Cerebral cortex最新文献

Mice communicate through high-frequency ultrasonic vocalizations, which are crucial for social interactions such as courtship and aggression. Although ultrasonic vocalization representation has been found in adult brain areas along the auditory pathway, including the auditory cortex, no evidence is available on the neuronal representation of ultrasonic vocalizations early in life. Using in vivo two-photon calcium imaging, we analyzed auditory cortex layer 2/3 neuronal responses to USVs, pure tones (4 to 90 kHz), and high-frequency modulated sweeps from postnatal day 12 (P12) to P21. We found that ACx neurons are tuned to respond to ultrasonic vocalization syllables as early as P12 to P13, with an increasing number of responsive cells as the mouse age. By P14, while pure tone responses showed a frequency preference, no syllable preference was observed. Additionally, at P14, USVs, pure tones, and modulated sweeps activate clusters of largely nonoverlapping responsive neurons. Finally, we show that while cell correlation decreases with increasing processing of peripheral auditory stimuli, neurons responding to the same stimulus maintain highly correlated spontaneous activity after circuits have attained mature organization, forming neuronal subnetworks sharing similar functional properties.

The levels-of-processing framework, proposing that deep encoding enhances retention, plays a crucial role in episodic memory research. Neuroimaging evidence highlights that increased activity of the left ventrolateral prefrontal cortex during deep encoding predicts subsequent memory success. However, cognitive mechanisms underlying this region's involvement in establishing and consolidating deep and shallow traces remain unclear. In this preregistered study, we investigated whether repetitive transcranial magnetic stimulation over the left ventrolateral prefrontal cortex versus the vertex differentially modulates the formation and maintenance of deep and shallow traces. Trains of 20 Hz online repetitive transcranial magnetic stimulation were delivered over the left ventrolateral prefrontal cortex or vertex during tasks involving pleasantness (deep) and alphabetical order (shallow) judgments of words. Following encoding, two recognition tests assessed immediate and 24-h delayed recognition of words. Compared to the vertex control, ventrolateral prefrontal stimulation selectively disrupted the formation of episodic memory under deep encoding conditions, evidenced by increased response time at encoding and reduced immediate recognition in the deep but not shallow condition. Notably, forgetting rates across the 24-h delay were similar for disrupted deep, intact deep, and shallow items, implying that the rate of trace decay is independent of the strength of trace formation. The constant trace decay indicates that distinct mechanisms are involved in establishing and maintaining episodic traces.

Previous studies have reported a correlation between anxiety disorders and changes in brain structure, yet the specific alterations in brain region volumes remain unclear. This study aimed to infer the causal relationship between anxiety disorders and changes in brain structure volume through Mendelian Randomization analysis. We selected 63 cortical structure volumes from the GWAS database as exposure data and anxiety disorder data from the FinnGen and UK Biobank databases as outcomes. We found a significant correlation between atrophy in the Left precentral volume area (Odds Ratio [OR] = 0.935, 95% Confidence intervals [CI]: 0.891-0.981, P value, P = 0.007) and an increased risk of anxiety disorders. Additionally, changes identified in specific brain regions, such as atrophy in the Right rostral anterior cingulate area (OR = 0.993, 95% CI: 0.987-0.999, P = 0.025) and increased volume in the Left superior parietal area (OR = 1.001, 95% CI: 1.000-1.001, P = 0.028), may correlate with an increased risk of anxiety disorders. Furthermore, both phenotypes demonstrated directional consistency in their respective and overall meta-analyzed OR values pre- and post-merger, enhancing the reliability of the results. This study elucidates the causal relationship between anxiety disorders and specific brain structures, providing new insights for further research into psychiatric disorders.

Slow gait speed and disrupted brain network connectivity are common in patients with Parkinson's disease (PD). This study aimed to clarify the relationship between gait speed and clinical characteristics in PD, and explore the underlying brain network mechanisms. Forty-two PD patients and 20 healthy controls (HC) were recruited. Statistical independent component analysis and correlation analysis were employed to investigate underlying neural mechanisms and relationships. PD patients exhibited significantly slower gait speed, which showed a significant negative correlation with postural instability and gait disturbance scores. Network connectivity analysis revealed decreased intranetwork functional connectivity (FC) within visual network (VN) and cerebellum network (CN), but increased internetwork FC between CN and both sensorimotor network (SMN) and frontoparietal network (FPN) in PD patients compared to HC. The slow gait speed PD subgroup demonstrated increased intranetwork FC within SMN and VN, along with decreased FC between VN and both FPN and default mode network. Correlation analyses revealed negative correlation between gait speed and FC of CN and positive correlation to FC of CN-SMN. Our study identified relationships between gait speed and clinical characteristics, and corresponding network connectivity alterations in PD patients, providing insights into the neural mechanisms underlying gait impairments in PD.

Bulimia nervosa (BN) has been observationally linked to the functional connectivity (FC) of large-scale brain networks, but the biological mechanisms remain unclear. This study used two-sample Mendelian randomization (MR) with genetic variations as instrumental variables (IVs) to explore potential causal relationships between FC and BN. Summary data from genome-wide association studies (GWAS) involving 2,564 individuals were analyzed to identify genetically predicted BN. Functional magnetic resonance imaging parameters and materials were sourced from the UK Biobank. The variables underwent independent component analysis processing by the database to generate the final GWAS dataset. Various methods, including MR Pleiotropy RESidual Sum and Outlier, MR Egger, and weighted median, were employed to detect heterogeneity and pleiotropy, with inverse variance weighting serving as the principal estimation method (P < 0.05). The FC imaging-derived phenotypes revealed that BN exerted a causal influence on the FC between large-scale networks, including the visual network, default mode network (DMN), frontoparietal network, somatosensory network (SSN), and ventral attention network. Additionally, BN had a causal impact on the within-network FC of both the DMN and SSN. The study provides evidence that BN leads to further changes in FC patterns within and between large-scale brain networks.

Understanding observed interpersonal touch, particularly the so-called affective touch targeting the CT fibers, is essential for social interactions. Research has documented that observing other people being touched activates the same cortical areas involved in direct tactile experiences. However, observing interpersonal touch also activates an inner simulation of the movements in the observer's motor system. Given the social and affective significance of CT-optimal touch, the present study tested the hypothesis that observing stroking touches targeting or not targeting the CT fibers system might distinctly influence motor resonance to vicarious touch. With this aim, we used single-pulse transcranial magnetic stimulation and motor-evoked potentials recording while participants observed video clips of interpersonal touch events at different stroking velocities. We found a modulation of motor system activity, particularly a decrease in corticospinal excitability, when observing CT-optimal touch as opposed to non-CT-optimal velocities, a mechanism that might aid in understanding the touchee's feelings during vicarious interpersonal touch. Moreover, participants with higher reliance on bodily cues to be emotionally aware showed greater motor suppression for CT-optimal compared to non-CT-optimal velocities. These results shed light on the complex interplay between motor and somatosensory systems in social touch perception and emphasize the importance of affective touch in human social interactions.

Altered reward processing has been repeatedly reported in Internet gaming disorder (IGD). However, it remains unclear whether these changes are linked to the severity of addictive symptoms or the extent of gaming experience. This study examined the neurophysiological responses regarding reward anticipation and consummation in individuals at different levels of gaming (including 22 casual gamers, 31 regular gamers, and 27 individuals with IGD) through a monetary incentive delay task. Three event-related potential components during reward anticipation-cue-related P300 (Cue-P3), contingent negative variation, and stimulus-preceding negativity (SPN)-and two during reward consummation-feedback-related negativity and feedback-related P300 (FB-P3)-were measured. We found that IGD individuals exhibited greater Cue-P3 but lower SPN amplitude compared to casual gamers, while regular gamers fell between the two without significant differences. Regressions indicated that more extensive gaming experience, rather than the severity of the symptoms, primarily contributed to the increased Cue-P3 in IGD. No group differences were found during reward consummation. Our results highlight disrupted reward anticipation processing in IGD, characterized by increased attention bias toward reward cues (Cue-P3) but diminished cognitive resources for reward anticipation (SPN) and emphasize the role of gaming experience in increased attention bias in IGD.

Subjective tinnitus, characterized by the perception of phantom sounds in the absence of external stimuli, presents significant challenges in both audiology and neurology. Once thought to primarily involve aberrant neural activity within auditory pathways, it is now understood to engage a broader array of neuroanatomical structures. This study investigated the connections between auditory, cognitive, and sensory processing regions, which are crucial for unraveling the complex neurobiological basis of tinnitus. Using high-resolution T1-weighted magnetic resonance imaging, we compared 52 individuals with subjective tinnitus with 52 age-matched healthy controls, focusing on cerebral cortex features, including fractal dimensionality, gyrification, and sulcal depth. Covariate analyses were conducted to explore the relationships between tinnitus duration, Tinnitus Handicap Inventory scores, anxiety score, and neuroanatomical changes. We found significant alterations in key brain regions involved in sensory processing, cognition, and emotional regulation, including the insula, lateral occipital cortex, middle frontal gyrus, and superior parietal lobule. These neuroanatomical changes were strongly correlated with the severity and chronicity of tinnitus symptoms. Our findings reveal profound structural changes in the brain associated with subjective tinnitus, offering valuable insights into the condition's underlying mechanisms and providing a potential framework for guiding future research and therapeutic interventions.

Contextual interference (CI) enhances learning by practicing motor tasks in a random order rather than a blocked order. One hypothesis suggests that the benefits arise from enhanced early perceptual/attentional processes, while another posits that better learning is due to highly activated mnemonic processes. We used high-density electroencephalography in a multi-scale analysis approach, including topographic analyses, source estimations, and functional connectivity, to examine the intertwined dynamics of attentional and mnemonic processes within short time windows. We recorded scalp activity from 35 participants as they performed an aiming task at three different distances, under both random and blocked conditions using a crossover design. Our results showed that topographies associated with processes related to perception/attention (N1, P3a) and working memory (P3b) were more pronounced in the random condition. Source estimation analyses supported these findings, revealing greater involvement of the perceptual ventral pathway, anterior cingulate and parietal cortices, along with increased functional connectivity in ventral alpha and frontoparietal theta band networks during random practice. Our results suggest that CI is driven, in the random compared to the blocked condition, by enhanced specific processes such as perceptual, attentional, and working memory processes, as well as large-scale functional networks sustaining more general attentional and executive processes.

Neuroscience research with public health relevance to emotional disorders examines brain-behavior relations. Joe LeDoux's legacy advances these efforts in ways that remain truly unique. While recognized for his basic science research, he also inspires applied researchers, guiding an agenda for clinical scientists: understanding the pathophysiology of altered subjective experiences in emotional disorders. For brain imaging, movie-watching approaches help clinicians realize this agenda due to movies' relative strength in evoking rich, meaningful subjective experiences. Here, we describe methodological advances in movie-watching paradigms that might sustain LeDoux's impact by facilitating the discovery of neural mechanisms generating complex emotional responses. Of note, while linking subjective emotion to pathophysiology is a first step, innovations in movie-watching designs, especially involving therapeutic techniques for emotional disorders, can boost clinical application. Leveraging research on pathophysiology to generate novel therapy reflects the clinical legacy sustained through Joe LeDoux's rousing career.