and suppresses reinstatement.

Alcohol use disorder (AUD) is a complex condition, and it remains unclear which specific neuronal substrates mediate alcohol-seeking and -taking behaviors. Engram cells and their related ensembles, which encode learning and memory, may play a role in this process. We aimed to assess the precise neural substrates underlying alcohol-seeking and -taking behaviors and determine how they may affect one another. Using FLiCRE (Fast Light and Calcium-Regulated Expression; a newly developed technique which permits the trapping of acutely activated neuronal ensembles) and operant self-administration (OSA), we tagged striatal neurons activated during alcohol-taking behaviors. We used FLiCRE to express an inhibitory halorhodopsin in alcohol-taking neurons, permitting loss-of-function manipulations. We found that the inhibition of OSA-tagged alcohol-taking neurons decreased both alcohol-seeking and -taking behaviors in future OSA trials. In addition, optogenetic inhibition of these OSA-tagged alcohol-taking neurons during extinction training facilitated the extinction of alcohol-seeking behaviors. Furthermore, inhibition of these OSA-tagged alcohol-taking neurons suppressed the reinstatement of alcohol-seeking behaviors, but, interestingly, it did not significantly suppress alcohol-taking behaviors during reinstatement. Our findings suggest that alcohol-taking neurons are crucial for future alcohol-seeking behaviors during extinction and reinstatement. These results may help in the development of new therapeutic approaches to enhance extinction and suppress relapse in individuals with AUD.

A bio-inspired reinforcement learning model that accounts for fast adaptation after punishment

Humans and animals can quickly learn a new strategy when a previously-rewarding strategy is punished. It is difficult to model this with reinforcement learning methods, because they tend to perseverate on previously-learned strategies − a hallmark of impaired response to punishment. Past work has addressed this by augmenting conventional reinforcement learning equations with ad hoc parameters or parallel learning systems. This produces reinforcement learning models that account for reversal learning, but are more abstract, complex, and somewhat detached from neural substrates. Here we use a different approach: we generalize a recently-discovered neuron-level learning rule, on the assumption that it captures a basic principle of learning that may occur at the whole-brain-level. Surprisingly, this gives a new reinforcement learning rule that accounts for adaptation and lose-shift behavior, and uses only the same parameters as conventional reinforcement learning equations. In the new rule, the normal reward prediction errors that drive reinforcement learning are scaled by the likelihood the agent assigns to the action that triggered a reward or punishment. The new rule demonstrates quick adaptation in card sorting and variable Iowa gambling tasks, and also exhibits a human-like paradox-of-choice effect. It will be useful for experimental researchers modeling learning and behavior.

Losing Control: Prefrontal Emotion Regulation Is Related to Symptom Severity and Predicts Treatment-Related Symptom Change in Adolescent Girls With Conduct Disorder

BackgroundEmotion regulation skills are linked to corticolimbic brain activity (e.g., dorsolateral prefrontal cortex [dlPFC] and limbic regions) and enable an individual to control their emotional experiences, thus allowing healthy social functioning. Disruptions in emotion regulation skills are reported in neuropsychiatric disorders, including conduct disorder or oppositional defiant disorder (CD/ODD). Clinically recognized means to ameliorate emotion regulation deficits observed in CD/ODD include cognitive or dialectical behavioral skills therapy as implemented in the START NOW program. However, the role of emotion regulation and its neural substrates in symptom severity and prognosis following treatment of adolescent CD/ODD has not been investigated. MethodsCross-sectional data including functional magnetic resonance imaging responses during emotion regulation (n = 114; average age = 15 years), repeated-measures assessments of symptom severity (pretreatment, posttreatment, long-term follow-up), and functional magnetic resonance imaging data collected prior to and following the START NOW randomized controlled trial (n = 44) for female adolescents with CD/ODD were analyzed using group comparisons and multiple regression. ResultsFirst, behavioral and neural correlates of emotion regulation were disrupted in female adolescents with CD/ODD. Second, ODD symptom severity was negatively associated with dlPFC/precentral gyrus activity during regulation. Third, treatment-related symptom changes were predicted by pretreatment ODD symptom severity and regulatory dlPFC/precentral activity. Additionally, pretreatment dlPFC/precentral activity and ODD symptom severity predicted long-term reductions in symptom severity following treatment for participants who received the START NOW treatment. ConclusionsOur findings demonstrate the important role that emotion regulation skills play in the characteristics of CD/ODD and show that regulatory dlPFC/precentral activity is positively associated with treatment response in female adolescents with CD/ODD.

The computational and neural substrates of individual differences in impulsivity under loss framework.

Numerous neuroimaging studies have identified significant individual variability in intertemporal choice, often attributed to three neural mechanisms: (1) increased reward circuit activity, (2) decreased cognitive control, and (3) prospection ability. These mechanisms that explain impulsivity, however, have been primarily studied in the gain domain. This study extends this investigation to the loss domain. We employed a hierarchical Bayesian drift-diffusion model (DDM) and the inter-subject representational similarity approach (IS-RSA) to investigate the potential computational neural substrates underlying impulsivity in loss domain across two experiments (n = 155). These experiments utilized a revised intertemporal task that independently manipulated the amounts of immediate and delayed-loss options. Behavioral results demonstrated positive correlations between the drift rate, measured by the DDM, and the impulsivity index K in Exp. 1 (n = 97) and were replicated in Exp. 2 (n = 58). Imaging analyses further revealed that the drift rate significantly mediated the relations between brain properties (e.g., prefrontal cortex activations and gray matter volume in the orbitofrontal cortex and precuneus) and K in Exp. 1. IS-RSA analyses indicated that variability in the drift rate also mediated the associations between inter-subject variations in activation patterns and individual differences in K. These findings suggest that individuals with similar impulsivity levels are likely to exhibit similar value processing patterns, providing a potential explanation for individual differences in impulsivity within a loss framework.

Are spatial terms rooted in geometry or force-dynamics? Yes.

Theories of spatial term meanings often focus on geometric properties of objects and locations as the key to understanding meaning. For example, in English, "The cat is on the mat" might engage geometric properties characterizing the figure ('cat', a point) and the ground ('mat', a plane) as well as the geometric relationship between the two objects ('on', + vertical, 0 distance from ground object). However, substantial literature suggests that geometric properties are far from sufficient to capture the meanings of many spatial expressions, and that instead, force-dynamic properties of objects that afford containment or support relationships may be crucial to the meanings of those expressions. I will argue that both approaches are needed to understand the variety of spatial terms that appear in language and further, that spatial terms fall into two distinct sets, one represented by geometric properties of figure and ground and their spatial relationships, and the other by the force-dynamic properties of objects and their relationships. This division of labor within spatial terms has many consequences, with the two types differing in the nature of the acquisition problem and likely learning mechanisms, the extent and kind of cross-linguistic variation that has been observed, and the application of pragmatic principles to spatial terms. Speculatively, the two types may also be rooted in different cognitive systems and their neural substrates.

Cerebellar nuclei cells produce distinct pathogenic spike signatures in mouse models of ataxia, dystonia, and tremor.

The cerebellum contributes to a diverse array of motor conditions, including ataxia, dystonia, and tremor. The neural substrates that encode this diversity are unclear. Here, we tested whether the neural spike activity of cerebellar output neurons is distinct between movement disorders with different impairments, generalizable across movement disorders with similar impairments, and capable of causing distinct movement impairments. Using in vivo awake recordings as input data, we trained a supervised classifier model to differentiate the spike parameters between mouse models for ataxia, dystonia, and tremor. The classifier model correctly assigned mouse phenotypes based on single-neuron signatures. Spike signatures were shared across etiologically distinct but phenotypically similar disease models. Mimicking these pathophysiological spike signatures with optogenetics induced the predicted motor impairments in otherwise healthy mice. These data show that distinct spike signatures promote the behavioral presentation of cerebellar diseases.

Decreased resting-state brain function in older adults predicts enlarged representational momentum.

Representational momentum (RM) refers to the phenomenon in which an observer's judgment of the final location of a previously viewed moving target is often displaced forward in the direction of motion. This phenomenon is an adaptive mechanism that compensates for neural processing delays and is closely associated with visual cortex function. However, the impact of age-related decline of visual cortex function on the manifestations of RM remains unclear. The present study examined differences in the RM effect between older (N = 82) and younger adults (N = 74) using a cursor-positioning task. Additionally, resting-state functional magnetic resonance imaging was used to explore the potential neural substrates that underlie these differences, employing amplitude of low-frequency fluctuation (ALFF, reflecting the intensity of neural activity) and regional homogeneity (ReHo, reflecting the synchronization of neural activity) as indicators. Our findings indicate a significant increase in RM among older adults compared with younger adults. Neuroimaging data revealed a significant decrease in ALFF and ReHo within extensive regions of the visual cortex in older adults, validating age-related differences in this cortical area. More importantly, ALFF values in the bilateral visual area 3 and ReHo values in the bilateral visual area 2 in older adults exhibited a strong negative correlation with their RM effects. These results suggest that larger RM in older adults may be functional compensation for aging of the visual cortex. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

Neural Substrates for Early Data Reduction in Fast Vision: A Psychophysical Investigation.

To ensure survival, the visual system must rapidly extract the most important elements from a large stream of information. This necessity clashes with the computational limitations of the human brain, so a strong early data reduction is required to efficiently process information in fast vision. A theoretical early vision model, recently developed to preserve maximum information using minimal computational resources, allows efficient image data reduction by extracting simplified sketches containing only optimally informative, salient features. Here, we investigate the neural substrates of this mechanism for optimal encoding of information, possibly located in early visual structures. We adopted a flicker adaptation paradigm, which has been demonstrated to specifically impair the contrast sensitivity of the magnocellular pathway. We compared flicker-induced contrast threshold changes in three different tasks. The results indicate that, after adapting to a uniform flickering field, thresholds for image discrimination using briefly presented sketches increase. Similar threshold elevations occur for motion discrimination, a task typically targeting the magnocellular system. Instead, contrast thresholds for orientation discrimination, a task typically targeting the parvocellular system, do not change with flicker adaptation. The computation performed by this early data reduction mechanism seems thus consistent with magnocellular processing.

Differential reorganization of episodic and semantic memory systems in epilepsy-related mesiotemporal pathology.

Declarative memory encompasses episodic and semantic divisions. Episodic memory captures singular events with specific spatiotemporal relationships, while semantic memory houses context-independent knowledge. Behavioural and functional neuroimaging studies have revealed common and distinct neural substrates of both memory systems, implicating mesiotemporal lobe (MTL) regions such as the hippocampus and distributed neocortices. Here, we explored declarative memory system reorganization in patients with unilateral temporal lobe epilepsy (TLE) as a human disease model to test the impact of variable degrees of MTL pathology on memory function. Our cohort included 31 patients with TLE as well as 60 age and sex-matched healthy controls, and all participants underwent episodic and semantic retrieval tasks during a multimodal MRI session. The functional MRI tasks were closely matched in terms of stimuli and trial design. Capitalizing on non-linear connectome gradient mapping techniques, we derived task-based functional topographies during episodic and semantic memory states, both in the MTL and in neocortical networks. Comparing neocortical and hippocampal functional gradients between TLE patients and healthy controls, we observed a marked topographic reorganization of both neocortical and MTL systems during episodic memory states. Neocortical alterations were characterized by reduced functional differentiation in TLE across lateral temporal and midline parietal cortices in both hemispheres. In the MTL, on the other hand, patients presented with a more marked functional differentiation of posterior and anterior hippocampal segments ipsilateral to the seizure focus and pathological core, indicating perturbed intrahippocampal connectivity. Semantic memory reorganization was also found in bilateral lateral temporal and ipsilateral angular regions, while hippocampal functional topographies were unaffected. Leveraging MRI proxies of MTL pathology, we furthermore observed alterations in hippocampal microstructure and morphology that were associated with TLE-related functional reorganization during episodic memory. Moreover, correlation analysis and statistical mediation models revealed that these functional alterations contributed to behavioural deficits in episodic, but again not semantic memory in patients. Altogether, our findings suggest that semantic processes rely on distributed neocortical networks, while episodic processes are supported by a network involving both the hippocampus and neocortex. Alterations of such networks can provide a compact signature of state-dependent reorganization in conditions associated with MTL damage, such as TLE.

Neural correlates of phonetic categorization under auditory (phoneme) and visual (grapheme) modalities.

We tested whether the neural mechanisms of phonetic categorization are specific to speech sounds or generalize to graphemes (i.e., visual letters) of the same phonetic label. Given that linguistic experience shapes categorical processing, and letter-speech sound matching plays a crucial role during early reading acquisition, we hypothesized sound phoneme and visual grapheme tokens representing the same linguistic identity might recruit common neural substrates, despite originating from different sensory modalities. Behavioral and neuroelectric brain responses (ERPs) were acquired as participants categorized stimuli from sound (phoneme) and homologous letter (grapheme) continua each spanning a /da/ - /ga/ gradient. Behaviorally, listeners were faster and showed stronger categorization of phoneme compared to graphemes. At the neural level, multidimensional scaling of the EEG revealed responses self-organized in a categorial fashion such that tokens clustered within their respective modality beginning ∼150-250 ms after stimulus onset. Source-resolved ERPs further revealed modality-specific and overlapping brain regions supporting phonetic categorization. Left inferior frontal gyrus and auditory cortex showed stronger responses for sound category members compared to phonetically ambiguous tokens, whereas early visual cortices paralleled this categorical organization for graphemes. Auditory and visual categorization also recruited common visual association areas in extrastriate cortex but in opposite hemispheres (auditory = left; visual=right). Our findings reveal both auditory and visual sensory cortex supports categorical organization for phonetic labels within their respective modalities. However, a partial overlap in phoneme and grapheme processing among occipital brain areas implies the presence of an isomorphic, domain-general mapping for phonetic categories in dorsal visual system.

Neural dynamics underlying minute-timescale persistent behavior in the human brain.

The ability to pursue long-term goals relies on a representations of task context that can both be maintained over long periods of time and switched flexibly when goals change. Little is known about the neural substrate for such minute-scale maintenance of task sets. Utilizing recordings in neurosurgical patients, we examined how groups of neurons in the human medial frontal cortex and hippocampus represent task contexts. When cued explicitly, task context was encoded in both brain areas and changed rapidly at task boundaries. Hippocampus exhibited a temporally dynamic code with fast decorrelation over time, preventing cross-temporal generalization. Medial frontal cortex exhibited a static code that decorrelated slowly, allowing generalization across minutes of time. When task context needed to be inferred as a latent variable, hippocampus encoded task context with a static code. These findings reveal two possible regimes for encoding minute-scale task-context representations that were engaged differently based on task demands.

The blushing brain: neural substrates of cheek temperature increase in response to self-observation.

Darwin proposed that blushing-the reddening of the face owing to heightened self-awareness-is 'the most human of all expressions'. Yet, relatively little is known about the underlying mechanisms of blushing. Theories diverge on whether it is a rapid, spontaneous emotional response that does not involve reflection upon the self or whether it results from higher-order socio-cognitive processes. Investigating the neural substrates of blushing can shed light on the mental processes underlying blushing and the mechanisms involved in self-awareness. To reveal neural activity associated with blushing, 16-20 year-old participants (n = 40) watched pre-recorded videos of themselves (versus other people as a control condition) singing karaoke in a magnetic resonance imaging scanner. We measured participants' cheek temperature increase-an indicator of blushing-and their brain activity. The results showed that blushing is higher when watching oneself versus others sing. Those who blushed more while watching themselves sing had, on average, higher activation in the cerebellum (lobule V) and the left paracentral lobe and exhibited more time-locked processing of the videos in early visual cortices. These findings show that blushing is associated with the activation of brain areas involved in emotional arousal, suggesting that it may occur independently of higher-order socio-cognitive processes. Our results provide new avenues for future research on self-awareness in infants and non-human animals.

Anterior cingulate cortex provides the neural substrates for feedback-driven iteration of decision and value representation

Adjusting decision-making under uncertain and dynamic situations is the hallmark of intelligence. It requires a system capable of converting feedback information to renew the internal value. The anterior cingulate cortex (ACC) involves in error and reward events that prompt switching or maintenance of current decision strategies. However, it is unclear whether and how the changes of stimulus-action mapping during behavioral adaptation are encoded, nor how such computation drives decision adaptation. Here, we tracked ACC activity in male mice performing go/no-go auditory discrimination tasks with manipulated stimulus-reward contingencies. Individual ACC neurons integrate the outcome information to the value representation in the next-run trials. Dynamic recruitment of them determines the learning rate of error-guided value iteration and decision adaptation, forming a non-linear feedback-driven updating system to secure the appropriate decision switch. Optogenetically suppressing ACC significantly slowed down feedback-driven decision switching without interfering with the execution of the established strategy.