Cerebral cortex最新文献

Listeners implicitly use statistical regularities to segment continuous sound input into meaningful units, eg transitional probabilities between syllables to segment a speech stream into separate words. Implicit learning of such statistical regularities in a novel stimulus stream is reflected in a synchronization of neural responses to the sequential stimulus structure. The present study aimed to test the hypothesis that neural tracking of the statistical stimulus structure is reduced in individuals with dyslexia who have weaker reading and spelling skills, and possibly also weaker statistical learning abilities in general, compared to healthy controls. To this end, adults with and without dyslexia were presented with continuous streams of (non-speech) tones, which were arranged into triplets, such that transitional probabilities between single tones were higher within triplets and lower between triplets. We found that the so-called Triplet Learning Index (ie the ratio of neural phase coherence at the triplet rate relative to the tone rate) was lower in adults with dyslexia compared to the control group. Moreover, a higher Triplet Learning Index was associated with better spelling skills. These results suggest that individuals with dyslexia have a rather broad deficit in processing structure in sound instead of a merely phonological deficit.

The phenomenon of beneficiaries ignoring benefactors' violations, ranging from everyday favors to bribes, is widespread yet lacks targeted theoretical and empirical attention. We propose a conceptual framework that includes "social debt" and "reciprocity bias," where "social debt" is defined as information about benefits bestowed by benefactors and "reciprocity bias" as the influence of social debt on beneficiaries' perceptions and decisions in situations involving the benefactor. To investigate this bias in moral perception and its cognitive-neural mechanisms, we manipulated three levels of social debt (none, less, more) by varying the amount of unasked benefits that benefactors bestowed upon participants. Participants then observed the distributor's fair or unfair allocation of resources to another person, while their electroencephalography (EEG) was recorded. Results indicate that more (vs. none/less) social debt reduces perceptions of unfairness toward benefactors' violations and enhances fairness perceptions of their norm adherence. This was, accompanied by the diminished fairness effect on fronto-centered P2 and a reversal fairness effect on the power of theta oscillations (4 to 7 Hz). These findings support a multilevel reciprocity bias in fairness perception, suggesting that strong social debt may heighten concern for benefactor's interests and increase the adaptive value of their violations at the cognitive-neural level.

The importance of nonmotor symptoms in understanding the pathogenesis of the heterogeneity of Parkinson's disease has been highlighted. However, the validation of specific brain network biomarkers in nonmotor symptom subtypes is currently lacking. By performing a new approach to compute functional connectivity with structural prior using magnetic resonance imaging, the present study computed both functional connectivity and fusional connectivity features in the nonmotor symptom subtypes of Parkinson's disease, one characterized by cognitive impairment with late onset and the other depression with early onset. The functional connectivity and fusional connectivity features centered at the left amygdala were both detected. The fusional features significantly enhanced the classification performance. The amygdala-postcentral and amygdala-orbital frontal features were critical for cognitive impairment with late onset detection, while the amygdala-temporooccipital features were crucial for depression with early onset detection. Additionally, the fusional connectivity features between the amygdala and the junction sulcus of parietooccipital and temporooccipital regions contributed significantly to differentiating cognitive impairment with late onset and depression with early onset. The within-subtype correlation analysis revealed that age at onset and cognitive scores were associated with features of amygdala-somatosensory/visual-motor processing areas in cognitive impairment with late onset, while related to features of amygdala-emotional processing areas in depression with early onset. Our findings highlighted distinct amygdala-centered fusional connectivity features related to diverse nonmotor symptoms in Parkinson's disease, offering new insights for pathogenesis-targeted treatments for specific Parkinson's disease subtypes.

Electroencephalography is instrumental in understanding neurophysiological mechanisms underlying working memory. While numerous studies have associated electroencephalography features to working memory, understanding causal relationships leads to better characterization of the neurophysiological mechanisms that are directly linked to working memory. Personalized causal modeling is a tool to discover these direct links between brain features and working memory performance. Therefore, we applied this approach to electroencephalography data from 66 adult healthy participants collected while performing a 3-back working memory task. Using graphical causal modeling, we discovered causal neural oscillations of working memory performance and compared the causal features between two groups: high and low performers. Total number of causal features in high performers was higher than low performers. Among the causal features, right temporal gamma oscillation was ~5 times (z-score = 3.87, P = 0.0001) more frequently a causal feature among high performers than low performers. However, the power of causal temporal gamma oscillation was not different between the two groups. Our findings suggest that one potential approach to improve working memory performance is to induce more causal gamma oscillations. This can be achieved by generating more local gamma entrainment over the right temporal cortex, rather than simply increasing gamma power.

In this Editorial, as the new Editor-in-Chief of Cerebral Cortex, I make a tribute to its well-known founders, late Patricia S. Goldman-Rakić and Paško Rakić. A couple with great synergies, they created a very special journal with unique spirit, one of the premier venues to publish the best neuroscience research. For the journal's future, my intentions are threefold: (i) to maintain and advance the high publication standards and traditions that contribute to the exceptional reputation of Cerebral Cortex in the scientific community, (ii) to follow the principles established by its founders, and (iii) to reflect novel trends in scientific publishing that have been crucially altered in recent years.

Tactile sensory information obtained from oneself or others may provide a calming effect and has been shown to enhance participants' motor control. The extent to which these touch activities may support motor inhibition and the related electrophysiological mechanisms remain unknown. Here, we investigated these effects in twenty healthy volunteers via electroencephalography under 3 touching conditions (self-touch, other-touch, and no-touch) during a stop-signal task. We found that both the self-touch and other-touch conditions resulted in better stopping accuracy and lower stop-signal reaction times than the no-touch condition. Additionally, these 2 touch conditions elicited larger N2 and P3 responses during successful inhibition of planned finger movements. Time-varying network analysis based on electroencephalography was further used to explore the differences in brain networks during conflict monitoring substages under different touch conditions. A top-down projection from the frontal cortex (Fz) to the parietal and occipital cortices was observed along with increased functional connectivity efficiency under touch conditions. These results indicate that tactile information may enhance neural processing efficiency in the human brain by eliciting larger event-related potential components and promoting information processing in the brain network during conflict monitoring processes, thereby contributing to the reactive inhibitory component of motor inhibition.

Different addictive drugs can impact the function and morphology of the brain in diverse ways. The insula cortex, an important brain node involved in craving and reward neural circuits in individuals with substance use disorders (including damage to the insula cortex), has been reported to reduce addictive behaviors. However, less is known about whether there is a functional difference between individuals with opioid and methamphetamine use disorders, especially regarding the function of the insula cortex. Fifty-eight individuals with opioid use disorder and sixty individuals with methamphetamine use disorder underwent resting-state and 3D-T1-weighted magnetic resonance imaging and completed craving questionnaires. Differences in insula subdivision resting-state functional connectivity between the groups were assessed, and their correlations with craving were analyzed. Compared with the methamphetamine group, the opioid group demonstrated increased connectivity of the right dorsal anterior insula but decreased connectivity of the right posterior insula and the left dorsal anterior insula/posterior insula/ventral anterior insula. Additionally, a negative correlation between functional connectivity and craving was observed in individuals with opioid and methamphetamine use disorders. This study provides insights into the various brain function connection patterns that are associated with different types of drug use with respect to opioid and methamphetamine use disorders.

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Glutamate, the primary excitatory neurotransmitter in the central nervous system (CNS), is regulated by the excitatory amino acid transporters glutamate transporter 1 (GLT-1) and glutamate aspartate transporter (GLAST). Following traumatic brain injury, extracellular glutamate levels increase, contributing to excitotoxicity, circuit dysfunction, and morbidity. Increased neuronal glutamate release and compromised astrocyte-mediated uptake contribute to elevated glutamate, but the mechanistic and spatiotemporal underpinnings of these changes are not well established. Using the controlled cortical impact model of TBI and iGluSnFR glutamate imaging, we quantified extracellular glutamate dynamics after injury. Three days postinjury, glutamate release was increased, and glutamate uptake and GLT-1 expression were reduced. Seven and 14 days postinjury, glutamate dynamics were comparable between sham and controlled cortical impact animals. Changes in peak glutamate response were unique to specific cortical layers and proximity to injury. This was likely driven by increases in glutamate release, which was spatially heterogeneous, rather than reduced uptake, which was spatially uniform. The astrocyte K+ channel, Kir4.1, regulates activity-dependent slowing of glutamate uptake. Surprisingly, Kir4.1 was unchanged after controlled cortical impact and accordingly, activity-dependent slowing of glutamate uptake was unaltered. This dynamic glutamate dysregulation after traumatic brain injury underscores a brief period in which disrupted glutamate uptake may contribute to dysfunction and highlights a potential therapeutic window to restore glutamate homeostasis.

Breathing meditation typically consists of directing attention toward breathing and redirecting attention when the mind wanders. As yet, we do not have a full understanding of the neural mechanisms of breath attention, in particular, how large-scale network interactions may be different between breath attention and rest and how these interactions may be modulated during periods of on-task and off-task attention to the breath. One promising approach may be examining fMRI measures including static connectivity between brain regions as well as dynamic, time-varying brain states. In this study, we analyzed static and dynamic functional connectivity in 72 adolescents during a breath-counting task (BCT), leveraging physiological respiration data to detect objective on-task and off-task periods. During the BCT relative to rest, we identified increases in static connectivity within attention-direction and orienting networks and anticorrelations between attention networks and the DMN. Dynamic connectivity analysis revealed four distinct brain states, including a DMN-anticorrelated brain state, proportionally more present during the BCT than the rest. We found there were distinct brain state markers of (i) breathing tasks vs rest and (ii) momentary on-task vs off-task attention within the BCT, yet in this analysis, no identifiable brain states reflecting between-individual behavioral variability.

Altered brain connectivity and atypical neural oscillations have been observed in autism, yet their relationship with autistic traits in nonclinical populations remains underexplored. Here, we employ electroencephalography to examine functional connectivity, oscillatory power, and broadband aperiodic activity during a dynamic facial emotion processing task in 101 typically developing children aged 4 to 12 years. We investigate associations between these electrophysiological measures of brain dynamics and autistic traits as assessed by the Social Responsiveness Scale, 2nd Edition (SRS-2). Our results revealed that increased facial emotion processing-related connectivity across theta (4 to 7 Hz) and beta (13 to 30 Hz) frequencies correlated positively with higher SRS-2 scores, predominantly in right-lateralized (theta) and bilateral (beta) cortical networks. Additionally, a steeper 1/f-like aperiodic slope (spectral exponent) across fronto-central electrodes was associated with higher SRS-2 scores. Greater aperiodic-adjusted theta and alpha oscillatory power further correlated with both higher SRS-2 scores and steeper aperiodic slopes. These findings underscore important links between facial emotion processing-related brain dynamics and autistic traits in typically developing children. Future work could extend these findings to assess these electroencephalography-derived markers as potential mechanisms underlying behavioral difficulties in autism.