Neuron神经元
Neuron(英文缩写 NEURON),ISSN 0896-6273,eISSN 1097-4199,中文译名:神经元 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 | 18.688 | Q1 |
| 2022 | 16.200 | Q1 |
| 2023 | 14.700 | Q1 |
| 2024 | 15.000 | Q1 |
| 2025 | 16.900 | Q1 |
Neuron 最新收录文献
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1. Toward a shared infrastructure for preclinical discovery: Why animal model tissue and biofluid biobanks are needed.
PMID:日期:2026-10-01Animal model tissues and biofluids are indispensable yet underused assets in preclinical research. We argue that standardized, shareable biobanks could reduce duplication, improve technical reproducibility, strengthen biomarker translation, lower animal use, and create scalable infrastructures for academia and industry.
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2. Circuit mechanisms of psychotic symptoms across disorders.
PMID:日期:2026-10-01Psychotic symptoms, including hallucinations, delusions, and disorganized thought, occur across psychiatric and neurological disorders, yet their underlying mechanisms remain poorly integrated across scales. Here, we propose a transdiagnostic framework in which disturbances in dopamine, glutamate, GABA, serotonin, and acetylcholine alter neuronal gain and synaptic efficacy, disrupting the precision weighting of sensory evidence, prediction errors, and internally generated representations. These local disturbances propagate through cortico-striato-thalamo-cortical circuits and large-scale functional networks, producing abnormal integration-segregation dynamics and unstable attractor states. This multilevel model links molecular and cellular perturbations to circuit dysfunction, network instability, and symptom expression while allowing distinct biological pathways to converge on shared computational vulnerabilities. Emerging neuroimaging, dynamical systems, and artificial intelligence approaches may enable individualized tests of these mechanisms and support more precise, circuit-informed interventions for psychotic symptoms.
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3. Lateral hypothalamic control of the striatal dopamine landscape during consummatory behavior.
PMID:日期:2026-10-01The lateral hypothalamic area (LHA) contains γ-aminobutyric acid (GABAergic) and glutamatergic neurons that converge on midbrain dopamine circuits, exerting opposing control over feeding and reinforcement. How these neurons behave during consummatory behavior and how they shape dopamine release across the striatum remains unresolved. Here, we show that LHA GABAergic and glutamatergic neurons independently scale their activity as mice consume rewarding and aversive solutions and that their balance sets a spatially organized dopamine landscape along the striatum's anterior-posterior axis: anterior regions track solution value and recent history, posterior regions encode sensorimotor features, and release at each site is controlled locally rather than propagated across subregions. This landscape tracks LHA activity, depends on it causally, and reinforces licking initiation. These results position the LHA as a central regulator of a striatum-wide dopamine landscape during consumption, providing a circuit-level framework for how the hypothalamus shapes motivated behavior.
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4. Two prefrontal-subcortical circuits estimate controllability and reflect its impact on learning.
PMID:日期:2026-10-01该文献暂无摘要。
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5. OpenFISH enables same-section spatial transcriptomics and MALDI-MSI integration.
5. OpenFISH实现同切片空间转录组学与MALDI-MSI整合PMID:日期:2026-09-29Integrating high-resolution spatial transcriptomics with metabolomics is essential for linking cellular identity to metabolic state, yet same-section, single-cell alignment is limited by incompatible substrates, chemistries, and imaging. We introduce OpenFISH, an open-source, low-cost, modular spatial transcriptomics platform and a matrix-assisted laser desorption ionization mass spectrometry imaging (MALDI-MSI)-compatible workflow. Through optimized tissue handling and a guided registration pipeline, OpenFISH enables cell-type-aware co-mapping of transcripts and metabolites. We demonstrate its utility by revealing cell-type-specific metabolic heterogeneity in the central nervous system and compartment-level metabolic zonation in the hippocampus. Exploratory 5xFAD experiments identify concordant cell-type-associated metabolic changes, including prominent phospholipid changes in microglia, metabolic shifts in excitatory neurons masked in aggregate analyses, and elevated lysophosphatidylethanolamine-related features in oligodendrocytes. OpenFISH also independently quantifies transposable-element activation after immune challenge and identifies candidate striatal D1-neuron patterning changes in Reeler mutants. This work provides an open, low-cost, and customizable framework for same-section spatial multi-omics.
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6. Time-resolved spectral parameterization: Recommendations and guidelines.
PMID:日期:2026-09-29Non-oscillatory, aperiodic activity, is an emerging signal of interest whose physiological and functional origins are just beginning to be probed for their potential link to systems-level physiology and cognition. But there are several pernicious, practical, and statistical hazards to be aware of when deploying spectral parameterization tools for disentangling oscillations and aperiodic activity over short, noisy time windows. In this primer, we provide a set of recommendations and guidelines for time-resolved and event-related spectral parameterization to help researchers meet these challenges. Specifically, we provide recommendations on how to optimize and assess model fits, how to report analysis decisions to maximize reproducibility, and what to do when spectral parameterization fails to identify the presence of oscillations. These recommendations will help guide the study of the distinct dynamics of periodic and aperiodic neural activity in cognition, behavior, and disease at fine timescales.
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7. An African ancestry-enriched H1 sub-haplotype challenges MAPT haplotype assignment and reveals distinct tau regulatory programs.
PMID:日期:2026-09-29The 17q21.31 inversion locus is among the strongest genetic modifiers of tau-related neurodegenerative disease, yet its structure and function across ancestries remain incompletely understood. By integrating long-read sequencing, transcriptomics from postmortem human brain tissue, induced pluripotent stem cell (iPSC)-derived neurons, and astrocytes, we identified H1_A, a previously unrecognized non-inverted H1 sub-haplotype enriched in individuals of African ancestry (AA). H1_A carries rs8070723, a variant widely used to define the protective H2 haplotype, revealing the limitations of current MAPT haplotype assignment in non-European populations. Across brain tissue and neural cell types, ancestry and haplotype influenced MAPT expression, tau isoform composition, extracellular matrix pathways, immune signaling, and oxidative stress responses. Functional studies further demonstrated effects on astrocyte migration and glutathione regulation. These findings uncover ancestry-dependent regulatory programs at 17q21.31 and provide a framework for more accurate interpretation of MAPT-associated risk in neurodegenerative disease.
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8. Cervical lymphadenectomy impairs brain lymphatic clearance and synaptic proteostasis.
PMID:日期:2026-09-29Meningeal lymphatic vessels drain brain fluid and waste into the cervical lymph nodes, but how removing these nodes during surgery affects brain health is unknown. Retrospective analysis of cancer patients who underwent neck lymphadenectomy without chemo-radiation therapy found that up to 25% developed mild-to-severe cognitive impairment, and neuroimaging showed accelerated temporal horn enlargement after bilateral surgery. To determine mechanistically how cervical lymphadenectomy contributes to cognitive impairment, mouse and rat models were utilized to phenocopy abrupt disruption of lymphatic flow to the cervical and submandibular nodes. Impaired lymphatic drainage induced a cerebrospinal fluid signature of metabolic stress and inflammation. In the hippocampus, redox stress drove oxidative posttranslational protein modifications and microaggregation with biochemical, molecular, and structural features distinct from amyloid aggregates in Alzheimer's models. Such changes were absent when lymphatic drainage was gradually reduced. The data link cognitive impairment following acute neck lymphadenectomy with the biochemical consequences of impaired metabolic waste clearance.
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9. Peripheral CXCR3 blockade mitigates T cell infiltration and neurodegeneration in a mouse model of tauopathy.
9. 外周CXCR3阻断减轻tau蛋白病小鼠模型中的T细胞浸润和神经退行性变PMID:日期:2026-09-28Chemokine receptor CXCR3 mediates T cell recruitment into inflamed tissues, but its role in tauopathies is unclear. Here, we show that hippocampal injection of interferon-γ (IFNγ) acutely triggers CXCL10 upregulation and brain parenchymal T cell infiltration. Genetic deletion or antibody-mediated blockade of CXCR3 prevented IFNγ-induced T cell infiltration. In a mouse model of tauopathy and neurodegeneration, chronic systemic anti-CXCR3 treatment markedly reduced parenchymal CD4 and CD8 T cell accumulation, attenuated neurodegeneration, and improved aspects of cognition. CXCR3 blockade decreased microglial MHC-II expression without broadly suppressing classical disease-associated inflammatory phenotypes. Single-cell RNA sequencing and flow cytometry further revealed a reduction in the proportion of activated CD4 T cell populations and elevated CD8 T cell terminal exhaustion in the brain. These findings identify CXCR3-dependent chemotaxis as a critical signaling pathway for subtypes of T cells linked to tau-mediated neurodegeneration and highlight CXCR3 blockade as a potential disease-modifying therapeutic strategy for tauopathies.
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10. A basolateral amygdala to dorsolateral striatum projection modulates stimulus-evoked motor behavior.
PMID:日期:2026-09-25The dorsal striatum is divided into dorsomedial (DMS) and dorsolateral (DLS) subregions, which support distinct aspects of motor learning. The basolateral amygdala (BLA) encodes emotionally salient information and can influence striatal function, but its connection to the sensorimotor DLS remains poorly understood. Using mice, we identify a direct, functional BLA-DLS projection that arises from a neuronal population distinct from BLA neurons projecting to the DMS. Although sparser than BLA-DMS inputs, BLA-DLS synapses preferentially targeted the distal dendrites of striatal projection neurons, positioning them to modulate heterosynaptic integration. Repeated optogenetic activation of BLA-DLS inputs potentiated stimulus-evoked grooming and induced heterosynaptic plasticity. This projection was also pathologically strengthened in compulsively grooming Sapap3 null mice. Together, these findings reveal a direct mechanism through which limbic input from the amygdala shapes sensorimotor striatal circuits and motor output.