The visual word form area (VWFA) has been proposed to function as a multiplex hub integrating both attentional and linguistic processing, yet how its functionally distinct subregions dynamically reconfigure their network connectivity across cognitive contexts remains unclear. This study examined resting-state and task-evoked functional connectivity of two VWFA subregions-posterior VWFA-1 and anterior VWFA-2-with predefined attention and language network regions of interest in 20 healthy adults performing a visuospatial flanker task and a Korean lexical decision task. We hypothesized that the posterior-to-anterior anatomical gradient corresponds to an attention-to-language functional role differentiation, observable both in intrinsic connectivity and in task-dependent reconfiguration. At rest, the VWFA exhibited a posterior-to-anterior intrinsic gradient, with VWFA-1 preferentially coupled to the attention network and VWFA-2 to language regions. Across both tasks, task context differentially shifted attention-network connectivity between VWFA-1 and VWFA-2, broadly following the intrinsic gradient. The alignment was only partial, however, as during lexical decision it was the posterior VWFA-1 rather than the anterior VWFA-2 that increased its coupling with the language network. Behaviorally, attention connectivity predicted accuracy across tasks from both subregions equivalently rather than from the gradient itself, suggesting a shared attention-based mechanism rather than gradient-specific contributions. Together, these findings provide preliminary support for the view that intrinsic VWFA organization shapes task-specific routing of attention network interactions, while behavioral performance converges on a shared attention-based mechanism.

This study used the sound-induced flash illusion (SIFI) paradigm to investigate how sensory congruency, audiovisual rhythm configurations, and momentary neural states jointly shape perceptual decisions by integrating trial-level EEG and behavioral data within a hierarchical Bayesian regression framework. Thirty healthy adults performed six beep-flash conditions (B0F1, B0F2, B1F1, B1F2, B2F1, and B2F2), encompassing two visual-only baseline conditions, two audiovisually congruent conditions, and two incongruent audiovisual illusion conditions, while response accuracy and reaction time (RT) were recorded together with prestimulus occipital α-band power, auditory and visual N1 amplitudes, and the centro-parietal positivity (CPP) indexing evidence accumulation. We first characterized condition effects and EEG-behavior relationships using repeated-measures ANOVAs and correlations, and then jointly modeled accuracy (Bernoulli likelihood with logit link; effects reported as odds ratios) and RT (Student-t likelihood on logRT; effects interpreted as percentage change in median RT) using trial-level hierarchical Bayesian regression, with model generalizability assessed via Pareto-smoothed importance sampling leave-one-out (PSIS-LOO) cross-validation. Behaviorally, unimodal and congruent conditions yielded faster and more accurate responses, whereas incongruent conditions-particularly the "2 beep-1 flash" configuration-produced elevated illusion rates and markedly prolonged RTs, highlighting the role of causal structure and signal reliability in cross-modal weighting. Neurally, higher trial-level prestimulus α power was reliably associated with reduced odds of a correct response, consistent with lower cortical excitability and a more conservative decision criterion; larger auditory N1 amplitudes predicted faster responses; and CPP slope closely tracked RT in descriptive analyses, consistent with its interpretation as an accumulation-to-bound signal. Model comparisons indicated that experimental conditions accounted for most of the behavioral variance, whereas EEG covariates added limited and non-robust incremental out-of-sample predictive value under the present linear additive specification. Nevertheless, prestimulus α showed a stable negative association with accuracy, and auditory N1 showed a weaker association with response speed, indicating that these neural measures remain theoretically informative even though they did not materially improve overall model generalizability.

Neurofeedback Training (NFT) employs real-time feedback on brain activity to empower participants to self-regulate cognitive functions within specific brain regions. Understanding the neurophysiological correlates of NFT is critically important, as these remain largely unclear, especially regard to their neural underpinnings. This study aims to investigate whether and to what extent NFT enhances attentional orientation and executive control in healthy adults, and to explore the potential electrophysiological features associated with these behavioral changes. Participants were divided into two groups: the neurofeedback group (NF, n = 19), who received real-time EEG signal feedback from the F3 electrode with training in the beta1 band (15-18 Hz); and the sham group (sham, n = 18), who watched pre-recorded videos unrelated to brain activity. Both groups underwent pre- and post-intervention assessments, which encompassed attention tasks and EEG data collection. Behavioral results demonstrated that the NF group achieved improvements in attention performance compared to the sham group. These findings were corroborated by event-related potential (ERP) data: post-intervention, the NF group exhibited enhanced N1 amplitudes during attention-orienting tasks and increased N2 amplitudes during executive control tasks. Furthermore, the NF group showed a phased increase in beta1 power during training, reaching statistical significance by the third session, whereas the sham group remained stable. These findings suggest that NFT may, to some extent, modulate attention-related neural activity, thereby potentially contributing to the enhancement of attentional task performance in healthy adults.

Depression is a common psychiatric disorder during pregnancy and the postnatal period. Consequently, antidepressant treatment is primordial for the safety of the mother and the neonate. Clomipramine (CMI) is a tricyclic antidepressant that has been prescribed even when the evidence suggests potential adverse effects on the neurodevelopment of the offspring, considering that antidepressant drugs can be transferred through breast milk. Nevertheless, in some cases, when the benefits outweigh the risks, it is used to treat severe depression in pregnant women. In rodents, postnatal administration of CMI causes persistent behavioral and neurophysiological alterations in adulthood. By contrast, a rewarding experience, such as mating, improves motivational and copulatory behavior in rodents through neuroplasticity in brain structures involved in reproduction. In a previous work, we reported that postnatal exposure to CMI disrupts the motivational and copulatory components of female sexual behavior during a single copulatory test. Therefore, the purpose of this study was to examine the effects of postnatal CMI treatment on female sexual behavior and reproductive tissues, and to determine whether sexual experience serves as a modulatory factor that ameliorates its potential impact on sexual performance. Female pups were divided in two groups, CMI group (30 mg/Kg) and the control group (NaCl 0.9%). Each group received a daily subcutaneous injection with CMI or saline solution from the 8th to 21st postnatal days. Behavioral test and histological analysis were performed at 3 months of age. The results indicated that postnatal CMI administration disrupts receptive but not proceptive behaviors. Repeated sexual encounters with males partially reversed the receptivity impairment in CMI-treated females, as it occurs in control rats. Histological data showed that CMI reduces the population of primordial and primary follicles; however, no morphological modifications were detected in the uterine layers. In conclusion, the data show that even when sexual experience partially improved copulatory behavior in female rats exposed to CMI during the postnatal period, ovarian development was affected, which could compromise fertility.

Hoxa5 encodes a transcription factor essential for embryonic patterning and organogenesis, with sustained expression in hindbrain precerebellar nuclei during postnatal development. Given prior evidence implicating HOXA5 in synaptogenesis and early postnatal circuit maturation, we investigated whether its inactivation during this critical developmental window contributes to neurodevelopmental disorder (NDD)-related phenotypes. Using previously generated transcriptomic data, we identified multiple deregulated genes classified as autism spectrum disorder (ASD) risk genes in the SFARI database, several of which are associated with a cerebellar phenotype in mice. We then performed a comprehensive behavioral assessment across motor, social, stereotypical, anxiety-related, and attentional domains in a postnatal inactivation mouse model (Hoxa5-cKO). Motor coordination, learning, gait, and sensorimotor functions were preserved. Social behavior assays yielded no consistent genotype-dependent effects, although results were sensitive to analytical methods and cohort variability. In contrast, Hoxa5-cKO mice exhibited increased stereotypical behaviors, including elevated scratching and marble burying, in the absence of anxiety- or locomotion-related confounds. Importantly, interpretation of social and cognitive phenotypes was impacted by well-known constraints of behavioral neuroscience. We discuss these downfalls and propose additional guidelines. Altogether, our findings indicate that postnatal Hoxa5 deficiency selectively enhances stereotyped behaviors without broadly affecting motor or social functions. The data support a model in which HOXA5 acts as a modulator of postnatal precerebellar circuit connectivity and/or function, with subtle behavioral consequences that require further research in specific genetic or environmental contexts.

Ketamine, a dissociative anesthetic, induces behavioral and molecular alterations associated with psychosis-like phenotypes. However, the epigenetic mechanisms bridging its cellular effects with behavioral outcomes are poorly defined. Here, we report that ketamine induces histone H3 Ser10 phosphorylation in both hippocampal neurons (HT22 cells) and the mouse hippocampus, an effect primarily driven by JNK activation. Critically, pharmacological inhibition of JNK with SP600125 not only reversed this epigenetic mark but also robustly attenuated ketamine-induced hyperlocomotion and cognitive deficits in mice. Integrated multi-omics analysis of the hippocampus 30 min post-ketamine revealed coordinated transcriptional and chromatin accessibility changes. We identified 262 differentially expressed genes (e.g., MAP3K9) enriched in MAPK signaling and neuroactive ligand-receptor pathways, alongside 165 differentially accessible regions, with motif analysis implicating CTCF as a key regulator. Our findings suggest that JNK-mediated H3S10 phosphorylation may play a critical role in linking ketamine exposure to psychosis-like phenotypes, providing a mechanistic framework that connects stress-sensitive signaling to rapid chromatin remodeling and sustained transcriptional reprogramming. This work unveils potential novel therapeutic targets for psychosis centered on the JNK-H3S10 phosphorylation axis.

Post-traumatic stress disorder (PTSD) is associated with cognitive impairments, anxiety, fear extinction deficits, and neurobiological alterations, particularly in the hippocampus. Oxidative stress, reduced brain-derived neurotrophic factor (BDNF), and dendritic remodeling are key contributors to these dysfunctions. This study investigated whether Ginkgo biloba extract, known for its antioxidant and neuroprotective properties, could ameliorate PTSD-like symptoms and hippocampal abnormalities in male rats exposed to the single prolonged stress (SPS) model. Adult male Wistar rats were exposed to SPS and treated with Ginkgo biloba extract (20 or 200 mg/kg) for 14 days. Behavioral assessments included anxiety-like behavior, fear extinction, spatial learning and memory, and working memory. Hippocampal tissue was analyzed for oxidative stress markers (MDA, SOD, TAC), BDNF expression (Western blot), and CA3 dendritic morphology (Golgi-Cox impregnation method). SPS exposure induced marked behavioral deficits, elevated oxidative stress, reduced BDNF expression, and dendritic atrophy in CA3 pyramidal neurons. Ginkgo biloba extract, particularly at a dose of 200 mg/kg, significantly attenuated anxiety-like behaviors, facilitated fear extinction, improved memory performance, reduced oxidative damage, restored BDNF levels, and reversed dendritic retraction and branching deficits in the CA3 region of the hippocampus. These findings demonstrate that Ginkgo biloba extract exerts neuroprotective effects against trauma-induced behavioral, molecular, and structural abnormalities in a validated animal model of PTSD. While promising, these results are based on preclinical data, and further studies are necessary to determine whether similar benefits can be translated to clinical populations.