Behavioral and Brain Functions最新文献

Background: Teams are inherently adaptive entities that continuously adapt to changes or disruptions in their tasks or environments. During collaboration, interbrain synchrony (IBS) emerges, reflecting the temporal alignment of neural activity between team members. Building on this, IBS has been proposed as a potential marker of teamwork, suggesting that IBS should be sensitive to changes in teamwork.

Purpose: The present study investigated whether IBS is sensitive to changes in teamwork. We hypothesized that disruptions in teamwork would be accompanied by alterations in IBS dynamics.

Methods: Ninety-eight healthy adults (mean age = 22.5 ± 3.22 years; 69 females, 65.1%) were assigned to forty-nine dyads. Each pair completed a 20-minute computer-based navigation task while their brain activity was simultaneously recorded using fNIRS hyperscanning. Dyads in the experimental group encountered an unexpected increase in task difficulty midway through the task, whereas those in the control group completed the task without disruption. We examined three features of IBS - its overall level, temporal slope trajectory, and the temporal recurrence patterns.

Results: Control analyses confirmed that IBS reliably emerged during the task (χ²(1) = 50.24, p < .001) and that the experimental manipulation successfully disrupted teamwork, as reflected in altered team behavioral responses in communication (χ²(1) = 8.48, p = 0.004) and performance (χ²(1) = 24.99, p < .001). Nevertheless, no evidence was found for disruption-related changes in IBS across the three features examined (all Time x Group interactions p > .05.

Conclusion: These findings raise the possibility that IBS may reflect a stable collective state rather than a reactive one, thereby challenging its interpretation as a direct marker of teamwork. Methodological considerations, including the operationalization of IBS, are also discussed as potential explanations for the lack of observed change in IBS.

Background: Electroacupuncture is widely accepted to treat pain related conditions, but detailed mechanisms remain unknown.

Objective: To explore cortical and subcortical subnuclei involved in electroacupuncture stimulation (EAS) analgesia by observing EAS's analgesic efficacy and c-fos expression changes, providing a basis for neural circuit research and clinical transcranial magnetic stimulation (TMS) therapy.

Design, setting, participants and interventions: A chronic inflammatory pain model was established using knee osteoarthritis (KOA). Bilateral Zusanli was selected for electroacupuncture intervention. Von Frey test, open field test, elevated plus maze, and tail suspension test, and immunohistochemical staining were performed.

Main outcomes measures: Changes in mechanical pain threshold and pain-related emotional behaviors and distribution of c-fos positive cells in cortical and subcortical nuclei.

Results: Electroacupuncture significantly increased mechanical pain thresholds in KOA model mice. KOA modeling caused c-fos downregulation in the motor cortex, insular cortex, secondary auditory cortex, dorsal peduncular cortex, temporal association cortex, caudate putamen, lateral septal nucleus, accumbens nucleus, and the anterior cortical amygdaloid area. Electroacupuncture at Zusanli reversed these changes, upregulating c-fos in abovementioned brain regions, and additionally upregulated c-fos expression in the granular insular cortex, extended amydala.

Conclusion: Inflammatory pain induces widespread inhibition of neuronal activity in cortical and subcortical nuclei. The core mechanisms of electroacupuncture analgesia may involve direct reversal of abnormal inhibition in the lateral septal nucleus, caudate putamen, accumbens nucleus, and the anterior cortical amygdaloid area and activation of the granular insular cortex, medial septal nucleus and the extended amygdala for pain information integration.

Background: Excessive stress leads to injury and dysfunction, but the underlying mechanism remains unclear. As a human longevity gene, forkhead box O3a (FoxO3a) is a transcription factor that regulates various cellular processes, including the response to oxidative stress, apoptosis, and autophagy. This study aims to explore whether FoxO3a in the dentate gyrus (DG) of the hippocampus is involved in the formation of anxiety- and depressive-like behavior and cognitive impairment in stressed rats and to investigate the detailed mechanism.

Methods: This study was conducted using the 6-week chronic unpredictable stress (CUS) model. Before the stress treatment, we injected an adeno-associated virus (AAV) vector to overexpress FoxO3a specifically in the DG. Following the 6-week CUS treatment, a series of behavioral tests was conducted. Depression-like behavior was assessed using the sucrose preference test (SPT) and the open field test (OFT). The state of desperation was assessed with the forced swim test (FST) and tail suspension test (TST). Anxiety-like behavior was measured in the elevated plus maze (EPM) and OFT. Cognitive function was examined using the Y-maze test (Y-maze), novel object recognition test (NORT), and Morris water maze test (MWM). The level of reactive oxygen species (ROS) and activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) were measured. The levels of inflammatory factors were detected by ELISA. Pathological injury in DG was observed using thionine staining. The expression levels of FoxO3a, brain-derived neurotrophic factor (BDNF), postsynaptic density protein 95 (PSD95), synaptophysin (SYN), and proliferation marker Ki67 (Ki67) were determined using western blot.

Results: CUS leads to various abnormal changes, including anxiety- and depressive-like behavior, cognitive impairment, oxidative stress, neuroinflammation, neuropathological alterations in the DG, and decreased expression of FoxO3a, BDNF, PSD95, SYN, and Ki67. All these abnormal changes were significantly alleviated by targeted AAV-FoxO3a injection in the DG.

Conclusions: In conclusion, our study demonstrates that the downregulation of FoxO3a induced by CUS in the DG triggers oxidative stress and inflammatory response, inhibits cell proliferation, and induces abnormal synaptic plasticity, ultimately leading to anxiety- and depressive-like behaviors and cognitive impairment.

Background: The effect of olfactory bulb (OB) and olfactory epithelium (OE) electrical stimulation on epileptiform activity and seizure-induced impairment on synaptic plasticity and memory was investigated in anesthetized and freely-moving animals.

Methods: Male Wistar rats were anesthetized with urethane (1.5 g/kg). Stimulating electrodes were bilaterally placed in either the OB or the OE. Another electrode was placed in the CA1 area for recording epileptiform discharges (EDs) following a pentylenetetrazol (PTZ, i.v.) injection and evoked field potentials following Schaffer collateral stimulation. Subjects were divided into PTZ and control groups. Each group received a 1 Hz stimulation either in the OB (OBS) or the OE (OES). ED threshold and duration, and the ability to generate long-term potentiation (LTP) were assessed. Finally, the effect of OBS on acute PTZ-induced seizures and working memory was investigated in freely-moving animals. OBS significantly increased the ED threshold when applied at 250 µA and decreased ED duration when applied at 125 and 250 µA.

Results: Applying OES had a small effect on the ED threshold but significantly decreased ED duration when applied at 125 and 250 µA. Both OBS and OES mitigated the PTZ-induced increase in basal synaptic transmission. Meanwhile, OBS and OES significantly restored the LTP generation following PTZ injection in anesthetized rats. In addition, applying OBS in freely-moving animals reduced the seizure severity and restored working memory impairment.

Conclusions: OB and OE may be considered effective stimulation targets for the attenuation of epileptiform activity and seizure severity. In addition, both OBS and OES decreased the seizure-induced impairment in LTP generation.

Background: Regular physical activity (PA) confers numerous benefits to both peripheral and cerebral health, including enhanced cardiovascular and muscular function, as well as improved cognitive performance and neuroplasticity. The hippocampus, a brain region highly sensitive to the effects of PA, has been consistently shown to undergo structural enhancements with sustained exercise. However, the impact of physical detraining-the cessation or significant reduction of regular PA-on hippocampal structure remains largely unexplored, particularly in humans. This study aimed to investigate whether a 14-day period of voluntary exercise reduction leads to measurable structural changes in the hippocampus, and whether these changes are associated with anxiety symptomatology.

Results: Paired t-tests analyses did not reveal significant changes in hippocampal volume for the whole sample. However, multiple regression analyses on volume change including physical fitness index and degree of moderate and vigorous PA reduction as independent variables, revealed a significant decrease in hippocampal gray matter volume following detraining in individuals with greater MVPA reduction. Notably, pre and post-detraining state anxiety levels were lower in participants who showed larger reductions in hippocampal volume.

Conclusions: These findings suggest that even short-term interruptions in regular physical activity may prompt rapid structural changes in the hippocampus, modulated by the extent of detraining. The observed relationship between hippocampal volume reduction and decreased state anxiety points to stress regulation as a potential mechanism. Further research is warranted to explore the functional significance and potential reversibility of these neuroplastic changes.

Background: The cytosolic 5'-nucleotidase II (NT5C2) enzyme has been implicated in both psychiatric disorders and metabolic traits, but whether these associations reflect a shared biological basis remains unclear. Here we combined cross-species approaches to investigate how reduced NT5C2 function shapes behavior.

Results: In Drosophila melanogaster, neuronal knockdown of the ortholog dNT5B increased activity around light-dark transitions, reduced sleep fragmentation, and selectively suppressed food intake under satiated conditions. Moreover, analysis of mouse phenotyping data revealed that whole-body Nt5c2 knockout alters locomotor activity, sensorimotor gating, and anxiety-related behaviors. Finally, human variant-trait associations showed reproducible enrichment in both metabolic domains, including body composition and BMI, and neuro-psychiatric outcomes such as schizophrenia, smoking, and anxiety.

Conclusions: Together, these phenotypic findings indicate that NT5C2 is a conserved neuro-metabolic regulator, linking energy-related pathways to specific behavioral dimensions that may underlie its pleiotropic impact on psychiatric and metabolic risk.

Background: This study aims to investigate the differences in neural network connectivity within the prefrontal cortex (PFC) among elderly individuals with normal cognition (NC), mild cognitive impairment (MCI), and Alzheimer's disease (AD) using functional near-infrared spectroscopy (fNIRS).

Results: Significant differences in functional connectivity (FC) strength were observed between the NC, MCI, and AD groups in several Brodmann areas (BA) pairs, including BA46.L-BA45.R and BA9.L-BA1.L. The most pronounced FC strength differences between the NC and MCI groups occurred at the 2nd -minute mark in BA45.R, while differences between the MCI and AD groups peaked at the 5th-minute mark in BA1.L. Additionally, the NC and MCI groups displayed FC strength differences during the first 2 minutes and first 3 minutes, again with BA45.R being central. FC strength between BA46.L-BA45.R was negatively correlated with Neuropsychiatric Inventory and Clinical Dementia Rating scores.

Conclusions: FC strength in the left dorsolateral PFC, where BA46.L and BA9.L are located, emerged as a key region for cortical dysfunction in cognitive impairment. Moreover, there were differences in FC across levels of cognitive impairment, and significant correlations between differences in FC strength in BA brain regions and cognitive level.

Social ties critically influence individual health and well-being, raising important questions about why some individuals occupy advantageous social network positions. While social cognition is known to play a key role, it remains unclear whether neural differences during social information processing is associated with variability in the social network structure. Using the Prisoner's Dilemma Game (PDG) combined with multilayered social network analysis, brain network analysis, and machine learning, we investigated how neural activation patterns relate to individual social network structures. The results revealed that individuals with a larger social network size were associated with (1) heightened nodal efficiency in the midcingulate cortex (MCC), (2) reduced efficiency in the inferior occipital gyrus (IOG), (3) enhanced functional connectivity between the anterior cingulate cortex-supplementary motor area (ACC-SMA) and olfactory-somatosensory regions, and (4) significantly negative predictive effects of nodal efficiency in both the IOG and hippocampus (as identified through machine learning). These findings demonstrate that efficient brain network organization, characterized by optimized integration in the cingulate cortex with a conflict monitoring function and selective suppression of visual attention and memory processing, is related to real-world social adaptation. Our study offers novel neurobiological insights into social networks, highlighting the crucial role of neural efficiency in social resource acquisition.

Background: Opioid use disorder is driven by neurobehavioral adaptations where environmental cues trigger relapse. Consequently, extinction therapy (ET) aims to modify drug-associated memories but has limited long-term efficacy. Recently, evidence suggested that glial cells may contribute to neuroplasticity phenomena in addiction. In this sense, this study examined whether aversive memories of morphine withdrawal and their extinction induce transcriptional changes in glial markers (gfap, aif1, itgam, klf4) in key memory-related regions: the basolateral amygdala (BLA) and hippocampus (dentate gyrus [DG] and CA1).

Results: Using the conditioned place aversion (CPA) paradigm in rats, we assessed avoidance behavior after naloxone-precipitated withdrawal and its extinction. Transcriptional analyses did not reveal major changes in the BLA. However, in CA1, downregulation of microglial markers cooccurred with aversive memory retrieval and restored after extinction. Moreover, one of the microglial markers, klf4, was reduced concomitantly with extinction memory retrieval in the DG. Correlation analyses showed negative associations between microglial markers and aversive memory strength, suggesting glial involvement in withdrawal-related learning.

Conclusions: These findings might indicate that microglial activity in CA1 plays a role in opioid withdrawal-associated memories, and extinction training might be returning these effects to basal levels. Therefore, targeting glial responses could provide new therapeutic strategies to prevent relapse.

Background: A common magnitude system-consistently involving the right intraparietal sulcus (IPS)-has been proposed to support the representation of space, time and numerosity. While shared mechanisms are acknowledged, domain-specific contributions have also been suggested. Among these, the role of the right precuneus remains debated, with inconclusive evidence regarding its involvement in spatial and temporal processing. Translating this question into the language domain and within a grounded cognition framework, we investigated the causal contribution of the IPS and precuneus to the processing of spatial and temporal concepts (e.g., circuit, eternity) using a state-dependent Transcranial Magnetic Stimulation (TMS) priming paradigm. Twenty healthy participants received stimulation over the IPS and precuneus, and a sham stimulation over the control site (vertex).

Results: Results showed that stimulation of the IPS abolished the priming effect observed under the sham control condition for both spatial and temporal concepts, whereas stimulation of the precuneus selectively disrupted priming for temporal concepts only.

Conclusions: These findings support the role of the right IPS as a key area for magnitude processing in language, while also highlighting a more specific contribution of the precuneus-particularly its ventral portion-to temporal concepts.