Medial Frontal Cortex Research Articles

Multimodal single-neuron, intracranial EEG, and fMRI brain responses during movie watching in human patients

We present a multimodal dataset of intracranial recordings, fMRI, and eye tracking in 20 participants during movie watching. Recordings consist of single neurons, local field potential, and intracranial EEG activity acquired from depth electrodes targeting the amygdala, hippocampus, and medial frontal cortex implanted for monitoring of epileptic seizures. Participants watched an 8-min long excerpt from the video “Bang! You’re Dead” and performed a recognition memory test for movie content. 3 T fMRI activity was recorded prior to surgery in 11 of these participants while performing the same task. This NWB- and BIDS-formatted dataset includes spike times, field potential activity, behavior, eye tracking, electrode locations, demographics, and functional and structural MRI scans. For technical validation, we provide signal quality metrics, assess eye tracking quality, behavior, the tuning of cells and high-frequency broadband power field potentials to familiarity and event boundaries, and show brain-wide inter-subject correlations for fMRI. This dataset will facilitate the investigation of brain activity during movie watching, recognition memory, and the neural basis of the fMRI-BOLD signal.

The date/delay effect in intertemporal choice: A combined fMRI and eye-tracking study.

Temporal discounting, the tendency to devalue future rewards as a function of delay until receipt, is influenced by time framing. Specifically, discount rates are shallower when the time at which the reward is received is presented as a date (date condition; e.g., June 8, 2023) rather than in delay units (delay condition; e.g., 30 days), which is commonly referred to as the date/delay effect. However, the cognitive and neural mechanisms of this effect are not well understood. Here, we examined the date/delay effect by analysing combined fMRI and eye-tracking data of N = 31 participants completing a temporal discounting task in both a delay and a date condition. The results confirmed the date/delay effect and revealed that the date condition led to higher fixation durations on time attributes and to higher activity in precuneus/PCC and angular gyrus, that is, areas previously associated with episodic thinking. Additionally, participants made more comparative eye movements in the date compared to the delay condition. A lower date/delay effect was associated with higher prefrontal activity in the date > delay contrast, suggesting that higher control or arithmetic operations may reduce the date/delay effect. Our findings are in line with hypotheses positing that the date condition is associated with differential time estimation and the use of more comparative as opposed to integrative choice strategies. Specifically, higher activity in memory-related brain areas suggests that the date condition leads to higher perceived proximity of delayed rewards, while higher frontal activity (middle/superior frontal gyrus, posterior medial frontal cortex, cingulate) in participants with a lower date/delay effect suggests that the effect is particularly pronounced in participants avoiding complex arithmetic operations in the date condition.

EEG-based major depressive disorder recognition by neural oscillation and asymmetry.

Major Depressive Disorder (MDD) is a pervasive mental health issue with significant diagnostic challenges. Electroencephalography (EEG) offers a non-invasive window into the neural dynamics associated with MDD, yet the diagnostic efficacy is contingent upon the appropriate selection of EEG features and brain regions. In this study, resting-state EEG signals from both eyes-closed and eyes-open conditions were analyzed. We examined band power across various brain regions, assessed the asymmetry of band power between the hemispheres, and integrated these features with clinical characteristics of MDD into a diagnostic regression model. Regression analysis found significant predictors of MDD to be beta2 (16-24 Hz) power in the Prefrontal Cortex (PFC) with eyes open (B = 20.092, p = 0.011), beta3 (24-40 Hz) power in the Medial Occipital Cortex (MOC) (B = -12.050, p < 0.001), and beta2 power in the Right Medial Frontal Cortex (RMFC) with eyes closed (B = 24.227, p < 0.001). Asymmetries in beta1 (12-16 Hz) power with eyes open (B = 28.047, p = 0.018), and in alpha (8-12 Hz, B = 9.004, p = 0.013) and theta (4-8 Hz, B = -13.582, p = 0.008) with eyes closed were also significant predictors. The study confirms the potential of multi-region EEG analysis in improving the diagnostic precision for MDD. By including both neurophysiological and clinical data, we present a more robust approach to understanding and identifying this complex disorder. The research is limited by the sample size and the inherent variability in EEG signal interpretation. Future studies with larger cohorts and advanced analytical techniques are warranted to validate and refine these findings.

A neuroanatomical and cognitive model of impaired social behaviour in frontotemporal dementia.

Impaired social cognition is a core deficit in frontotemporal dementia (FTD). It is most commonly associated with the behavioural-variant of FTD, with atrophy of the orbitofrontal and ventromedial prefrontal cortex. Social cognitive changes are also common in semantic dementia, with atrophy centred on the anterior temporal lobes. The impairment of social behaviour in FTD has typically been attributed to damage to the orbitofrontal cortex and/or temporal poles and/or the uncinate fasciculus that connects them. However, the relative contributions of each region are unresolved. In this review, we present a unified neurocognitive model of controlled social behaviour that not only explains the observed impairment of social behaviours in FTD, but also assimilates both consistent and potentially contradictory findings from other patient groups, comparative neurology and normative cognitive neuroscience. We propose that impaired social behaviour results from damage to two cognitively- and anatomically-distinct components. The first component is social-semantic knowledge, a part of the general semantic-conceptual system supported by the anterior temporal lobes bilaterally. The second component is social control, supported by the orbitofrontal cortex, medial frontal cortex and ventrolateral frontal cortex, which interacts with social-semantic knowledge to guide and shape social behaviour.

Dual-Process Theory of Thought and Inhibitory Control: An ALE Meta-Analysis.

The dual-process theory of thought rests on the co-existence of two different thinking modalities: a quick, automatic, and associative process opposed to a slow, thoughtful, and deliberative process. The increasing interest in determining the neural foundation of the dual-process distinction has yielded mixed results, also given the difficulty of applying the fMRI standard approach to tasks usually employed in the cognitive literature. We report an activation likelihood estimation (ALE) meta-analysis to investigate the neural foundation of the dual-process theory of thought. Eligible studies allowed for the identification of cerebral areas associated with dual-process theory-based tasks without differentiating between fast and slow thinking. The ALE algorithm converged on the medial frontal cortex, superior frontal cortex, anterior cingulate cortex, insula, and left inferior frontal gyrus. These structures partially overlap with the cerebral areas recurrently reported in the literature about the neural basis of the dual-process distinction, where the PARCS theory-based interpretation emphasizes the role of the right inferior gyrus. The results confirm the potential (but still almost unexplored) common ground between the dual-process literature and the cognitive control literature.

Amygdala structure and function and its associations with social-emotional outcomes in a low-risk preterm sample

Amygdala atypical volume development and functional connectivity (FC) at small gestational ages (GA) have been found across childhood. This adult-oriented study assesses whether altered amygdala structure and function is present following low-risk preterm birth. T1-weighted and resting-state functional MRI images of 33 low-risk preterm (30–36 weeks’ GA) and 29 full-term (37–42 weeks’ GA) young adults of both sexes, aged between 20 and 32 years old, were analyzed using FreeSurfer (v6.0.0) and Coon Toolbox (v21.a). The social-emotional assessment included Happé’s Strange Stories Test, the Moral Judgment Test, Delay-Discounting Test, Adult Self Report, and Emotion Regulation Questionnaire. No differences were found in social-emotional outcomes or amygdala volumes between the groups. Low-risk preterm young adults showed increased FC between the left amygdala, right amygdala and medial frontal cortex (MedFC) (F = 9.89, p-FWE = 0.009) at cluster level compared to their full-term peers. However, significant results at connection level were not observed between left and right amygdala. Lastly, increased FC at cluster level between the right amygdala and MedFC, and left amygdala and MedFC, was related to better social-emotional outcomes only in low-risk preterm young adults (F = 6.60, p-FWE = 0.036) at cluster level. At connection level, in contrast, only right amygdala–MedFC increased FC was significantly associated with better social-emotional outcomes. This study reveals that low-risk prematurity does not have an effect on social-emotional outcomes or structural amygdala volumes during young adulthood. However, individuals who were considered to be at a lower risk of exhibiting neurodevelopmental alterations following preterm birth demonstrated increased FC between the left and right amygdala and MedFC.

GABAergic imbalance in Parkinson’s disease–related depression determined with MEGA-PRESS

ObjectiveThe pathogenesis of depression in patients with Parkinson’s disease (PD) is poorly understood. Therefore, this study aimed to explore the changes in γ-aminobutyric acid (GABA) and glutamate plus glutamine (Glx) levels in patients with PD with or without depression determined using MEscher-GArwood Point Resolved Spectroscopy (MEGA-PRESS). Materials and methodsA total of 83 patients with primary PD and 24 healthy controls were included. Patients with PD were categorized into depressed PD (DPD, n = 19) and nondepressed PD (NDPD, n = 64) based on the 17-item Hamilton Depression Rating Scale. All participants underwent T1-weighted imaging and MEGA-PRESS sequence to acquire GABA+ and Glx values. The MEGA-PRESS sequence was conducted using 18.48 mL voxels in the left thalamus and medial frontal cortex. The GABA+, Glx, and creatine values were quantified using Gannet 3.1 software. ResultsThe GABA+ and Glx values were not significantly disparate between patients with PD and controls in the thalamus and medial frontal cortex. However, the levels of N-acetyl aspartate/creatine and choline/creatine in the left thalamus were significantly lower in patients with PD than in controls (P = .031, P = .009). The GABA+/Water and GABA+/Creatine in the medial frontal cortex were higher in DPD than in NDPD (P = .001, P = .004). The effects of depression on Glx or other metabolite levels were not evident, and no significant difference in metabolite values was noted in the left thalamus among all groups (P > .05). ConclusionsGABA+ levels increased in the medial frontal cortex in DPD, which may be more closely related to depressive pathology. Thus, alterations in GABAergic function in special brain structures may be related to the clinical manifestations of PD symptoms, and hence mediating this function might help in treating depression in PD.

Common and distinct BOLD correlates of Simon and flanker conflicts which can(not) be reduced to time-on-task effects.

The ability to identify and resolve conflicts between standard, well-trained behaviors and behaviors required by the current context is an essential feature of cognitive control. To date, no consensus has been reached on the brain mechanisms involved in exerting such control: while some studies identified diverse patterns of activity across different conflicts, other studies reported common resources across conflict tasks or even across simple tasks devoid of the conflict component. The latter reports attributed the entire activity observed in the presence of conflict to longer time spent on the task (i.e., to the so-called time-on-task effects). Here, we used an extended Multi-Source Interference Task (MSIT) which combines Simon and flanker types of interference to determine shared and conflict-specific mechanisms of conflict resolution in fMRI and their separability from the time-on-task effects. Large portions of the activity in the dorsal attention network and decreases of activity in the default mode network were shared across the tasks and scaled in parallel with increasing reaction times. Importantly, the activity in the sensory and sensorimotor cortices, as well as in the posterior medial frontal cortex (pMFC) - a key region implicated in conflict processing - could not be exhaustively explained by the time-on-task effects.

Frontal and anterior temporal hypometabolism post chemoradiation in head and neck cancer: A real-world PET study.

Adverse neurological effects after cancer therapy are common, but biomarkers to diagnose, monitor, or risk stratify patients are still not validated or used clinically. An accessible imaging method, such as fluorodeoxyglucose positron emission tomography (FDG PET) of the brain, could meet this gap and serve as a biomarker for functional brain changes. We utilized FDG PET to evaluate which brain regions are most susceptible to altered glucose metabolism after chemoradiation in patients with head and neck cancer (HNCa). Real-world FDG PET images were acquired as standard of care before and after chemoradiation for HNCa in 68 patients. Linear mixed-effects voxelwise models assessed changes after chemoradiation in cerebral glucose metabolism quantified with standardized uptake value ratio (SUVR), covarying for follow-up time and patient demographics. Voxelwise analysis revealed two large clusters of decreased glucose metabolism in the medial frontal and polar temporal cortices following chemoradiation, with decreases of approximately 5% SUVR after therapy. These findings provide evidence that standard chemoradiation for HNCa can lead to decreased neuronal glucose metabolism, contributing to literature emphasizing the vulnerability of the frontal and anterior temporal lobes, especially in HNCa, where these areas may be particularly vulnerable to indirect radiation-induced injury. FDG PET shows promise as a sensitive biomarker for assessing these changes.

Volumetric brain assessment of long-term head and neck cancer survivors

BackgroundRadiation therapy (RT) for locally advanced head and neck cancer (HNC) often exposes subcortical brain structures to radiation. We performed this study to assess region-specific brain volumetrics in a population of long term HNC survivors. Methods and MaterialsForty HNC survivors were enrolled at a mean of 6.4 years from completion of RT. Patients underwent a research MRI protocol that included a 3D T1- weighted whole-brain scan on a 3 Tesla MRI scanner. Voxel based morphometry was performed using the Computational Anatomy Toolbox with the Neuromorphometrics atlas. Healthy controls from the Human Connectome Project were used as a comparison cohort. Study participants also completed a comprehensive neurocognitive assessment. ResultsThe final study cohort consisted of 38 participants after excluding 2 participants due to image quality. HNC survivors displayed widespread reduction in gray matter (GM) brain region volumes that included bilateral medial frontal cortex, temporal lobe, hippocampus, supplemental motor area, and cerebellum. Greater radiation exposure was associated with reduced GM volume in the left ventral diencephalon (r = -0.512, p = 0.003). Associations between cognition and regional GM volumes were identified for motor coordination and bilateral cerebellum (left, r = 0.444, p = 0.009; right, r = 0.372, p = 0.030), confrontation naming and left amygdala (r = 0.382, p = 0.026), verbal memory and bilateral thalamus (left, r = 0.435, p = 0.010; right, r = 0.424, p = 0.012), right amygdala (r = 0.339, p = 0.050), and right putamen (r = 0.364, p = 0.034). ConclusionsReductions in GM were observed within this cohort of primarily non-nasopharyngeal HNC survivors as compared to a control sample. GM volumes were associated with performance in multiple cognitive domains. Results of this exploratory study support the need for investigation of anatomic brain changes as an important translational corollary to cognitive problems among HNC survivors.

Neuromodulation of choice-induced preference changes: the tDCS study of cognitive dissonance.

Difficult choices between two equally attractive options result in a cognitive discrepancy between dissonant cognitions such as preferences and actions often followed by a sense of psychological discomfort known as cognitive dissonance. It can lead to changes in the desirability of options: the chosen option becomes more desirable, whereas the rejected option is devalued. Despite the ample experimental evidence to show this effect, the neural mechanisms and timing of such choice-induced preference changes are not fully understood. In this study, we used transcranial direct current stimulation (tDCS) to modulate the activity of the posterior medial frontal cortex (pMFC), which has been associated with conflict monitoring and choice-induced preference changes in neuroimaging studies. Prior to a revised version of Brehm's free-choice paradigm, participants in two experiments underwent cathodal (inhibitory) or anodal (excitatory) tDCS of the pMFC compared to sham (placebo) stimulation prior to the choice phase. Our results showed that cathodal tDCS significantly decreased the choice-induced preference change relative to a sham, but only in direct comparisons of rejected options. No significant effect of anodal tDCS in comparison with sham was observed. This study replicates the general behavioral effect of cognitive dissonance and provide partial support for the theory of the pMFC contribution to choice-related cognitive dissonance and subsequent preference changes, with possible limitations of an under-sampling for the obtained effect size and an asymmetry in the inhibitory-excitatory effects of non-invasive tDCS.

Neurophysiological mechanisms of exploration and exploitation in high-functioning autism: Magnetoencephalographic study

Intolerance of uncertainty and high sensitivity to the threat of failure are believed to contribute to chronic anxiety in individuals with high-functioning autism. This study examines the influence of these personality traits on the brain processes involved in decision-making in a probabilistic setting among autism patients. Furthermore, we explore the causal relationship between these personality traits and chronic anxiety in individuals with high-functioning autism. Twenty-one high-functioning autistic individuals who are intolerant to uncertainty, aged 19 to 46, and 21 neurotypical volunteers of the same age, carried out a probabilistic choice experiment with two alternatives. One option yielded a monetary profit of 70% of the time, while the other brought only a 30% gain. Following each selection, the subjects received feedback on their decision and gradually learned, through trial and error, to prefer the more advantageous option. From this point forward, we consider frequent selections of a beneficial stimulus to align with the internal utility model, specifically the exploitation strategy. On the other hand, sporadic choices of a detrimental stimulus correspond to an exploration strategy, which may prove disadvantageous in a stable environment but enables adaptation to unforeseen changes in the surroundings. We hypothesized that there are characteristic differences in brain activity reflecting exploration and exploitation strategies between groups, which would emerge during the decision-making period and after internal feedback evaluation regarding advantageous and disadvantageous choices [1]. Beta oscillations (16–30 Hz) were analyzed in the magnetoencephalographic recordings. The decrease in beta oscillation power below baseline during the period between stimulus presentation and subjects’ response indicates activation in brain regions related to decision-making strategy. Conversely, an increase in beta oscillation power following feedback signaling a disadvantageous choice reflects a mechanism that reinforces internal value models in current task conditions [1]. The cortical sources of beta oscillations in 448 cortical areas were estimated using the sLoreta technique at the single-trial level. Mixed linear models (LMM) were used for statistical analysis with correction for multiple comparisons via the FDR method for the number of cortical areas analyzed. The study concentrated on the time interval for decision-making (–900 to –300 ms prior to the motor action of choice) and the post-feedback period (500 to 900 ms after the commencement of the feedback presentation) [1]. Based on questionnaire results, individuals with high-functioning autism exhibited a significantly lower tolerance for uncertainty and a greater intolerance for uncertainty when compared to neurotypical participants. The study generated two primary findings. Initially, the extent of brain activity during decision-making differed in control subjects and subjects with autism based on the type of choice, with exact opposition. Opting for an advantageous vs. disadvantageous choice was linked with reduced activation of the inferior temporal, parietal, and medial frontal cortex regions in control subjects and elevated activation in these regions for subjects with autism spectrum disorder. These findings suggest that neurotypical individuals utilize fewer neural resources and exhibit decreased emotional response while deciding in favor of a known profitable outcome compared to opting for an uncertain choice — one that is more likely to result in a negative outcome based on previous experiences. Individuals with autism allocate disproportionate amounts of attention and emotional resources towards planning actions that are deemed safe and offer only a probable (though not definite) advantage. Conversely, the prospect of failure due to risky behavior induces a comparatively muted response in their brains. Second, our internal evaluation of feedback focused on variations in functional activity within the orbitofrontal and lateral prefrontal cortical areas during exploratory (disadvantageous) choices between individuals with autism and control subjects. As previously reported, neurotypical subjects demonstrated significant beta synchronization following negative feedback after disadvantageous choices [1]. Contrary to control participants, individuals with autism spectrum disorder exhibited a lack of synchronization in frontal beta oscillations following losses incurred from unfavorable selections. This observation may indicate insufficient reinforcement of the internal utility model, which typically strengthens in response to negative outcomes that align with predicted results [1]. Overall, our study found that individuals on the autism spectrum with a high intolerance for uncertainty exhibit significantly increased activation of brain decision-making systems in situations that are perceived to be low-risk and with a high probability of a successful outcome. These findings clarify the reasons behind the puzzling rise in anxiety and autonomic reactivity among individuals in situations where they anticipate rewards, which are not inherently aversive unlike fear of punishment [2].

Elevated VCAM-1 levels in peripheral blood are associated with brain structural and functional alterations in major depressive disorder

BackgroundVascular cell adhesion molecule-1 (VCAM-1) is a well-known biomarker of endothelial activation. This study aimed to determine whether changes in peripheral VCAM-1 levels occurred in major depressive disorder (MDD) patients and explored immune-brain interactions based on neuroimaging. MethodsThis study included 165 subjects (80 healthy controls [HCs] and 85 MDD patients). Of them, 133 underwent magnetic resonance imaging. VCAM-1 was measured using a commercially available Enzyme-Linked Immunosorbent Assay kit following the manufacturer's instructions. The gray matter volume (GMV) and surface-based functional connectivity (FC) were calculated based on Schaefer parcellation 400 parcels. ResultsCompared with the HCs, MDD patients exhibited significantly higher level of VCAM-1. The correlation analysis showed that VCAM-1 had a significant negative correlation with GMV of the right medial frontal cortex (MFC) and postcentral (PostCG). The mediation analyses showed that VCAM-1 mediated the association between group and GMV of PostCG and the FC of left ventral prefrontal cortex (vPFC) with right inferior parietal lobe (IPL). ConclusionsThis study showed that a high level of VCAM-1 was associated to the decreased GMV in the right MFC and PostCG, and mediated the FC of the left vPFC with right IPL. These findings suggested that VCAM-1 might contribute to the etiology of MDD by influencing brain structure and function. LimitationsThe cross-sectional design makes it difficult to determine the causal relationship and dynamic effect among VCAM-1, brain structure/function features, and depressive symptoms.

The Sporadic Early‐Onset Alzheimer’s Disease Signature of Regional Atrophy

AbstractBackgroundIn EOAD, the localization of neurodegeneration is often more prominent in posterior lateral temporal, lateral and medial parietal, frontal, or occipital cortex relative to the medial and ventral temporal cortical localization of typical LOAD. Convergently, neuropathological investigations have identified a “hippocampal‐sparing” form of AD that is often present in younger patients. For these reasons, imaging biomarkers of neurodegeneration in EOAD, such as Magnetic Resonance Imaging (MRI) measures of atrophy, likely need to be different than those of neurodegeneration in typical LOAD. Although prior neuroimaging work has advanced our understanding of anatomical abnormalities in EOAD, these studies have included small samples, most composed of amnestic EOAD dementia and none focused on developing an MRI biomarker specific to EOAD. Such a disease‐signature MRI biomarker has been established and validated in LOAD dementia and has proven to be powerful in predicting progressive decline in people with MCI or who were cognitively unimpaired and in predicting molecular biomarker status. An a priori‐defined regional atrophy signature may also be helpful in constraining the analysis of MRI data in studies of putative disease‐modifying therapies.MethodLEADS is an observational study which includes annual MRI. In this analysis, we used FreeSurfer to define the sporadic EOAD atrophy signature in a small sample of MGH EOAD patients, and investigated its reproducibility in LEADS, as well as the magnitude of atrophy and its relationship to clinical measures.ResultThe EOAD signature is robustly reproducible across the two independent patient cohorts, with prominent atrophy in caudal lateral temporal cortex, inferior parietal lobule, and posterior cingulate and precuneus cortex, with relative sparing of medial temporal lobe structures. Comparing patients to controls, Cohen’s d effect sizes within various regions ranged from 0.99 to 1.98.ConclusionThis study demonstrates the specific cortical regions with most prominent atrophy in patients with sporadic EOAD; this signature of regional atrophy will be used to examine longitudinal change.

Effects of rTMS Intervention on Functional Neuroimaging Activities in Adolescents with Major Depressive Disorder Measured Using Resting-State fMRI.

Repetitive transcranial magnetic stimulation (rTMS) to the left dorsolateral prefrontal cortex (L-DLPFC) is commonly used for the clinical treatment of major depressive disorder (MDD). The neuroimaging biomarkers and mechanisms of rTMS are still not completely understood. This study aimed to explore the functional neuroimaging changes induced by rTMS in adolescents with MDD. A total of ten sessions of rTMS were administrated to the L-DLPFC in thirteen adolescents with MDD once a day for two weeks. All of them were scanned using resting-state functional magnetic resonance imaging at baseline and after rTMS treatment. The regional homogeneity (ReHo), amplitude of low-frequency fluctuation (ALFF), and the subgenual anterior cingulate cortex (sgACC)-based functional connectivity (FC) were computed as neuroimaging indicators. The correlation between changes in the sgACC-based FC and the improvement in depressive symptoms was also analyzed. After rTMS treatment, ReHo and ALFF were significantly increased in the L-DLPFC, the left medial prefrontal cortex, bilateral medial orbital frontal cortex, and the left ACC. ReHo and ALFF decreased mainly in the left middle occipital gyrus, the right middle cingulate cortex (MCC), bilateral calcarine, the left cuneus, and the left superior occipital gyrus. Furthermore, the FCs between the left sgACC and the L-DLPFC, the right IFGoper, the left MCC, the left precuneus, bilateral post-central gyrus, the left supplementary motor area, and the left superior marginal gyrus were enhanced after rTMS treatment. Moreover, the changes in the left sgACC-left MCC FC were associated with an improvement in depressive symptoms in early improvers. This study showed that rTMS treatment in adolescents with MDD causes changes in brain activities and sgACC-based FC, which may provide basic neural biomarkers for rTMS clinical trials.

The shared and unique neural correlates of personal semantic, general semantic, and episodic memory.

One of the most common distinctions in long-term memory is that between semantic (i.e., general world knowledge) and episodic (i.e., recollection of contextually specific events from one's past). However, emerging cognitive neuroscience data suggest a surprisingly large overlap between the neural correlates of semantic and episodic memory. Moreover, personal semantic memories (i.e., knowledge about the self and one's life) have been studied little and do not easily fit into the standard semantic-episodic dichotomy. Here, we used fMRI to record brain activity while 48 participants verified statements concerning general facts, autobiographical facts, repeated events, and unique events. In multivariate analysis, all four types of memory involved activity within a common network bilaterally (e.g., frontal pole, paracingulate gyrus, medial frontal cortex, middle/superior temporal gyrus, precuneus, posterior cingulate, angular gyrus) and some areas of the medial temporal lobe. Yet the four memory types differentially engaged this network, increasing in activity from general to autobiographical facts, from autobiographical facts to repeated events, and from repeated to unique events. Our data are compatible with a component process model, in which declarative memory types rely on different weightings of the same elementary processes, such as perceptual imagery, spatial features, and self-reflection.

Neural mechanisms for executive control of speed-accuracy trade-off

The medial frontal cortex (MFC) plays an important but disputed role in speed-accuracy trade-off (SAT). In samples of neural spiking in the supplementary eye field (SEF) in the MFC simultaneous with the visuomotor frontal eye field and superior colliculus in macaques performing a visual search with instructed SAT, during accuracy emphasis, most SEF neurons discharge less from before stimulus presentation until response generation. Discharge rates adjust immediately and simultaneously across structures upon SAT cue changes. SEF neurons signal choice errors with stronger and earlier activity during accuracy emphasis. Other neurons signal timing errors, covarying with adjusting response time. Spike correlations between neurons in the SEF and visuomotor areas did not appear, disappear, or change sign across SAT conditions or trial outcomes. These results clarify findings with noninvasive measures, complement previous neurophysiological findings, and endorse the role of the MFC as a critic for the actor instantiated in visuomotor structures.

Neuromodulation of the Left Inferior Frontal Cortex Affects Social Monitoring during Motor Interactions.

Motor interactions require observing and monitoring a partner's performance as the interaction unfolds. Studies in monkeys suggest that this form of social monitoring might be mediated by the activity of the ventral premotor cortex (vPMc), a critical brain region in action observation and motor planning. Our previous fMRI studies in humans showed that the left vPMc is indeed recruited during social monitoring, but its causal role is unexplored. In three experiments, we applied online anodal or cathodal transcranial direct current stimulation over the left lateral frontal cortex during a music-like interactive task to test the hypothesis that neuromodulation of the left vPMc affects participants' performance when a partner violates the agent's expectations. Participants played short musical sequences together with a virtual partner by playing one note each in turn-taking. In 50% of the trials, the partner violated the participant's expectations by generating the correct note through an unexpected movement. During sham stimulation, the partner's unexpected behavior led to a slowdown in the participant's performance (observation-induced posterror slowing). A significant interaction with the stimulation type showed that cathodal and anodal transcranial direct current stimulation induced modulation of the observation-induced posterror slowing in opposite directions by reducing or enhancing it, respectively. Cathodal stimulation significantly reduced the effect compared to sham stimulation. No effect of neuromodulation was found when the partner behaved as expected or when the observed violation occurred within a context that was perceptually matched but noninteractive in nature. These results provide evidence for the critical causal role that the left vPMc might play in social monitoring during motor interactions, possibly through the interplay with other brain regions in the posterior medial frontal cortex.

The changes of intrinsic connectivity contrast in young smokers.

Previous studies demonstrated that reward circuit plays an important role in smoking. The differences of functional and structural connectivity were found among several brain regions such as thalamus and frontal lobe. However, few studies focused on functional connectivity (FC) in whole-brain voxel level of young smokers. In this study, intrinsic connectivity contrast (ICC) was used to perform voxel-based whole-brain analyses in 55 young smokers and 55 matched non-smokers to identify brain regions with significant group differences. ICC results showed that the connectivity of young smokers in medial frontal cortex (MedFC), supramarginal gyrus anterior division left (L_aSMG), central opercular cortex left (L_CO) and middle frontal gyrus left (L_MidFG) showed a significantly lower trend compared with the non-smokers. The seed-based FC analysis about MedFC indicated that young smokers showed reduced connectivity between the MedFC and left hippocampus, left amygdala compared to non-smokers. Correlation analysis showed that the ICC of MedFC in young smokers was significantly negatively correlated with Fagerstrom test for nicotine dependence (FTND) and Questionnaire on Smoking Urges (QSU). The FC between the MedFC and left hippocampus, left amygdala was significantly negatively correlated with Pack_years. The mediation analysis indicated that ICC of MedFC completely mediated FTND and QSU of young smokers. The results suggest that nicotine accumulation may affect the communication of the frontal lobe with the whole brain to some extent, leading to changes in smoking cravings. The above research also provides in-depth insights into the mechanism of adolescent smoking addiction and related intervention treatment.

Different Faces of Medial Beta-Band Activity Reflect Distinct Visuomotor Feedback Signals.

Beta-band (13-35 Hz) modulations following reward, task outcome feedback, and error have been described in cognitive and/or motor adaptation tasks. Observations from different studies are, however, difficult to conciliate. Among the studies that used cognitive response selection tasks, several reported an increase in beta-band activity following reward, whereas others observed increased beta power after negative feedback. Moreover, in motor adaptation tasks, an attenuation of the postmovement beta rebound follows a movement execution error induced by visual or mechanical perturbations. Given that kinematic error typically leads to negative task-outcome feedback (e.g., target missed), one may wonder how contradictory modulations, beta power decrease with movement error versus beta power increase with negative feedback, may coexist. We designed a motor adaptation task in which female and male participants experience varied feedbacks-binary success/failure feedback, kinematic error, and sensory-prediction error-and demonstrate that beta-band modulations in opposite directions coexist at different spatial locations, time windows, and frequency ranges. First, high beta power in the medial frontal cortex showed opposite modulations well separated in time when compared in success and failure trials; that is, power was higher in success trials just after the binary success feedback, whereas it was lower in the postmovement period compared with failure trials. Second, although medial frontal high-beta activity was sensitive to task outcome, low-beta power in the medial parietal cortex was strongly attenuated following movement execution error but was not affected by either the outcome of the task or sensory-prediction error. These findings suggest that medial beta activity in different spatio-temporal-spectral configurations play a multifaceted role in encoding qualitatively distinct feedback signals.SIGNIFICANCE STATEMENT Beta-band activity reflects neural processes well beyond sensorimotor functions, including cognition and motivation. By disentangling alternative spatio-temporal-spectral patterns of possible beta-oscillatory activity, we reconcile a seemingly discrepant literature. First, high-beta power in the medial frontal cortex showed opposite modulations separated in time in success and failure trials; power was higher in success trials just after success feedback and lower in the postmovement period compared with failure trials. Second, although medial frontal high-beta activity was sensitive to task outcome, low-beta power in the medial parietal cortex was strongly attenuated following movement execution error but was not affected by the task outcome or the sensory-prediction error. We propose that medial beta activity reflects distinct feedback signals depending on its anatomic location, time window, and frequency range.