Quantifying Population-level Neural Tuning Functions Using Ricker Wavelets and the Bayesian Bootstrap.

Experience changes the tuning of sensory neurons, including neurons in retinotopic visual cortex, as evident from work in humans and non-human animals. In human observers, visuo-cortical re-tuning has been studied during aversive generalization learning paradigms, in which the similarity of generalization stimuli (GSs) with a conditioned threat cue (CS+) is used to quantify tuning functions. This work utilized pre-defined tuning shapes reflecting prototypical generalization (Gaussian) and sharpening (Difference-of-Gaussians) patterns. This approach may constrain the ways in which re-tuning can be characterized, for example if tuning patterns do not match the prototypical functions or represent a mixture of functions. The present study proposes a flexible and data-driven method for precisely quantifying changes in neural tuning based on the Ricker wavelet function and the Bayesian bootstrap. The method is illustrated using data from a study in which university students (n = 31) performed an aversive generalization learning task. Oriented gray-scale gratings served as CS+ and GSs and a white noise served as the unconditioned stimulus (US). Acquisition and extinction of the aversive contingencies were examined, while steady-state visual event potentials (ssVEP) and alpha-band (8-13 Hz) power were measured from scalp EEG. Results showed that the Ricker wavelet model fitted the ssVEP and alpha-band data well. The pattern of re-tuning in ssVEP amplitude across the stimulus gradient resembled a generalization (Gaussian) shape in acquisition and a sharpening (Difference-of-Gaussian) shape in an extinction phase. As expected, the pattern of re-tuning in alpha-power took the form of a generalization shape in both phases. The Ricker-based approach led to greater Bayes factors and more interpretable results compared to prototypical tuning models. The results highlight the promise of the current method for capturing the precise nature of visuo-cortical tuning functions, unconstrained by the exact implementation of prototypical a-priori models.

Unpredictable threat increases early event-related potential amplitudes and cardiac acceleration: A brain-heart coupling study.

In the face of unpredictable threat, rapid processing of external events and behavioral mobilization through early psychophysiological responses are crucial for survival. While unpredictable threat generally enhances early processing, it would seem adaptive to particularly increase sensitivity for unexpected events as they may signal danger. To examine this possibility, n = 77 participants performed an auditory oddball paradigm and received unpredictable shocks in threat but not in safe contexts while a stream of frequent (standard) and infrequent (deviant) tones was presented. We assessed event-related potentials (ERP), heart period (HP), and time-lagged within-subject correlations of single-trial EEG and HP (cardio-EEG covariance tracing, CECT) time-locked to the tones. N1 and P2 ERP amplitudes were generally enhanced under threat. The P3 amplitude was enhanced to deviants versus standards and this effect was reduced in the threat condition. Regarding HP, both threat versus safe and unexpected versus expected tones led to stronger cardiac acceleration, suggesting separate effects of threat and stimulus expectancy on HP. Finally, CECTs revealed two correlation clusters, indicating that single-trial EEG magnitudes in the N1/P2 and P3 time-windows predicted subsequent cardiac acceleration. The current results show that an unpredictable threat context enhances N1 and P2 amplitudes and cardiac acceleration to benign auditory stimuli. They further suggest separable cortical correlates of different effects on cardiac activity: an early N1/P2 correlate associated with threat-effects on HP and a later P3 correlate associated with expectedness-effects. Finally, the results indicate that unpredictable threat attenuates rather than enhances the processing of unexpected benign events during the P3 latency.

Sustained selective attention to chromatic information enhances visuocortical gain at the population level.

Prior work in selective attention research has shown that colour-selective attention enhances neural activity in visuocortical areas sensitive to the attended colour while suppressing activity in areas sensitive to ignored colours. However, it is currently unclear whether this effect is limited to attending to specific colour hues or extends to chromatic information more broadly. To investigate this question, we used steady-state visual evoked potentials (ssVEPs) frequency tagging to quantify participants' visuocortical responses to specific elements embedded in arrays of flickering, randomly moving mid-complex patterns. Participants were instructed to attend to either coloured or greyscale patterns while ignoring the others. We found that attending to either coloured or greyscale patterns produced robust increases in ssVEP amplitudes both compared to ignored stimuli and to baseline. There was however no evidence of suppressed responses to ignored patterns. These findings demonstrate that attentional selection based on the presence or absence of chromatic information prompts selectively enhanced visuocortical processing but this selective amplification is not accompanied by suppression of unattended stimuli. Findings are consistent with theoretical notions that predict strong competition between specific exemplars within a given feature dimension, such as red or green, but weak competition between broadly defined stimulus categories, such as chromatic versus non-chromatic.

Feature-based Attentional Amplitude Modulations of the Steady-state Visual Evoked Potentials Reflect Blood Oxygen Level Dependent Changes in Feature-sensitive Visual Areas.

Recent EEG studies have investigated basic principles of feature-based attention by means of frequency-tagged random dot kinematograms in which different colors are simultaneously presented at different temporal frequencies to elicit steady-state visual evoked potentials (SSVEPs). These experiments consistently showed global facilitation of the to-be-attended random dot kinematogram-a basic principle of feature-based attention. SSVEP source estimation suggested that posterior visual cortex from V1 to area hMT+/V5 is broadly activated by frequency-tagged stimuli. What is presently unknown is whether the feature-based attentional facilitation of SSVEPs is a rather unspecific neural response including all visual areas that follow the "on/off," or whether SSVEP feature-based amplitude enhancements are driven by activity in visual areas most sensitive to a specific feature, such as V4v in the case of color. Here, we leverage multimodal SSVEP-fMRI recordings in human participants and a multidimensional feature-based attention paradigm to investigate this question. Attending to shape produced significantly greater SSVEP-BOLD covariation in primary visual cortex compared with color. SSVEP-BOLD covariation during color selection increased along the visual hierarchy, with greatest values in areas V3 and V4. Importantly, in area hMT+/V5, we found no differences between shape and color selection. Results suggest that SSVEP amplitude enhancements in feature-based attention is not an unspecific enhancement of neural activity in all visual areas following the "on/off." These findings open new avenues to investigating neural dynamics of competitive interactions in specific visual areas sensitive to a certain feature in a more economical way and better temporal resolution compared with fMRI.

Higher amplitudes in steady-state visual evoked potentials driven by square-wave versus sine-wave contrast modulation - A dual-laboratory study.

Steady-state visual evoked potentials (ssVEPs) are an established tool for assessing visuocortical responses in visual perception and attention. They have the same temporal frequency characteristics as a periodically modulated stimulus (e.g., in contrast or luminance) that drives them. It has been hypothesized that the amplitude of a given ssVEP may depend on the shape of the stimulus modulation function, but the size and robustness of these effects is not well established. The current study systematically compared the effect of the two most common functions in the ssVEP literature, square-wave and sine-wave functions. Across two laboratories, we presented mid-complex color patterns to 30 participants with square-wave or sine-wave contrast modulation and at different driving frequencies (6 Hz, 8.57 Hz, 15 Hz). When ssVEPs were analyzed independently for the samples, with each laboratory's standard processing pipeline, ssVEP amplitudes in both samples decreased at higher driving frequencies and square-wave modulation evoked higher amplitudes at lower frequencies (i.e., 6 Hz, 8.57 Hz) compared to sine-wave modulation. These effects were replicated when samples were aggregated and analyzed with the same processing pipeline. In addition, when using signal-to-noise ratios as outcome measures, this joint analysis indicated a somewhat weaker effect of increased ssVEP amplitudes to square-wave modulation at 15 Hz. The present study suggests that square-wave modulation should be used in ssVEP research when the goal is to maximize signal amplitude or signal-to-noise ratio. Given effects of modulation function across laboratories, and data processing pipelines, the findings appear robust to differences in data collection and analysis.

Using expectation violation models to improve the outcome of psychological treatments.

Expectations are a central maintaining mechanism in mental disorders and most psychological treatments aim to directly or indirectly modify clinically relevant expectations. Therefore, it is crucial to examine why patients with mental disorders maintain dysfunctional expectations, even in light of disconfirming evidence, and how expectation-violating situations should be created in treatment settings to optimize treatment outcome and reduce the risk of treatment failures. The different psychological subdisciplines offer various approaches for understanding the underlying mechanisms of expectation development, persistence, and change. Here, we convey recommendations on how to improve psychological treatments by considering these different perspectives. Based on our expectation violation model, we argue that the outcome of expectation violation depends on several characteristics: features of the expectation-violating situation; the dynamics between the magnitude of expectation violation and cognitive immunization processes; dealing with uncertainties during and after expectation change; controlled and automatic attention processes; and the costs of expectation changes. Personality factors further add to predict outcomes and may offer a basis for personalized treatment planning. We conclude with a list of recommendations derived from basic psychology that could contribute to improved treatment outcome and to reduced risks of treatment failures.

Alpha-2 Adrenoreceptor Antagonist Yohimbine Potentiates Consolidation of Conditioned Fear.

BACKGROUND: Hyperconsolidation of aversive associations and poor extinction learning have been hypothesized to be crucial in the acquisition of pathological fear. Previous animal and human research points to the potential role of the catecholaminergic system, particularly noradrenaline and dopamine, in acquiring emotional memories. Here, we investigated in a between-participants design with 3 groups whether the noradrenergic alpha-2 adrenoreceptor antagonist yohimbine and the dopaminergic D2-receptor antagonist sulpiride modulate long-term fear conditioning and extinction in humans. METHODS: Fifty-five healthy male students were recruited. The final sample consisted of n = 51 participants who were explicitly aware of the contingencies between conditioned stimuli (CS) and unconditioned stimuli after fear acquisition. The participants were then randomly assigned to 1 of the 3 groups and received either yohimbine (10 mg, n = 17), sulpiride (200 mg, n = 16), or placebo (n = 18) between fear acquisition and extinction. Recall of conditioned (non-extinguished CS+ vs CS-) and extinguished fear (extinguished CS+ vs CS-) was assessed 1 day later, and a 64-channel electroencephalogram was recorded. RESULTS: The yohimbine group showed increased salivary alpha-amylase activity, confirming a successful manipulation of central noradrenergic release. Elevated fear-conditioned bradycardia and larger differential amplitudes of the N170 and late positive potential components in the event-related brain potential indicated that yohimbine treatment (compared with a placebo and sulpiride) enhanced fear recall during day 2. CONCLUSIONS: These results suggest that yohimbine potentiates cardiac and central electrophysiological signatures of fear memory consolidation. They thereby elucidate the key role of noradrenaline in strengthening the consolidation of conditioned fear associations, which may be a key mechanism in the etiology of fear-related disorders.

A Revised Framework for the Investigation of Expectation Update Versus Maintenance in the Context of Expectation Violations: The ViolEx 2.0 Model.

Expectations are probabilistic beliefs about the future that shape and influence our perception, affect, cognition, and behavior in many contexts. This makes expectations a highly relevant concept across basic and applied psychological disciplines. When expectations are confirmed or violated, individuals can respond by either updating or maintaining their prior expectations in light of the new evidence. Moreover, proactive and reactive behavior can change the probability with which individuals encounter expectation confirmations or violations. The investigation of predictors and mechanisms underlying expectation update and maintenance has been approached from many research perspectives. However, in many instances there has been little exchange between different research fields. To further advance research on expectations and expectation violations, collaborative efforts across different disciplines in psychology, cognitive (neuro)science, and other life sciences are warranted. For fostering and facilitating such efforts, we introduce the ViolEx 2.0 model, a revised framework for interdisciplinary research on cognitive and behavioral mechanisms of expectation update and maintenance in the context of expectation violations. To support different goals and stages in interdisciplinary exchange, the ViolEx 2.0 model features three model levels with varying degrees of specificity in order to address questions about the research synopsis, central concepts, or functional processes and relationships, respectively. The framework can be applied to different research fields and has high potential for guiding collaborative research efforts in expectation research.

Why expectations do or do not change after expectation violation: A comparison of seven models.

Individuals are often confronted with events that violate their expectations, but disconfirming evidence does not always lead to expectation change. We review seven theoretical models on how individuals cope with disconfirming expectations: associative learning theories, the ViolEx Model, the model of coping with expectation disconfirmation (Roese & Sherman, 2007), the Meaning Maintenance Model, the Predictive Processing Framework, Expectancy Violations Theory, and the Expectation-Disconfirmation Model of consumer satisfaction. We focus on the proposed processes that relate to persistence or change of expectations. We discuss similarities and differences between the models. Three core coping processes are identified across most of these models - minimization of the importance of expectation-disconfirming evidence, search for/production of future expectation-confirming evidence, and expectation change. Suggestions for refinements and extensions of the models as well as for future empirical work on model testing are drawn.

Extinction-resistant attention to long-term conditioned threat is indexed by selective visuocortical alpha suppression in humans.

Previous electrophysiological studies in humans have shown rapid modulations of visual attention after conditioned threat vs. safety cues (<500 ms post-stimulus), but it is unknown whether this attentional prioritization is sustained throughout later time windows and whether it is robust to extinction. To investigate sustained visual attention, we assessed visuocortical alpha suppression in response to conditioned and extinguished threat. We reanalysed data from N = 87 male participants that had shown successful long-term threat conditioning and extinction in self reports and physiological measures in a two-day conditioning paradigm. The current EEG time-frequency analyses on recall test data on Day 2 revealed that previously threat-conditioned vs. safety cues evoked stronger occipital alpha power suppression from 600 to 1200 ms. Notably, this suppression was resistant to previous extinction. The present study showed for the first time that threat conditioning enhances sustained modulation of visuocortical attention to threat in the long term. Long-term stability and extinction resistance of alpha suppression suggest a crucial role of visuocortical attention mechanisms in the maintenance of learned fears.

Aversive Imagery Causes De Novo Fear Conditioning.

In classical fear conditioning, neutral conditioned stimuli that have been paired with aversive physical unconditioned stimuli eventually trigger fear responses. Here, we tested whether aversive mental images systematically paired with a conditioned stimulus also cause de novo fear learning in the absence of any external aversive stimulation. In two experiments (N = 45 and N = 41), participants were first trained to produce aversive, neutral, or no imagery in response to three different visual-imagery cues. In a subsequent imagery-based differential-conditioning paradigm, each of the three cues systematically coterminated with one of three different neutral faces. Although the face that was paired with the aversive-imagery cue was never paired with aversive external stimuli or threat-related instructions, participants rated it as more arousing, unpleasant, and threatening and displayed relative fear bradycardia and fear-potentiated startle. These results could be relevant for the development of fear and related disorders without trauma.

Fear Extinction Recall Modulates Human Frontomedial Theta and Amygdala Activity.

Human functional magnetic resonance imaging (fMRI) and electroencephalography (EEG) studies, as well as animal studies, indicate that the amygdala and frontomedial brain regions are critically involved in conditioned fear and that frontomedial oscillations in the theta range (4-8 Hz) may support communication between these brain regions. However, few studies have used a multimodal approach to probe interactions among these key regions in humans. Here, our goal was to bridge the gap between prior human fMRI, EEG, and animal findings. Using simultaneous EEG-fMRI recordings 24 h after fear conditioning and extinction, conditioned stimuli presented (CS+E, CS-E) and not presented during extinction (CS+N, CS-N) were compared to identify effects specific to extinction versus fear recall. Differential (CS+ vs. CS-) electrodermal, frontomedial theta (EEG) and amygdala responses (fMRI) were reduced for extinguished versus nonextinguished stimuli. Importantly, effects on theta power covaried with effects on amygdala activation. Fear and extinction recall as indicated by theta explained 60% of the variance for the analogous effect in the right amygdala. Our findings show for the first time the interplay of amygdala and frontomedial theta activity during fear and extinction recall in humans and provide insight into neural circuits consistently linked with top-down amygdala modulation in rodents.

Fearfulness, neuroticism/anxiety, and COMT Val158Met in long-term fear conditioning and extinction.

Individual differences in long-term stability of fear memories are of potential relevance for stable dispositions related to threat processing, such as neuroticism/anxiety and fearfulness. As previous research suggests a prominent role of dopamine for the retention of conditioned and extinguished fear, dopaminergic gene polymorphisms may also relate to individual differences in fear stability. While the COMT Val158Met polymorphism causes individual differences in prefrontal dopamine, its associations with human long-term fear extinction are currently unknown. Here, n = 30/29/28 healthy male Val/Val, Val/Met and Met/Met carriers, respectively, underwent a two-day differential conditioning paradigm with fear acquisition and extinction on Day 1 and a recall test on Day 2 with recordings of EEG and ECG. Fearfulness but not neuroticism/anxiety predicted fear bradycardia (i.e., heart period slowing) during Day 1 fear acquisition while it did not affect extinction or Day 2 fear recall. In contrast, COMT Val158Met significantly modulated Day 2 fear recall as evident in fear bradycardia and Late Positive Potential (LPP) amplitudes while it did not affect Day 1 fear or extinction learning. Furthermore, exploratory analyses revealed that individual differences in fear bradycardia during Day 2 extinction recall depended on Day 1 extinction success. Importantly, this contingency was (a) modulated by COMT Val158Met and (b) significantly reduced in high vs. low neuroticism/anxiety. The present study indicates that (a) individual differences in dopaminergic genotypes may affect the long-term stability of fear memories and (b) fearfulness vs. neuroticism/anxiety might play distinct roles in initial fear reactions vs. long-term stability of fear memories, respectively.

Reliability and robustness of feedback-evoked brain-heart coupling after placebo, dopamine, and noradrenaline challenge.

External and internal performance feedback triggers not only neural but also cardiac modulations, suggesting communication between brain and heart during feedback processing. Using Cardio-Electroencephalographic Covariance Tracing (CECT), it has accordingly been shown that feedback-evoked centromedial single-trial EEG at the P300 latency intraindividually predicts subsequent changes in heart period - the so called N300H phenomenon. While previous findings suggest that the N300H depends on serotonin, its relationship to central dopamine and noradrenaline is currently unknown. Here, we tested (1) the psychometric properties of this CECT-based component and (2) its putative catecholaminergic mechanisms. N = 54 healthy male participants received either a α2-adrenoceptor antagonist (yohimbine, 10 mg; n = 18), D2-dopamine-receptor antagonist (sulpiride, 200 mg; n = 18), or a placebo (n = 18). Afterwards, they performed a gambling task with feedback after each trial, while EEG and ECG were recorded. Feedback successfully evoked a significant N300H both across all 54 participants and within each substance group. Importantly, we show that N300H can be reliably measured in a priori defined time windows with as few as 240 feedback trials and is relatively unaffected when removing extreme single-trial values. However, we could not find any significant substance effects on N300H magnitude as well as on univariate feedback-related measures (FRN, P300, heart period). Altogether, the N300H component proves as a robust and reliable marker of cortico-cardiac coupling evoked by feedback. Furthermore, these findings suggest a subordinate role of catecholamines (i.e., noradrenaline and dopamine) and sympathetic pathways in feedback-evoked brain-heart communication as measured with N300H.

A pragmatic comparison of noise burst and electric shock unconditioned stimuli for fear conditioning research with many trials.

Several methods that are promising for studying the neurophysiology of fear conditioning (e.g., EEG, MEG) require a high number of trials to achieve an adequate signal-to-noise ratio. While electric shock and white noise burst are among the most commonly used unconditioned stimuli (US) in conventional fear conditioning studies with few trials, it is unknown whether these stimuli are equally well suited for paradigms with many trials. Here, N = 32 participants underwent a 260-trial differential fear conditioning and extinction paradigm with a 240-trial recall test 24 h later and neutral faces as conditioned stimuli. In a between-subjects design, either white noise bursts (n = 16) or electric shocks (n = 16) served as US, and intensities were determined using the most common procedure for each US (i.e., a fixed 95 dB noise burst and a work-up procedure for electric shocks, respectively). In addition to differing US types, groups also differed in closely linked US-associated characteristics (e.g., calibration methods, stimulus intensities, timing). Subjective ratings (arousal/valence), skin conductance, and evoked heart period changes (i.e., fear bradycardia) indicated more reliable, extinction-resistant, and stable conditioning in the white noise burst versus electric shock group. In fear conditioning experiments where many trials are presented, white noise burst should serve as US.

Conditioned and extinguished fear modulate functional corticocardiac coupling in humans.

Although the conditioned cardiac fear response is an important index of psychophysiological fear processing, underlying neural mechanisms remain unclear. N = 22 participants underwent differential fear conditioning and extinction with face pictures as conditioned stimuli (CS) and loud noise bursts as aversive unconditioned stimulus (US) on Day 1 and a recall test 1 day later. We assessed ERPs, evoked heart period (HP), and time-lagged within-subject correlations of single-trial EEG amplitude and HP as index for corticocardiac coupling in response to the CS. Fear-conditioned stimuli (CS+) triggered cardiac deceleration during fear acquisition and recall. Meanwhile, only during Day 1 acquisition, CS+ evoked larger late positivities in the ERP than CS-. Most importantly, during Day 2 recall, stimulus-evoked single-trial EEG responses in the time window between 250 and 500 ms predicted the magnitude of cardiac fear responses 2 to 5 s later. This marker of corticocardiac coupling selectively emerged in response to not previously extinguished CS+ but was absent in response to CS- or previously extinguished CS+. The present results provide first evidence that fear conditioning and extinction modulate functional corticocardiac coupling in humans. Underlying mechanisms may involve subcortical structures enhancing corticocardiac transmission to facilitate processing of consolidated conditioned fear.

Prefrontal oscillations during recall of conditioned and extinguished fear in humans.

Human neuroimaging studies indicate that the anterior midcingulate cortex (AMC) and the ventromedial prefrontal cortex (vmPFC) play important roles in the expression and extinction of fear, respectively. Electrophysiological rodent studies further indicate that oscillatory neuronal activity in homolog regions (i.e., prelimbic and infralimbic cortices) changes during fear expression and fear extinction recall. Whether similar processes occur in humans remains largely unexplored. By assessing scalp surface EEG in conjunction with LORETA source estimation of CS-related theta and gamma activity, we tested whether a priori defined ROIs in the human AMC and vmPFC similarly modulate their oscillatory activity during fear expression and extinction recall, respectively. To this end, 42 healthy individuals underwent a differential conditioning/differential extinction protocol with a Recall Test on the next day. In the Recall Test, nonextinguished versus extinguished stimuli evoked an increased differential (CS(+) vs CS(-)) response with regard to skin conductance and AMC-localized theta power. Conversely, extinguished versus nonextinguished stimuli evoked an increased differential response with regard to vmPFC-localized gamma power. Finally, individuals who failed to show a suppressed skin conductance response to the extinguished versus nonextinguished CS(+) also failed to show the otherwise observed alterations in vmPFC gamma power to extinguished CS(+). These results indicate that fear expression is associated with AMC theta activity, whereas successful fear extinction recall relates to changes in vmPFC gamma activity. The present work thereby bridges findings from prior rodent electrophysiological research and human neuroimaging studies and indicates that EEG is a valuable tool for future fear extinction research.

Panic disorder and serotonin reuptake inhibitors predict coupling of cortical and cardiac activity.

Panic attacks, the cardinal symptom of panic disorder (PD), are characterized by intense physiological reactions including accelerated heart activity. Although cortical processes are thought to trigger and potentiate panic attacks, it is unknown whether individuals with PD have a general tendency to show elevated cortico-cardiac interactions, which could predispose them for brain-driven modulations of heart activity during panic. Consistent with this hypothesis, serotonin, a highly relevant neurotransmitter for panic and PD presumably affects the cortical control of the heart. The current study thus aimed to test whether PD and serotonin reuptake inhibitor (SRI) intake are related to cortico-cardiac interactions in the absence of acute panic. Human participants with PD (N=22), major depression (MD, clinical control group, N=21) or no psychiatric diagnosis (healthy control group, N=23) performed a gambling task. To measure cortico-cardiac coupling, the within-subject covariation of single-trial EEG after feedback presentation and subsequent changes in heart period was determined. As in prior studies, there was a significant time-lagged covariation of EEG and heart activity indicating that trial-by-trial fluctuations of feedback-evoked EEG amplitude determined how much heart activity accelerated seconds later. Importantly, this covariation pattern was significantly potentiated in PD vs control participants. Moreover, concurrent SRI intake further augmented brain-heart covariation in individuals with PD and MD. The present findings demonstrate that PD and serotonin are associated with altered brain-heart interactions in a non-panic situation. Future work should clarify whether brain-heart coupling has a causal role in PD, for example by facilitating panic attacks.

Brain-heart coupling at the P300 latency is linked to anterior cingulate cortex and insula--a cardio-electroencephalographic covariance tracing study.

Prior work on the coupling of cortical and cardiac responses to feedback demonstrated that feedback-evoked single-trial EEG magnitudes 300 ms post-stimulus predict the degree of subsequent cardiac acceleration. The main goal of the current study was to explore the neural sources of this phenomenon using (a) independent component analysis in conjunction with dipole fitting and (b) low resolution electromagnetic tomography (LORETA) in N=14 participants who performed a gambling task with feedback presented after each trial. It was shown that independent components localized near anterior cingulate cortex produced robust within-subjects correlations with feedback-evoked heart-period, suggesting that anterior cingulate cortex activity 300ms after feedback presentation predicts the strength of subsequent cardiac acceleration. Moreover, interindividual differences in evoked left insular cortex LORETA-estimated activity at around 300ms moderated within-subjects EEG-heart period correlations. These results suggest that key regions of central autonomic control are involved in cortico-cardiac coupling evoked by feedback stimuli.