Neuroscience最新文献

{"title":"Comprehensive analysis of the prognostic value and immune infiltration of Uridine Monophosphate Synthetase (UMPS) in Pan-Glioma.","authors":"Dong He, Xiaokun Jiang, Jinfeng Ma, Jinyan Chen, Yongfei Zhang, Xixi Dou, Qingwen Jia, Qian Liu, Ping Xie, Zhen Zhang","doi":"10.1016/j.neuroscience.2025.09.056","DOIUrl":"https://doi.org/10.1016/j.neuroscience.2025.09.056","url":null,"abstract":"<p><p>Uridine Monophosphate Synthetase (UMPS) is a pivotal enzyme in nucleotide metabolism, playing a crucial role in the synthesis of purine and thymidine nucleotides. These nucleotides are essential for DNA and RNA synthesis, thereby impacting cell growth, proliferation, and immune function. In glioblastoma (GBM), a highly malignant primary brain tumor, nucleotide metabolism is abnormally active, and UMPS expression is significantly upregulated. This study aimed to investigate the expression patterns, prognostic potential, and functional roles of UMPS in GBM, as well as its correlation with immune infiltration. Our findings revealed that UMPS expression is elevated in GBM compared to normal tissues and correlates positively with WHO grades of central nervous system tumors. High UMPS expression was associated with shorter overall survival, disease-specific survival, and progression-free interval. Furthermore, This study is the first to reveal that UMPS promotes an immunosuppressive microenvironment in glioma through dual regulation of tumor cell nucleotide metabolism and immune suppression. This establishes a novel link between a metabolic enzyme and immune evasion, providing a new perspective for targeting UMPS in metabolism-immunity combination therapy. Its novelty lies in breaking through the traditional framework of metabolic enzyme research by reframing UMPS as a key node connecting core tumor metabolism to the remodeling of the immune microenvironment. Our study highlights UMPS as a potential therapeutic target in GBM, where modulating its activity or expression could disrupt nucleotide metabolism, inhibit tumor growth, and enhance immune responses.</p>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145225750","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Voluntary exercise combined with environmental enrichment during adolescence promotes sociability and maintains excitation-inhibition balance of Amygdala’s synaptic transmission in mice","authors":"Xinqi Yang ,&nbsp;Qiong Zhou ,&nbsp;Yangyang Cao ,&nbsp;Xin Lyu ,&nbsp;Qianting Xu ,&nbsp;Yuejun Zhou ,&nbsp;Jiachun Zuo ,&nbsp;Wei Meng","doi":"10.1016/j.neuroscience.2025.09.041","DOIUrl":"10.1016/j.neuroscience.2025.09.041","url":null,"abstract":"<div><div>Social behavior is a complex social trait in animal survival, which is influenced by intrinsic states and environmental factors. The basolateral complex of the amygdala (BLA) has been demonstrated to play a pivotal role in regulating social behavior. The effects of physical exercise and environmental enrichment on social behavior and the underlying neural mechanisms remain poorly understood. This study investigated how 5 weeks of single voluntary wheel running exercise (Ex) or Ex combined with environmental enrichment (Ex + EE) from postnatal day 21 (post-weaning) affects social behavior and BLA synaptic transmission in male mice. The results showed that single Ex enhanced sociability, accompanied by a significant increase in mEPSCs’ frequency/amplitude of BLA pyramidal neurons, suggesting that voluntary exercise during adolescence may promote social behavior by potentiating excitatory synaptic afferents of BLA pyramidal neurons. Further, Ex + EE more effectively enhanced sociability and increased both mEPSCs’ frequency/amplitude and mIPSCs’ frequency/amplitude in BLA pyramidal neurons. The concurrent potentiation of excitatory and inhibitory synaptic transmission in BLA pyramidal neurons highlights the potential key role of excitation-inhibition balance of BLA synaptic afferents in modulating social behavior. These findings provide a possible amygdala mechanism underlying the effects of physical exercise and environmental enrichment during adolescence on social behavior.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"587 ","pages":"Pages 14-22"},"PeriodicalIF":2.8,"publicationDate":"2025-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145213131","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Assessment of elephant claustrum by combined histological analysis and high-resolution micro-CT","authors":"Chao Fang ,&nbsp;Anne Schnurpfeil ,&nbsp;Lennart Eigen ,&nbsp;Olivia Heise ,&nbsp;Tabea Pottek ,&nbsp;Johannes Alkofer ,&nbsp;Thomas Hildebrandt ,&nbsp;Tim Salditt ,&nbsp;Robert K. Naumann ,&nbsp;Michael Brecht","doi":"10.1016/j.neuroscience.2025.09.044","DOIUrl":"10.1016/j.neuroscience.2025.09.044","url":null,"abstract":"<div><div>Analysis of the brain architecture of the three extant elephant species is challenging, because of the vast size of their brains. We identified the elephant claustrum in histological Nissl-stained sections from small parts of an Asian (<em>Elephas maximus</em>) and an African savanna elephant (<em>Loxodonta africana</em>) brain. We find that the elephant claustrum is organized into islands of widely differing volume and cell numbers. We attempted to resolve these islands in virtual elephant brain sections from a 3 T Magnetic Resonance (MR) scanner, but found that the resolution was insufficient for such an analysis. We then transferred one hemisphere of an adult female African elephant brain into an ascending alcohol series. After degassing, we scanned the entire hemisphere in a micro-computed tomography (micro-CT) scanner with a resolution of 67 µm³ and parts of the hemisphere with a resolution of 26 µm³. Such scans provided sufficient resolution to estimate the total volume of the elephant claustrum in one hemisphere: 1453 mm³, corresponding to 0.22 % of cortical gray matter volume. In conjunction with our histological data, we estimate that the elephant claustrum in the same hemisphere contains 7.61 million neurons, or 0.27 % of cortical neurons (2869.86 million neurons). These values fit well with known cortico-claustral allometric relationships. Although elephant claustrum structure is widely distributed and organized into irregular islands, its volume follows the typical mammalian pattern, and micro-CT scans provide sufficient resolution to resolve small structures in large brains.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"587 ","pages":"Pages 131-138"},"PeriodicalIF":2.8,"publicationDate":"2025-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145213332","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Rehabilitation, neuroplasticity, and machine learning: Approaching artificial intelligence for equitable health systems","authors":"Esraa M. Qansuwa ,&nbsp;Hadeer N. Atalah ,&nbsp;Mohamed M. Salama","doi":"10.1016/j.neuroscience.2025.09.050","DOIUrl":"10.1016/j.neuroscience.2025.09.050","url":null,"abstract":"<div><div>Recently, technology has evolved significantly in the rehabilitation process for neurological disorders and neurodegenerative diseases, focusing on neuroplasticity. Neuroplasticity, as a fundamental base of brain rehabilitation, is the change in the output of neural circuits in response to the stimulus of the input activity. The physiological and anatomical changes that occur following a brain insult compel the brain to rewire for the sake of reacquiring lost functions or behaviors in a driven form of neural plasticity called neurorehabilitation. One of the main challenges in neuroscience research is the accurate visualization of the brain structure and brain connectivity related to behaviors and memory. Building machine learning predictive models for brain disorders associated with neural circuits and brain plasticity defects is a promising early detection tool for some mental health disorders. Machine learning is becoming more impactful in neuroimaging because it can discern intricate patterns in multidimensional and multimodal data. This technology may then be utilized to generate data-driven classifications and predictions for specific patients. In this review, we discuss main ideologies of neuroplasticity concepts as well as the concept of neuroplasticity induction and neural circuit defects associated with neurodegenerative disorders, in addition to discussing some applications of artificial intelligence of machine learning (ML) models for the future vision of early mental health detection in low- and middle-income countries. This review considers how the health system stratifies rehabilitation and utilizes large data sets for strengthening health systems.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"587 ","pages":"Pages 38-46"},"PeriodicalIF":2.8,"publicationDate":"2025-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145213280","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Kinaesthetic motor imagery in writer's cramp dystonia reveals writing specific abnormalities in the occipital lobe.","authors":"A Baumann, C A Gless, A Knutzen, O Granert, I Tödt, J Schmidt, T Gerke, S Wolff, C Marquardt, K Witt, Kirsten E Zeuner","doi":"10.1016/j.neuroscience.2025.09.042","DOIUrl":"https://doi.org/10.1016/j.neuroscience.2025.09.042","url":null,"abstract":"<p><p>Studies on motor imagery (MI) in writer's cramp (WC) dystonia are limited but may offer insights into impaired motor planning without the influence of dystonic co-contraction. This study used functional magnetic resonance imaging (fMRI) to compare executed writing and drawing of circles with kinaesthetic motor imagery in 18 WC patients and 18 healthy controls. Kinematic analysis confirmed the abnormal signature of WC by demonstrating a decreased frequency and an increased number of inversions during writing in WC patients. fMRI showed decreased BOLD activation during MI, with similar regions activated as in motor execution. Between-group differences during drawing demonstrated reduced activity in the bilateral precentral areas, left supplementary motor area, and right frontal medial area in WC patients. Imagined drawing revealed diminished activation in the left sensorimotor cortex, left superior frontal area, and right cerebellum (Vermis 4/5, Vermis 6, and Cerebellum 6) in WC patients. Writing and imagined writing led to abnormal activation in the superior occipital area and cuneus in WC patients. Direct comparison of writing and drawing in execution and MI conditions displayed a writing-specific deficit in the cuneus and occipital areas. We conclude that MI in WC dystonia offers a valuable opportunity to observe neural activity in similar regions as during motor execution. The observed writing-specific activation deficits in the occipital lobe may reflect dysfunction in the integration of printed/written features or a correlate of disrupted somatosensory processing.</p>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145192220","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Structural and functional abnormalities in relevant brain regions of patients with insomnia disorders: a systematic review and multimodal neuroimaging meta-analysis.","authors":"Si-Ning Li, Ying Yu, Bo Hu, Hao Xie, Pan Dai, Shu-Qi Qiao, Xin-Yu Cao, Yan-Yan Cui, Yang Yang, Lin-Feng Yan","doi":"10.1016/j.neuroscience.2025.09.039","DOIUrl":"https://doi.org/10.1016/j.neuroscience.2025.09.039","url":null,"abstract":"<p><strong>Objective: </strong>Insomnia disorder (ID) has emerged as a significant public health concern in recent years. Research has demonstrated that the occurrence of ID is associated with abnormalities in brain structure and function. However, a consistent conclusion regarding the convergent changes in brain function and structure in individuals with ID has yet to be reached. Therefore, the purpose of this study is to synthesize previous researches through meta-analysis to investigate the changes in imaging-based cerebral structure and function of patients with ID.</p><p><strong>Methods: </strong>We searched the PubMed, MEDLINE, and Web of Science databases for studies published as of October 28, 2024, which involved differences in cerebral gray matter volume (GMV) or spontaneous neural activity (represented by amplitude of low frequency fluctuation, ALFF) between ID patients and HC. The effective peak coordinates and t-values corresponding to brain regions were extracted from the literature and seed-based d-mapping software was used for subsequent analysis.</p><p><strong>Results: </strong>Compared to the HC group, ALFF of ID group was increased in the right amygdala (AMYG.R), left median network, and cingulum (DCG.L) and decreased in right cerebellar hemisphere lobule VIII. GMV of ID group was increased in the right inferior temporal gyrus (ITG.R) and right insular (INS.R) and decreased in right median network, and cingulum (DCG.R).</p><p><strong>Conclusion: </strong>In ID patients, the areas of functional abnormality were not consistent with structural abnormality, indicating a structural-functional coupling dysfunction, but the related brain regions were both associated with cognitive impairment and emotional disorders.</p>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145192223","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"GlyT1 inhibition promotes post-ischemic neuroprotection in the MCAO model","authors":"Daniel Pereira Cavalcante ,&nbsp;Antônio Ítalo dos Santos Nunes ,&nbsp;Gustavo Almeida de Carvalho ,&nbsp;Renato Santiago Gomez ,&nbsp;Leandro do Prado Assunção ,&nbsp;Alexandre Melo Bailão ,&nbsp;Mauro Cunha Xavier Pinto","doi":"10.1016/j.neuroscience.2025.09.033","DOIUrl":"10.1016/j.neuroscience.2025.09.033","url":null,"abstract":"<div><div>Glycine transporter type 1 (GlyT1) regulates extracellular glycine levels and modulates N-methyl-D-aspartate receptor (NMDAR) activity, positioning it as a promising target in excitotoxic and ischemic conditions. While previous studies have shown that GlyT1 inhibition prior to injury confers neuroprotection, its therapeutic potential in a post-ischemic context remains unclear. Here, we investigated the neuroprotective effects of NFPS, a selective GlyT1 inhibitor, administered after the induction of permanent middle cerebral artery occlusion (MCAO) in mice. NFPS (1.25, 2.5, or 5.0 mg/kg, i.p.) was administered once daily for three days, beginning 24 h post-ischemia. NFPS treatment significantly reduced infarct volume and improved motor function in a dose-dependent manner. Additionally, NFPS reduced reactive oxygen species, nitric oxide, and lipid peroxidation, alongside adjustments in antioxidant enzymes and glutathione-related activity. Proteomic analysis of cortical tissue from healthy mice treated with NFPS revealed enrichment of pathways related to glutamatergic synapse, Parkinson disease, and dopaminergic synapse pathways, suggesting modulation of synaptic plasticity and metabolic resilience. Western blot analysis confirmed an increase in GluN2A and a decrease in GluN2B expression, consistent with a shift toward prosurvival NMDAR signaling. Collectively, these findings demonstrate that post-ischemic GlyT1 inhibition with NFPS confers robust neuroprotection through coordinated regulation of excitotoxicity and oxidative stress, supporting its potential as a therapeutic strategy for ischemic stroke.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"587 ","pages":"Pages 56-66"},"PeriodicalIF":2.8,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145186539","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Activin A protects against lipopolysaccharide/TNF-α induced damage of dopaminergic neurons both in vivo and in vitro by regulating mitochondrial fusion","authors":"Yue Zhang ,&nbsp;Shuxiang Tian ,&nbsp;Mingguang Niu ,&nbsp;Han Yang ,&nbsp;Lulu Liu ,&nbsp;Yuyang Kang ,&nbsp;Yanyan Yin","doi":"10.1016/j.neuroscience.2025.09.043","DOIUrl":"10.1016/j.neuroscience.2025.09.043","url":null,"abstract":"<div><div>There is increasing evidence that the pathogenesis of Parkinson’s disease (PD) is closely related to mitochondrial dysfunction and iron deposition. Activin A (Act A) is a homodimeric cytokine from the TGF-β superfamily and has neuroprotective effects in various neurological diseases. However, the specific mechanisms by which Act A exerts a neuronal protective effect in PD remain unclear. In this study, we selected lipopolysaccharide (LPS) −induced PD model mice to investigate the mechanism of protective effects of Act A on neurons, focusing on its effects on the expression of mitochondrial dynamics and ferroptosis related proteins. Meanwhile, the human neuroblastoma cell line SH-SY5Y was selected in vitro to detect mitochondrial membrane potential and reactive oxygen species (ROS) levels to clarify the potential molecular mechanism of Act A in PD. The results of the study showed that Act A attenuated dopaminergic neuron damage in the LPS-induced PD model mice, possibly through regulating mitochondrial dynamics, inhibiting ferroptosis, and reducing ROS. Additionally, mitochondrial fusion inhibitor (MFI8) increased the intracellular ROS levels, while Act A attenuated MFI8-mediated ROS elevation. In conclusion, our results suggest that Act A is involved in the onset and development of PD and may exert neuronal protective effects by regulating mitochondrial fusion.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"587 ","pages":"Pages 108-122"},"PeriodicalIF":2.8,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145186565","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"An overview of adjunctive therapies and alternatives to reperfusion management to reduce cerebral infarct size.","authors":"Jacqueline B Anderson Enni, Robert A Kloner","doi":"10.1016/j.neuroscience.2025.09.022","DOIUrl":"https://doi.org/10.1016/j.neuroscience.2025.09.022","url":null,"abstract":"<p><p>Stroke remains a leading cause of morbidity and mortality, imposing a substantial financial burden on healthcare systems and significantly impacting survivors' quality of life. Endovascular recanalization through thrombolysis and/or thrombectomy is the current standard of care for ischemic stroke. However, these interventions are constrained by a narrow therapeutic window, and stroke outcomes remain suboptimal despite timely treatment. Clinical evidence suggests a strong correlation between infarct size and adverse clinical outcomes. This review explores existing literature and emerging therapeutic strategies beyond endovascular recanalization that aim to reduce cerebral infarct size. It identifies a variety of interventions that have shown therapeutic potential, particularly in animal models. However, it highlights that findings from animal studies have yet to be extensively translated into humans and may be an asset to improving neurological recovery and overall patient outcomes. Additionally, this review emphasizes the need for adjunctive therapies to complement standard reperfusion treatment, with the goal of improving neurological recovery and overall patient outcomes.</p>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145177019","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Single-cell RNA sequencing reveals the ameliorative effects of Kai-Xin-San on depression via regulating neuroplasticity and inflammation in the hypothalamus of rats","authors":"Xiaoxi Li ,&nbsp;Yiming Hua ,&nbsp;Huiling Li ,&nbsp;Yingnan Feng ,&nbsp;Chao Wu ,&nbsp;Xin Hu ,&nbsp;Zhichao Zhang ,&nbsp;Xiaojiang Zhou ,&nbsp;Xianzhe Dong","doi":"10.1016/j.neuroscience.2025.09.037","DOIUrl":"10.1016/j.neuroscience.2025.09.037","url":null,"abstract":"<div><div>Kai-Xin-San (KXS) is widely used as a traditional Chinese herbal formula for treating depression, while its regulatory mechanisms on the hypothalamic microenvironment remain unclear. This study systematically elucidated the molecular mechanisms by which KXS alleviates chronic unpredictable mild stress (CUMS)-induced depression in rats through single-cell RNA sequencing (scRNA-seq) combined with behavioral and molecular biology experiments. Behavioral tests revealed that KXS significantly ameliorated depressive-like behaviors in CUMS-induced rats. The scRNA-seq analysis of 45,482 hypothalamic cells isolated from control rats, CUMS-induced rats, KXS-treated rats and fluoxetine-treated rats revealed nine major cell types. The transcriptional atlas of these cells revealed that CUMS reduced the numbers of astrocytes and adipocytes, while increasing the number of proinflammatory microglia and endothelial cells. KXS intervention restored astrocyte subpopulations (Astro_1), upregulated the protein expression of mitochondrial metabolism-related enzyme CPT1A, reduced the M1/M2 microglial polarization ratio, suppressed the protein expression of proinflammatory cytokines TNF-α and CXCL10, and elevated the protein expression of anti-inflammatory TGF-β. KXS remodeled hypothalamic intercellular communication networks, enhancing astrocyte-neuron interactions. The protein expression of neuronal nuclear antigen, microtubule-associated protein 2, synapsin, and postsynaptic density-95 in hypothalamus was significantly increased in KXS group, which reflected changes in the number of neurons and altered synaptic plasticity. Our study is the first to demonstrate that KXS can alleviate depression through the inhibition of proactivity, restoration of astrocytic mitochondrial metabolism, and reshaping of neuro-astrocyte interaction networks to enhance synaptic plasticity through scRNA-seq in hypothalamus. These results provide a theoretical foundation for the development of hypothalamic microenvironment-targeted antidepressant strategies.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"587 ","pages":"Pages 47-55"},"PeriodicalIF":2.8,"publicationDate":"2025-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145177040","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}