Emotional intelligence (EI) is one\'s ability to monitor one\'s own and other\'s emotions and the use of emotional information to enhance thought and action. Previous behavioral studies have shown that EI is separable into trait EI and ability EI, which are known to have distinct characteristics at the behavioral level. A relevant and unanswered question is whether both forms of EI have a dissociable neural basis. Previous studies have individually explored the neural underpinnings of trait EI and ability EI, but there has been no direct comparison of the neural mechanisms underlying these two types of emotional intelligence. The present study addresses this question by using resting-state fMRI to examine the correlational pattern between the regional amplitude of low-frequency fluctuations (ALFF) of the brain and individuals\' trait EI and ability EI scores. We found that trait EI scores were positively correlated with the ALFF in the bilateral superior temporal gyrus, and negatively correlated with the ALFF in the ventral medial prefrontal cortex. In contrast, ability EI scores were positively correlated with the ALFF in the insula. Taken together, these results provide preliminary evidence of dissociable neural substrates between trait EI and ability EI.

This study explored whether amygdala reactivity predicted the greed personality trait (GPT) using both task-based and resting-state functional connectivity analyses (ntotal = 452). In Cohort 1 (n = 83), task-based functional magnetic resonance imaging (t-fMRI) results from a region-of-interest (ROI) analysis revealed no direct correlation between amygdala reactivity to fearful and angry faces and GPT. Instead, whole-brain analyses revealed GPT to robustly negatively vary with activations in the right ventromedial prefrontal cortex (vmPFC), supramarginal gyrus, and angular gyrus in the contrast of fearful + angry faces > shapes. Moreover, task-based psychophysiological interaction (PPI) analyses showed that the high GPT group showed weaker functional connectivity of the vmPFC seed with a top-down control network and visual pathways when processing fearful or angry faces compared to their lower GPT counterparts. In Cohort 2, resting-state functional connectivity (rs-FC) analyses indicated stronger connectivity between the vmPFC seed and the top-down control network and visual pathways in individuals with higher GPT. Comparing the two cohorts, bilateral amygdala seeds showed weaker associations with the top-down control network in the high group via PPI analyses in Cohort 1. Yet, they exhibited distinct rs-FC patterns in Cohort 2 (e.g., positive associations of GPT with the left amygdala-top-down network FC but negative associations with the right amygdala-visual pathway FC). The study underscores the role of the vmPFC and its functional connectivity in understanding GPT, rather than amygdala reactivity.

Dysfunctional glutamatergic neurotransmission contributes importantly to the pathophysiology of depression. However, the underlying neural mechanisms of glutamatergic dysfunction remain poorly understood. Here, we employed chronic unpredictable mild stress (CUMS) to induce depression-like behavior in male mice and to assess the alterations of glutamatergic system within the ventromedial prefrontal cortex (vmPFC). Male mice subjected to CUMS showed an increase in levels of glutamate content, synaptosomal GluN2B-NMDA receptors (GluN2B-NMDARs) and phosphorylated synaptosomal associated protein 25 KD of Ser187 (pSer187-SNAP25), which is involved in synaptic vesicular fusion processes in the vmPFC. Downregulation of pSer187-SNAP25 via the TAT-S187 fusion peptide efficiently alleviated CUMS-induced depressive-like behaviors in male mice by reversing the increase of glutamate content and synaptosomal GluN2B-NMDARs. These findings demonstrated a critical role for pSer187-SNAP25-mediated glutamatergic dysfunction in CUMS-induced depressive-like behaviors, suggesting the potential of pS187-SNAP25 inhibitors for further investigation on depression management.

Schemas provide a scaffold onto which we can integrate new memories. Previous research has investigated the brain activity and connectivity underlying schema-related memory formation. However, how schemas are represented and reactivated in the brain, in order to enhance memory, remains unclear. To address this issue, we used an object-location spatial schema that was learned over multiple sessions, combined with similarity analyses of neural representations, to investigate the reactivation of schema representations of object-location memories when a new object-scene association is learned. In addition, we investigated how this reactivation affects subsequent memory performance under different strengths of schemas. We found that reactivation of a schema representation in the lateral occipital cortex (LOC) during object-scene encoding affected subsequent associative memory performance only in the schema-consistent condition and increased the functional connectivity between the LOC and the parahippocampal place area. Taken together, our findings provide new insight into how schema acts as a scaffold to support the integration of novel information into existing cortical networks and suggest a neural basis for schema-induced rapid cortical learning.

Chronic pain patients often have anxiety disorders, and some of them suffer from anxiety even after analgesic administration. In this study, we investigated the role of AMPAR-mediated synaptic transmission in the ventromedial prefrontal cortex (vmPFC) in chronic pain-induced persistent anxiety in mice and explored potential drug targets. Chronic inflammatory pain was induced in mice by bilateral injection of complete Freund\'s adjuvant (CFA) into the planta of the hind paws; anxiety-like behaviours were assessed with behavioural tests; S-nitrosylation and AMPAR-mediated synaptic transmission were examined using biochemical assays and electrophysiological recordings, respectively. We found that CFA induced persistent upregulation of AMPAR membrane expression and function in the vmPFC of anxious mice but not in the vmPFC of non-anxious mice. The anxious mice exhibited higher S-nitrosylation of stargazin (an AMPAR-interacting protein) in the vmPFC. Inhibition of S-nitrosylation by bilaterally infusing an exogenous stargazin (C302S) mutant into the vmPFC rescued the surface expression of GluA1 and AMPAR-mediated synaptic transmission as well as the anxiety-like behaviours in CFA-injected mice, even after ibuprofen treatment. Moreover, administration of ZL006, a small molecular inhibitor disrupting the interaction of nNOS and PSD-95 (20 mg·kg-1·d-1, for 5 days, i.p.), significantly reduced nitric oxide production and S-nitrosylation of AMPAR-interacting proteins in the vmPFC, resulting in anxiolytic-like effects in anxious mice after ibuprofen treatment. We conclude that S-nitrosylation is necessary for AMPAR trafficking and function in the vmPFC under chronic inflammatory pain-induced persistent anxiety conditions, and nNOS-PSD-95 inhibitors could be potential anxiolytics specific for chronic inflammatory pain-induced persistent anxiety after analgesic treatment.

For centuries, scientists have pondered why people would help others at a cost to themselves even in the absence of expectation for future benefit. While a growing body of neuroimaging studies has suggested that the ventromedial prefrontal cortex (vmPFC) may be particularly critical for the regulation of altruistic behavior. However, evidence is still lacking in the field of neuroscience regarding the causal link between the region of vmPFC and pure altruistic behavior. In the present study, we designed a modified dictator game with a binary choice in the contexts of gain and loss that aimed to provide a simple and direct measure of participants\' altruistic tendency. Using tDCS, we found that modulating the activity of vmPFC could significantly alter altruistic behaviors. Specifically, anodal stimulation of the vmPFC resulted in increasing altruistic choices compared with the cathodal stimulation, and the effect was found both in the gain and loss contexts. In addition, the subsequent inferences about others\' altruistic behaviors were correlated with their own choices, and cathodal vmPFC stimulation resulted in a lower inference than sham stimulation in the gain context.

By including four different time intervals and controlling for behavioral confounds, Tallman et al. (this issue) found that brain connectivity of cortical regions with the vmPFC or with the hippocampus changed over time, although hippocampal activity did not change significantly. This study shed light on how memory is consolidated as it ages. Further studies could clarify the extent to which other factors, such as memory content, influence brain connectivity with more than two time intervals. The roles of different cortical regions in memory consolidation should also be addressed.

As a major contributor to the development of depression, rumination has proven linked with aberrant default-mode network (DMN) activity. However, it remains unclear how the spontaneous spatial and temporal activity of DMN underlie the association between rumination and depression. To illustrate this issue, behavioral measures and resting-state functional magnetic resonance images were connected in 2 independent samples (NSample1 = 100, NSample2 = 95). Fractional amplitude of low-frequency fluctuations (fALFF) and regional homogeneity (ReHo) were used to assess spatial characteristic patterns, while voxel-wise functional concordance (across time windows) (VC) and Hurst exponent (HE) were used to assess temporal dynamic patterns of brain activity. Results from both samples consistently show that temporal dynamics but not spatial patterns of DMN are associated with rumination. Specifically, rumination is positively correlated with HE and VC (but not fALFF and ReHo) values, reflecting more consistent and regular temporal dynamic patterns in DMN. Moreover, subregion analyses indicate that temporal dynamics of the ventromedial prefrontal cortex (VMPFC) reliably predict rumination scores. Furthermore, mediation analyses show that HE and VC of VMPFC mediate the association between rumination and depression. These findings shed light on neural mechanisms of individual differences in rumination and corresponding risk for depression.

Owing to high heterogeneity and comorbidity, the shared and unique neural mechanisms underlying the development of anxiety and major depressive disorders remain unclear. Using a dimensional model describing shared versus unique symptoms associated with anxiety and depression, this study investigated how longitudinal changes in symptom dimensions relate to threat neurocircuitry.
Participants were 18- to 19-year-olds (N = 279, 186 females) who completed self-report measures of anxiety and depression at baseline and at 10, 20, and 30 months. Linear slopes of symptom dimensions of general distress, fear, and anhedonia-apprehension were estimated through a trilevel factorial model. In addition, functional magnetic resonance imaging scans were obtained while participants performed Pavlovian fear conditioning tasks at baseline and 30 months, including three phases of fear acquisition, extinction, and extinction recall. Neural responses in regions of interest related to threat neural circuitry (e.g., amygdala, ventromedial prefrontal cortex, and subgenual anterior cingulate cortex) were extracted.
Linear mixed models used to estimate relationships between changes of symptom dimensions and neural responses revealed two major findings: 1) greater neural responses to threatening stimuli during fear acquisition at baseline were associated with a greater increase in fear symptoms during the 30-month prospective period; and 2) elevated neural responses to the extinguished stimulus during extinction recall at 30 months were negatively associated with changes in general distress, suggesting that greater increases in general distress are associated with larger deficits in extinction memory.
These findings improve our understanding of pathophysiological pathways underlying the development of anxiety and depression, while separating symptom dimensions that are shared versus unique between the two disorders.

There is evidence indicating that people are more likely to take risks when they are sleep-deprived than during resting wakefulness (RW). The ventromedial prefrontal cortex (vmPFC) could have a crucial psychophysiological role in this phenomenon. However, the intrinsic patterns of functional organization of the human vmPFC and their relationship with risk-taking during sleep deprivation (SD) are unclear. This study investigated the relationship between functional connectivity in the vmPFC and cerebral cortex and the risk-taking tendency after SD. The study participants were 21 healthy college students who underwent functional magnetic resonance imaging twice in the resting state, once during RW and once after 36 h of SD. The vmPFC was analyzed bilaterally for functional connectivity between the regions of interest. Correlation analysis was performed to evaluate changes in functional connectivity between the vmPFC and the cerebral cortex and risk-taking before and after SD. A single night of SD produced a definite deficit in functional connectivity between the vmPFC and thalamus bilaterally and an increase in functional connectivity between the vmPFC and dorsolateral prefrontal cortex (dlPFC) and the parietal lobe. We also found that the likelihood of risk-taking was positively correlated with increased functional connectivity between the vmPFC and dlPFC and negatively correlated with decreased functional connectivity between the vmPFC and thalamus bilaterally. These results demonstrate that lack of sleep substantially impairs functional connectivity between the vmPFC and the cerebral cortex, which in turn predicts the risk-taking behavior found after SD.