Behavioural Brain Research最新文献

This study explores how cognitive style diversity (differences in information processing among team members) influences group creativity through interpersonal neural mechanisms. 116 college students were assigned to high-diversity (HD) groups (mix of field-independent and field-dependent individuals) or low-diversity (LD) groups (homogeneous cognitive styles). Both groups completed a creative task (umbrella design) and a routine task (desk purchase) while their prefrontal cortex (PFC) and right temporoparietal junction (r-TPJ) activity was monitored via fNIRS. Results revealed that HD groups produced significantly more novel ideas than LD groups. fNIRS data showed enhanced brain synchronization in HD groups within the frontal pole and dorsolateral prefrontal cortex (DLPFC). Field-independent individuals dominated neural interactions in HD groups, with delayed inter-brain synchronization positively correlating with creative novelty. Findings suggest cognitive diversity fosters group creativity through complementary neural coordination between field-independent and field-dependent individuals.

Previous research has linked psychiatric disorders to alterations in the aperiodic exponent-a measure of excitatory-inhibitory (E/I) balance derived from resting-state EEG that reflects broadband, non-oscillatory brain activity. This measure also appears sensitive to age-related neurodevelopmental changes. In this study, we investigated whether the aperiodic exponent varies with age in children and adolescents diagnosed with adjustment disorder (AD) or oppositional defiant disorder (ODD), compared to age-matched healthy controls. While healthy participants showed no significant association between age and the aperiodic exponent, both clinical groups exhibited a pronounced nonlinear relationship. Specifically, the exponent was lower in early childhood and early adulthood, but peaked around 9 to 10 years of age. This U-shaped developmental trajectory suggests a deviation from normative brain maturation in AD and ODD and points to temporally specific alterations in cortical E/I balance. These findings underscore the potential of the aperiodic exponent as a developmentally sensitive neural marker of externalising psychopathology and may inform age-tailored diagnostic and intervention strategies in child and adolescent psychiatry.

Growing evidence suggests that resveratrol possesses neuroprotective properties against arsenic toxicity. This study investigated whether resveratrol could ameliorate arsenic-induced depression-like behaviors in male Naval Medical Research Institute (NMRI) mice and explored potential molecular mechanisms. Mice were exposed to arsenic (50mg/L in drinking water) for 4 weeks and treated with resveratrol (10 or 20mg/kg). Behavioral assessments included the hole-board test (HBT) for exploratory behavior, and the sucrose splash test (SST), tail suspension test (TST), and forced swim test (FST) for depression-like behaviors. The mRNA levels of Bdnf, Creb1, and Dvl1 in the brain were analyzed by qRT-PCR. Arsenic exposure induced significant depression-like behaviors, characterized by decreased grooming in SST and increased immobility in TST and FST. Resveratrol treatment prevented these behavioral alterations and exhibited intrinsic antidepressant effects in naïve mice, with dose-dependent reductions in immobility time (FST) and increased grooming (SST). Notably, resveratrol (20mg/kg) enhanced rearing frequency in naïve mice and decreased it in the arsenic-treated mice. At the molecular level, arsenic downregulated Bdnf expression, while resveratrol restored its levels. In contrast, no significant changes in Creb1 and Dvl1 expression were observed. These findings indicate that resveratrol mitigates arsenic-induced depression-like behaviors primarily through the modulation of Bdnf-dependent pathways, independent of Creb1 and Dvl1. These results position resveratrol as a potential antidepressant and underscore its therapeutic promise for mood disorders associated with environmental toxicant exposure.

Chronic neuropathic pain affects 7-10% of the population and is often accompanied by emotional impairments, greatly reducing the quality of life of patients. Recently, we showed that in the chronic constriction injury (CCI) model of experimental neuropathic pain, female (but not male) rats showed a delayed but progressive development of mechanical and cold allodynia, which did not improve over time. In this work, we characterised the CCI-induced nociceptive and emotional impairments at earlier (2 weeks) and later (8 weeks) time points in both male and female rats. Both neuropathic males and females developed mechanical allodynia from week 1 onwards; however, males were shown to recover earlier at week 3, corroborated by sciatic nerve histopathology. Importantly, both males and females displayed cold allodynia throughout the experimental period (8 weeks). Regarding emotional impairments, males showed a more anxious and depressive phenotype than females, independently of CCI. Electrophysiological recordings suggest time-dependent changes in descending inhibition from the rostral ventromedial medulla (RVM) in response to CCI-induced neuropathic pain. Altogether, our results show the existence of sex-specific differences in the development and maintenance of CCI-induced nociceptive and emotional impairments, highlighting the need to include female subjects in the study of neuropathic pain mechanisms and treatments.

Rapid and precise activation of the laryngeal musculature, particularly the thyroarytenoid (TA), is required for the production of rat ultrasonic vocalizations (USVs). Although the role of the TA in USV production has been established through denervation and excised larynx studies, how TA muscle dysfunction affects USV acoustics remains unknown. This study examined how iatrogenic, transmuscular vocal fold injury influences USV production by comparing acoustic parameters between rats receiving bilateral transmuscular vocal fold injury (including the TA muscle) versus sham surgery. Twenty adult male rats were randomly assigned to injury or sham groups and assessed at 30 or 60 days post-surgery. USVs were recorded at each timepoint (pre- and post-surgery) and analyzed for changes in principal frequency, frequency complexity (standard deviation and sinuosity), power (intensity of the USV), tonality, and duration. Injury significantly decreased USV frequency complexity and reduced the likelihood of producing frequency-modulated vocalizations in both post-surgical time groups. These findings demonstrate that while TA muscle integrity is crucial for frequency modulation, it is not necessary for basic USV production, offering new insights into the biomechanical role of the TA muscle in rat vocalization and laying the groundwork for investigating therapeutic interventions targeting laryngeal muscle function.

Astrocytes are one of the glial cells of the nervous system. These cells reach their maximum number in the first two weeks after birth. Therefore, during this period they are sensitive to adverse conditions, including separation from the mother. One of the factors is the stress-modulating hormone oxytocin (OT). Adolescent male Wistar rats were used in this study. Rat pups were subjected to the MS protocol for 180 min per day from postnatal day 1-21 (postnatal day (PND)). Then, from PND 22-34, OT was administered intranasally (2 μg/μl, for 7 days). Behavioral assessments were performed on PND 35-37, we prespecified glial fibrillary acidic protein (GFAP)+ astrocyte density and morphology as the primary outcome, given astrocytes' active roles in synaptic plasticity, stress regulation, and oxytocin signaling; the neuron degeneration ratio and p38/p-p38 expression were treated as secondary outcomes. MS did not alter locomotion; it increased anxiety-like behavior in the Zero Maze Test (ZMT) (but not in the Open Field Test (OFT)) and elevated olfactory thresholds. MS also increased the degenerated/healthy neuron ratio and p38/p-p38 protein levels, and reduced GFAP+ astrocyte density and process size in hippocampal CA1; OT partly reversed these glial/inflammatory changes without affecting the neuron degeneration ratio. These findings suggest that OT could serve as a therapeutic agent to improve some of the adverse behavioral and histological effects of MS in modern societies.

Stroke represents a leading cause of non-traumatic prolonged disorders of consciousness (pDoC). Given the prefrontal cortex's critical role in consciousness, this study aimed to explore the abnormalities in the prefrontal network in post-stroke pDoC patients. Using resting-state functional near-infrared spectroscopy (fNIRS), we acquired data from 21 post-stroke pDoC patients and 19 age- and gender-matched healthy controls (HC). Based on the Coma Recovery Scale-Revised, patients were classified into 12 with minimally conscious state (MCS) and 9 with unresponsive wakefulness syndrome (UWS). We analyzed and compared functional connectivity and topological properties of the prefrontal network across groups. Compared to HCs, the pDoC group exhibited extensively weakened functional connectivity and disrupted network topology, as evidenced by a lower clustering coefficient (Cp), reduced local efficiency (Eloc), global efficiency (Eg) and a longer characteristic path length (Lp). Reductions in key nodal metrics which including nodal clustering coefficient (NCp), nodal efficiency (Ne), and degree centrality (DC) were also observed across several prefrontal regions. In the direct comparison between patient subgroups, the MCS group demonstrated significantly stronger functional connectivity within the right premotor and supplementary motor cortex (PreM & SMA_R) than the UWS group, but conversely, showed weaker connectivity within the left frontopolar area (FPA_L). Consequently, assessing prefrontal network integrity with portable fNIRS holds promise for identifying potential biomarkers to diagnose and monitor post-stroke prolonged disorders of consciousness.

Oxytocin (OT), a neuropeptide known for its role in social behavior, has unclear neural mechanisms when administered intranasally, especially across different ages. Brain entropy (BEN), a metric of neural irregularity, shows promise for revealing OT's neurophysiological effects. This study examined whether BEN could detect neural changes induced by intranasal OT and how these effects are modulated by age. In a randomized, double-blind, placebo-controlled trial, young adults (YA) and older adults (OA) were assigned to receive intranasal OT or placebo (PL). Using fMRI-based BEN mapping, we identified a significant age-dependent effect in the left temporoparietal junction (TPJ), where OT increased BEN in YA but decreased it in OA. Further analyses showed OT also elevated the fractional amplitude of low-frequency fluctuations (fALFF) in the same region, particularly in YA. Additionally, OT enhanced functional connectivity within the left TPJ and between the left and right TPJ in both age groups. These results establish BEN as a sensitive biomarker capable of capturing age-specific OT effects, providing information beyond traditional measures of oscillatory power and temporal synchronization. The findings suggest that the timing of post-administration brain state changes under OT may vary with age, potentially due to differences in OT receptor density.

Arginine vasopressin (AVP) is well established in regulating social cognition and emotional responses in males. However, its roles in these processes in females and the underlying circuit mechanisms, remain poorly understood. In this study, female mice spent significantly more time sniffing the anogenital region of unfamiliar conspecifics compared to familiar individuals. Fiber photometry recordings revealed that the calcium activity in paraventricular nucleus of the hypothalamus (PVN) AVP neurons was elevated when sniffing unfamiliar mice relative to familiar ones. No significant differences were observed during non-social exploratory behaviors such as bedding sniffing or self-grooming, indicating a specific involvement of these neurons in social investigation. Retrograde tracing using cholera toxin B (CTB) confirmed direct projections from AVP neurons in the PVN to the medial amygdala (MeA). Chemogenetic inhibition of the PVN-MeA AVPergic pathway impaired social recognition and reduced anxiety-like behaviors. Furthermore, bilateral microinjection of the V1a receptor (V1aR) antagonist into the MeA decreased both anxiety-like behaviors and social investigation toward unfamiliar mice. These findings demonstrate that the AVPergic projection from the PVN to the MeA modulates social cognition and emotional state in female mice, providing a circuit mechanism for social and affective dysregulation and offering potential targets for the treatment of related neuropsychiatric disorders.