Frontiers in Synaptic Neuroscience前沿突触神经科学
Frontiers in Synaptic Neuroscience(英文缩写 FRONT SYNAPTIC NEURO),ISSN 1663-3563,eISSN 1663-3563,中文译名:前沿突触神经科学 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：2025-11-01 至 2026-10-31，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 | 3.567 | Q3 |
| 2022 | 3.700 | Q2 |
| 2023 | 2.800 | Q2 |
| 2024 | 4.100 | Q1 |
| 2025 | 6.900 | Q1 |
Frontiers in Synaptic Neuroscience 最新收录文献
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2. Sleep disturbances as an early indicator of psychotic disorders in adolescents and young adults.
2. 睡眠障碍是青少年和年轻人精神障碍的早期指标PMID:日期:2026-09-04Sleep disturbances are increasingly recognized as clinically relevant markers in the early detection of psychotic disorders among adolescents and young adults. These disturbances, including insomnia, circadian rhythm disruptions, parasomnias, and fragmented sleep, affect up to 70% of individuals at clinical high risk for psychosis, rising to 80% in fully developed schizophrenia. This review synthesizes current evidence on the relationship between sleep problems and early psychotic symptoms, emphasizing their potential as observable and possibly modifiable indicators of illness onset. Neurobiological mechanisms suggest overlapping pathways for both sleep problems and the development of psychotic symptoms involving dopaminergic, serotonergic, and hormonal dysregulation, which are additionally exacerbated by psychological factors such as stress, substance use, and poor sleep hygiene. Screening methods, such as self-report questionnaires, actigraphy, and polysomnography, have demonstrated utility in identifying individuals at risk. Furthermore, sleep-focused interventions, particularly cognitive behavioral therapy, show promise in alleviating both sleep and psychiatric symptoms. Despite methodological limitations of available research, including heterogeneous study designs and short follow-ups, sleep assessment can represent a low-cost, scalable tool for early intervention. Future research should prioritize longitudinal, multimodal studies and explore personalized, sleep-centered preventive strategies. Furthermore, sleep disorders could be considered not only as early signs of developing psychosis but also as a potential therapeutic target in psychosis prevention.
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3. Activation of silent synapses driven by emerging technologies: mechanisms, disease associations, and prospects for clinical translation.
PMID:日期:2026-09-03Silent synapses represent a unique class of synaptic connections that are non-functional at rest but possess the potential to become functional, serving as a critical reservoir for neural plasticity. Their activation mechanisms not only challenge traditional models of synaptic maturation but also provide novel insights into brain function regulation and disease pathology. This article provides a systematic review of the regulatory mechanisms underlying silent synapse activation, encompassing pre-synaptic calcium signaling-mediated vesicle cycling and active zone (AZ) optimization, post-synaptic -amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) membrane insertion and post-synaptic density protein 95 (PSD-95) anchoring, Mg blockade release by N-methyl-D-aspartate receptor (NMDAR), as well as synergistic integration of upstream signaling pathways. Additionally, it explores the roles of astrocytes, epigenetic modifications, ubiquitin-proteasome systems, and autophagy-lysosomal systems in multi-level regulatory processes. Notably, abnormal regulation of silent synapses exhibits two contrasting pathological patterns in diseases: "desilencing impairment" (e.g., Alzheimer's disease, depression) and "abnormally excessive desilencing" (e.g., drug addiction, chronic pain), which establishes a theoretical framework for targeted interventions. The study further evaluates the applicability and limitations of emerging technologies-including high-resolution imaging, single-cell omics, optogenetics, and AI-driven brain-inspired computing-in silent synapse research, while systematically summarizing clinical advancements, current challenges, and future directions, aiming to inform both fundamental neuroscience studies and therapeutic interventions.
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4. Zebrafish as a translational model for peptide-mediated synaptic dysfunction related to obesity.
4. 斑马鱼作为肥胖相关肽介导突触功能障碍的转化模型PMID:日期:2026-08-10Obesity-driven synaptic dysfunction is increasingly recognized as a key mechanism linking metabolic disorders to neurodegenerative diseases. This review aims to explore the utility of zebrafish () as a translational model to investigate these mechanisms and screen peptide-based therapeutic strategies. Owing to their optical transparency, genetic tractability, and suitability for high-throughput screening, zebrafish provide a powerful platform for studying neuronal circuitry and evaluating bioactive peptides . Current evidence on pathophysiological processes underlying obesity-related synaptic impairment, including central resistance to metabolic hormones, oxidative stress, and the chronic inflammatory state, which promotes persistent immune activation and neuroinflammation. In addition, the persistence of these disturbances in the organism can lead to dysfunctions and pathologies, such as Parkinson's and Alzheimer's diseases, both of which are discussed in more detail in this review. Also, particular emphasis is placed on the roles of glial cells and the gut-brain axis in modulating synaptic integrity. We highlight how cutting-edge technologies, such as live neural imaging and single-cell transcriptomics, are accelerating peptide discovery and mechanism-of-action studies in zebrafish. Furthermore, we discuss emerging therapeutic peptides such as GLP-1 analogs and BDNF-based molecules that modulate inflammatory pathways, restore insulin signaling, and enhance neuronal resilience. Collectively, the evidence positions zebrafish as a robust model not only for elucidating disease mechanisms but also for advancing peptide-based interventions targeting synaptic dysfunction in obesity.
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6. Heterosynaptic NMDA receptor plasticity in hippocampal dentate granule cells.
PMID:日期:2026-07-22The dentate gyrus is a key relay station that controls information transfer from the entorhinal cortex to the hippocampus proper. This process relies heavily on dendritic integration by dentate granule cells (GCs) of excitatory synaptic inputs from the medial and lateral entorhinal cortex via medial and lateral perforant paths (MPP and LPP, respectively). Inputs from the entorhinal cortex onto GCs exhibit activity-dependent long-term plasticity of N-methyl-D-aspartate receptor (NMDAR)-mediated synaptic transmission. However, the properties, underlying mechanisms, and input-specificity of this plasticity remain poorly understood. Here, we examined NMDAR plasticity rules at MPP-GC and LPP-GC synapses using physiologically relevant stimulation patterns in acute hippocampal slices from rats and mice. Unlike MPP-GC synapses, LPP-GC synapses did not express homosynaptic NMDAR-LTP. Additionally, inducing NMDAR-LTP at MPP-GC synapses potentiated NMDAR transmission at distal LPP-GC synapses. The same stimulation protocol induced homosynaptic α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR)-LTP at MPP-GC synapses but heterosynaptic AMPAR-LTD at distal LPP synapses, indicating that NMDAR and AMPAR plasticity are controlled by different plasticity rules. Notably, heterosynaptic but not homosynaptic NMDAR-LTP required Ca release from intracellular, ryanodine receptor-dependent Ca stores. Lastly, genetic deletion of the GluN2D subunit from GCs or selective antagonism of GluN2D-containing NMDARs abolished heterosynaptic LTP. Heterosynaptic NMDAR-mediated LTP may have important consequences for the dendritic integration of functionally distinct excitatory inputs by dentate granule cells.
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7. Correction: Automated ROI detection allows rapid quantification of synaptic activity across tens of thousands of synapses in cell culture.
PMID:日期:2026-07-20[This corrects the article DOI: 10.3389/fnsyn.2026.1832103.].
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8. The how and why for multiple forms of hippocampal LTP.
PMID:日期:2026-07-10Activity-induced Long-Term Potentiation (LTP)-characterized as it is by rapid induction, synapse specificity, and remarkable persistence-has long been considered a primary substrate for memory encoding. There has however been considerable debate about the cellular mechanisms responsible for producing the potentiated state. It seems that much of the confusion can be traced to an implicit assumption that there is a single form of stable potentiation. However, features of LTP in Schaffer-commissural (SC) input to CA1 and perforant path projections from entorhinal cortex to dentate gyrus (DG), show that different nodes of the hippocampal circuit express different types of LTP and that distinctions can be found even within the same population of synapses. For the SC system, brief theta burst stimulation (TBS) elicits LTP that is expressed by an expansion of the spine, postsynaptic density and associated AMPA receptor pool, and stabilized by reorganization of the actin cytoskeleton. Both sexes employ these mechanisms but females rely on locally synthesized estrogen and synaptic estrogen receptors to set processes in motion whereas males more heavily rely on metabotropic NMDA receptor signaling. Extended theta burst trains, high frequency stimulation (HFS), and spike timing paradigms engage mechanisms of LTP induction that differ from those produced by the minimal TBS. And an even more radical form of potentiation is expressed at lateral perforant path (LPP) connections with the DG. In this case, LTP is triggered postsynaptically but expressed presynaptically by increased transmitter release with an endocannabinoid providing the requisite retrograde messenger. These sex- and region-specific differences in plasticity have meaningful consequences for episodic memory encoding and vulnerability to neurological insults.
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9. High-frequency, high-intensity electrical stimulation selectively activates human fast-spiking interneurons.
PMID:日期:2026-06-26Electrical brain stimulation has been used to treat epilepsy with therapeutic success, but without complete understanding of its cellular mechanisms of seizure suppression. Using acute human brain slices obtained from pharmaco-resistant epilepsy patients, we delivered high-frequency, high-intensity extracellular electrical stimulation while recording from neocortical layer 2/3 pyramidal neurons (PNs), fast-spiking interneurons (FSINs), and non-fast-spiking interneurons (nFSINs). Electrical stimulation led to an increasingly selective activation of FSINs at higher stimulation frequencies, which consistently fired with high fidelity throughout prolonged stimulation periods while both PNs and nFSINs were suppressed rapidly. In addition, stimulation caused a long-term rebalancing of synaptic weights through selective and differential depression of synaptic inputs, resulting in an approximately twofold increase in the normalized excitatory-to-inhibitory postsynaptic conductance at FSINs while not affecting PNs, thereby providing support for FSIN activation toward increased inhibitory tone and network stabilization. These stimulation-induced effects were accompanied by only minimal changes in neuronal intrinsic excitability.
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10. Calcium at the crossroads of the immunometabolic signaling and comorbidity in schizophrenia.
10. 钙在精神分裂症免疫代谢信号传导与共病交汇点中的作用PMID:日期:2026-06-15该文献暂无摘要。