NEUROSCIENCE神经科学
NEUROSCIENCE(英文缩写 NEUROSCIENCE),ISSN 0306-4522,eISSN 1873-7544,中文译名:神经科学 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-09-27 至 2026-09-27，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 3.708 | Q3 |
| 2022 | 3.300 | Q3 |
| 2023 | 2.900 | Q2 |
| 2024 | 2.800 | Q3 |
| 2025 | 3.300 | Q2 |
NEUROSCIENCE 最新收录文献
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2. Multi-omics integration identifies VIM and LGALS3 as apoptosis-associated genes in astrocytes after traumatic brain injury.
PMID:日期:2026-10-15Apoptosis contributes substantially to neurological deficits after traumatic brain injury (TBI), yet the molecular drivers and cellular regulation of astrocyte-associated apoptosis remain poorly defined. We integrated bulk RNA-seq, single-cell RNA-seq, and spatial transcriptomics to identify apoptosis-related hub genes in TBI. Differentially expressed genes were intersected with apoptosis-related genes and ranked by protein-protein interaction network topology. Astrocyte heterogeneity was examined through sub-clustering, pseudotime, regulon, and in silico transcription-factor perturbation analyses. Findings were validated in vivo using a Feeney weight-drop model and in vitro using an astrocyte scratch model, with Western blot, immunofluorescence co-staining, siRNA knockdown, wound-healing, CCK-8, and flow-cytometric apoptosis assays. VIM and LGALS3 were identified as the apoptosis-related hub genes and showed reproducible injury-associated upregulation across multiple independent datasets. Single-cell analysis showed their expression in a reactive astrocyte subpopulation, with levels rising along the homeostatic-to-reactive trajectory. CEBPB, FOSL1/FOSL2, and MAFF showed higher regulon activity in TBI-reactive astrocytes, and there in silico knockout shifted reactive astrocytes toward the homeostatic state. Spatially, both transcripts accumulated in the lesion core and peri-lesional zones, coinciding with elevated apoptotic activity. Western blot confirmed their upregulation in vivo and in vitro, and immunofluorescence co-staining of injured cortical tissue showed their expression in GFAP-positive astrocytes; silencing either genes reduced astrocyte migration, and flow cytometry together with an increased cleaved-caspase-3/caspase-3 ratio indicated enhanced apoptotic signaling. In astrocytes after TBI, VIM and LGALS3 modulate migration and apoptotic signaling, representing candidate molecular markers and potential therapeutic targets for secondary brain injury that warrant further validation.
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3. Autophagy as a mechanistic link between physical exercise and Alzheimer's disease.
PMID:日期:2026-10-15Alzheimer's Disease (AD), the most prevalent cause of dementia worldwide, is a neurodegenerative disorder that currently has no cure. A growing body of evidence suggests that physical exercise is a potential non-pharmacological strategy in the treatment of AD. Recent findings highlight the involvement of autophagy in the modulatory actions of physical exercise for AD. Here, we present a narrative review of the current knowledge on how exercise impacts AD, specifically focusing on its regulation of autophagic activity in animal models of AD. Evidence from rodent studies further demonstrates that exercise may influence AD-related pathology through autophagy-lysosomal regulation, lysosomal homeostasis, and mitochondrial quality control, but direct human evidence remains limited. This review uniquely positions exercise-induced autophagy regulation as a central mechanistic hub, offering a novel paradigm for developing lifestyle-based interventions for AD.
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4. Integrative insights into ε subunit-containing GABAA receptors: exploring non-canonical modulation by zolpidem.
PMID:日期:2026-10-15Zolpidem is a widely prescribed hypnotic agent that has been reported to produce paradoxical neurological effects in a subset of patients with conditions such as disorders of consciousness and other forms of neurological injury, including transient improvements in arousal and function. The mechanisms underlying these responses remain incompletely understood. This review critically synthesizes evidence supporting the hypothesis that non-canonical ε subunit-containing GABAA receptors, may contribute to these atypical effects of zolpidem. Evidence from heterologous expression systems indicates that incorporation of the ε subunit can alter GABAA receptor gating and reduce sensitivity to classical benzodiazepine-site ligands, with some studies reporting zolpidem-dependent modulation. However, these findings are derived primarily from recombinant systems and do not establish the existence, distribution, or functional significance of defined ε-containing receptor assemblies in native brain tissue. In vivo studies have reported altered ε subunit expression following neurological injury together with behavioural responses to zolpidem, although these associations remain correlative. Computational modelling and molecular docking studies further suggest the possibility of non-canonical ligand-receptor interactions, but these predictions have yet to be validated experimentally. Collectively, the available evidence identifies ε-containing GABAA receptors as a biologically plausible but unproven contributor to the paradoxical neurological effects of zolpidem. By integrating findings across molecular, experimental, and computational studies, this review highlights key limitations in the current evidence base and outlines priorities for future research aimed at determining whether ε-containing GABAA receptors play a causal role in zolpidem-induced neurological responses.
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5. Automated autism spectrum disorder detection using EEG signals and time-frequency visibility graphs.
PMID:日期:2026-10-15Early and objective screening of Autism Spectrum Disorder (ASD) remains challenging because conventional diagnosis primarily relies on behavioural assessment and clinical observation. To address this limitation, this study proposes a dual-domain computational framework for automated EEG-based ASD classification by integrating complementary time-frequency analysis with Horizontal Visibility Graph (HVG)-based network modelling. Four time-frequency decomposition techniques, namely the Short-Time Fourier Transform (STFT), Discrete Wavelet Transform (DWT), Wigner-Ville Distribution (WVD), and Superlet Transform (SLT), were employed to characterise the non-stationary dynamics of resting-state EEG signals. The resulting time-frequency representations were transformed into HVG networks, from which 17 graph-theoretic descriptors were extracted and evaluated using conventional machine learning classifiers, including a Soft Voting Ensemble. Among the investigated methods, the DWT-HVG framework combined with the Soft Voting Ensemble achieved the best performance, yielding an accuracy of 93.54%, sensitivity of 94.32%, specificity of 92.76%, F1-score of 93.62%, balanced accuracy of 93.54%, and an Area Under the Curve (AUC) of 98.17% using stratified 10-fold cross-validation. Statistical analysis using the Wilcoxon signed-rank test further confirmed the superiority of the DWT-based representation over the STFT, WVD, and SLT-based approaches. These findings demonstrate that integrating multiresolution time-frequency analysis with HVG-based graph-theoretic feature extraction provides an accurate, interpretable, and computationally efficient framework for objective EEG-based ASD screening.
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6. Aftereffects of 1-week chronic intermittent hypoxia on the jaw muscle electromyographic activities during sleep in young adult rats.
PMID:日期:2026-10-15Obstructive sleep apnea (OSA) is associated with increased jaw muscle activity during sleep across a wide age range from childhood to adulthood. However, the contribution of intermittent hypoxia to jaw muscle activity remains unclear. We hypothesized that chronic intermittent hypoxia (CIH) enhances arousal-related jaw muscle activity during sleep through neuroplastic changes in trigeminal motor system in young adult rats. Six-week-old rats were exposed to CIH (nadir O_2, 5%) for 6 h/day during the light phase for 1 week. At 7 weeks of age, immunohistochemical analyses were performed to assess FosB expression in brainstem regions containing trigeminal premotor neurons and dopamine-β-hydroxylase-positive fiber density in the trigeminal motor nucleus. At 7 weeks of age after CIH exposure, electrophysiological recordings were conducted to analyze masseter and digastric muscle activity during sleep-wake cycles. CIH increased FosB expression in multiple brainstem regions containing trigeminal premotor neurons and enhanced noradrenergic fiber density in both dorsolateral and ventromedial regions of the trigeminal motor nucleus. Sleep architecture, electroencephalography spectral power, and open-field behavior remained unchanged between groups. While masseter muscle activity was stable across vigilance states, CIH selectively increased digastric muscle activity during arousal from sleep. One-week CIH induces plasticity in trigeminal circuits and enhances arousal-related jaw-opening muscle responsiveness in young adult rats, without altering overall sleep structure.
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7. Behavioral and transcriptional divergence across rat strains differing in the nervous system excitability.
PMID:日期:2026-10-15Trait differences in nervous system excitability may contribute to individual variation in behavioral reactivity and stress susceptibility, but the associated molecular organization remains poorly understood. We examined behavioral and transcriptional divergence in two selectively bred rat strains with contrasting excitability thresholds: high-threshold, low-excitability (HT) and low-threshold, high-excitability (LT). LT rats showed strongly reduced acoustic startle responsiveness, whereas multivariate analysis of open field and elevated plus maze behavior separated the strains along axes reflecting defensive behavior, exploration, avoidance, and risk assessment. Prolonged emotional-pain stress shifted HT and LT rats, but not outbred Wistar, toward increased defensive behavior and reduced exploration. Gene set enrichment analysis of hippocampal and amygdalar RNA-seq data revealed region-specific molecular divergence between the selected strains. The amygdala showed only limited pathway-level differences, mainly involving interferon-related signatures. The hippocampus showed broader differences: metabolic, proteostatic, secretory, and synaptic vesicle-related gene sets were enriched toward the LT-upregulated end of the ranked gene list, whereas glial, inflammatory, hypoxia-, apoptosis-, and tissue-remodeling-related gene sets were enriched toward the HT-upregulated end. In addition, the transcriptional excitation/inhibition (E/I) index was significantly lower in the hippocampus of LT rats, while no comparable difference was detected in the amygdala. These findings identify the hippocampus as a major site of transcriptional divergence associated with inherited excitability thresholds and suggest that high trait excitability may be accompanied by compensatory E/I-related molecular organization. More broadly, excitability appears not as a simple linear driver of reactivity, but as a trait around which distinct behavioral and molecular regulatory states can be organized.
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8. CNNM2 in schizophrenia: multilevel evidence of genetic susceptibility, magnesium homeostasis, neurodevelopment and cognitive dysfunction.
PMID:日期:2026-10-15Schizophrenia (SCZ) is a common psychiatric disorder with a complex, genetically and environmentally influenced etiology, but the specific pathogenesis remains unclear. In recent years, the SCZ susceptibility gene CNNM2 (encoding cyclin M2) located at the 10q24.32-33 locus has received widespread attention. The well-validated SCZ risk interval 10q24.32-33 harbors two independent risk variants: rs11191580 in NT5C2 (significantly associated with CNNM2 mRNA and protein levels) and rs7914558 in CNNM2. Results from functional genomic analyses indicate that lower CNNM2 expression is significantly associated with SCZ. Imaging genetics studies have demonstrated that carriers of risk alleles of CNNM2 SNPs exhibit alterations in brain structure. Animal model studies have revealed that Cnnm2 downregulation in mice leads to impairments in sensorimotor gating and cognitive function. As an Mg transporter, CNNM2 primarily maintains systemic Mg homeostasis. According to clinical studies, a proportion of patients with SCZ exhibit reduced Mg concentrations in plasma and cerebrospinal fluid. CNNM2 dysfunction may contribute to the pathology of SCZ by disrupting Mg homeostasis, thereby affecting neurodevelopment and synaptic plasticity. A systematic consolidation of current evidence supporting the involvement of CNNM2 in SCZ pathogenesis provides a direction for further investigation of the pathological mechanisms underlying this disease, and for identification of novel targets for clinical intervention..
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9. Exploring the antidepressant-like effects of cannabidiol and/or temozolomide in female mice with induced glioblastoma.
PMID:日期:2026-10-15Temozolomide (TMZ), the gold standard drug used for the treatment of glioblastoma, is known to affect healthy brain proliferating cells, inhibiting adult hippocampal neurogenesis. Since most antidepressants mediate their beneficial effect through this process and given the large proportion of glioblastoma patients with depressive symptoms, this preclinical study evaluated the interaction between TMZ and cannabidiol (CBD), a cannabinoid compound with antidepressant-like potential. To do so, adult female nude mice were intracranially implanted with GL261 tumor cells and treated with TMZ (5 mg/kg) or PBS twice a week. Additionally, animals received CBD (30-45 mg/kg) 5 days/week (1 dose/day) rendering two groups (PBS-CBD vs. TMZ-CBD). To control for the effects of TMZ alone a group of mice was treated with vehicle (TMZ-Veh). MRI was used to evaluate tumor growth and/or its suppression by treatment. Antidepressant-like responses were assessed under stressful settings (forced-swim or tail-suspension tests) and brain samples were collected to evaluate hippocampal neuroplasticity/neurotoxicity markers. The main results showed that the combined treatment with TMZ-CBD decreased tumor volume, induced signs of antidepressant-like responses, while modulated hippocampal FADD as compared to PBS-CBD female mice. However, these effects were no different than the ones observed by TMZ-Veh, suggesting that TMZ alone was sufficient to observe the behavioral and neurochemical responses, and that adding a concomitant CBD treatment did not change that outcome. This data adds to our recent studies suggesting some beneficial affective-like responses induced by TMZ in rodents, while validating them in a female mice model with induced glioblastoma.
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10. Exploring the protective potential of remote ischemic conditioning-induced miRNAs in stroke.
PMID:日期:2026-10-15Remote ischemic conditioning (RIC) is a non-invasive strategy that mitigates ischemic injury, partly through circulating microRNAs. Emerging evidence suggests that miRNAs may modulate angiogenesis, which is essential for post-stroke recovery. This study investigated the effect of four RIC-induced miRNAs (RIC-miRNAs), miR-16-5p, miR-144-3p, miR-182-5p, and miR-451a, in immortalized human brain microvascular endothelial cells (IM-HBMECs) exposed to inflammatory conditions in vitro. Transcriptomic and in silico analysis were used to identify target genes of RIC-miRNAs. Two angiogenesis-related genes, SLIT2 and TEK, were validated in vitro. as functional targets of miR-16-5p and miR-144-3p, respectively. Rare variant burden analyses in UK Biobank data associated TEK variants with reduced ischemic stroke risk and regulatory SLIT2 variants with increased stroke risk. Functional enrichment analysis further linked the RIC-miRNA-associated targets to the regulation of apoptotic processes, cytokine production, and sprouting angiogenesis. These findings suggest that miR-16-5p and miR-144-3p may modulate endothelial pathways involved in cell death, inflammatory signaling, and vascular remodeling during the response to stroke.