Neuroscience bulletin最新文献

Inner Ear Organoids: A Hydrogel-Based Platform for Drug Screening and Deafness Modeling. 内耳类器官：基于水凝胶的药物筛选和耳聋建模平台。

IF 5.8 2区医学

Neuroscience bulletin Pub Date : 2025-10-21 DOI: 10.1007/s12264-025-01479-0

Yuyu Cao, Xiaotao Liu, Renjie Chai, Zuhong He

引用次数: 0

Selectively Labeling and Distinguishing Adrenergic and Noradrenergic Neurons in the Sympathetic Nervous System. 交感神经系统肾上腺素能和去肾上腺素能神经元的选择性标记和区分。

IF 5.8 2区医学

Neuroscience bulletin Pub Date : 2025-10-18 DOI: 10.1007/s12264-025-01522-0

Guodong Pang, Yuyan Shi, Jiayi Shen, Tianyu Shao, Fengchao Wang, Yijing Wang, Cheng Zhan

{"title":"Selectively Labeling and Distinguishing Adrenergic and Noradrenergic Neurons in the Sympathetic Nervous System.","authors":"Guodong Pang, Yuyan Shi, Jiayi Shen, Tianyu Shao, Fengchao Wang, Yijing Wang, Cheng Zhan","doi":"10.1007/s12264-025-01522-0","DOIUrl":"https://doi.org/10.1007/s12264-025-01522-0","url":null,"abstract":"The sympathetic nervous system, with adrenaline and noradrenaline as key neurotransmitters, plays a vital role in regulating physiological functions. However, distinguishing between adrenergic and noradrenergic neurons has been challenging. This study used CRISPR/Cas9 technology to generate Net-Cre and Pnmt-p2a-Cre transgenic mouse lines. The results showed that gene editing did not affect the normal reproduction and development of these mice, and their stress levels were comparable to those of wild-type mice. In the central nervous system (CNS), noradrenergic neurons are distributed mainly in the brainstem and other regions, whereas adrenergic neurons are distributed specifically in the ventrolateral medulla (VLM) and the nucleus of the solitary tract (NTS). In the peripheral nervous system (PNS), more than 98% of neurons in the sympathetic ganglia are noradrenergic. AAV-based tracing of the locus coeruleus (LC) revealed that LC noradrenaline transporter (NET) neurons had extensive long-distance projections, whereas phenylethanolamine-N-methyltransferase (PNMT) neurons had short-range projections. These transgenic mouse lines provide a powerful tool for further research on the functions of adrenergic and noradrenergic neurons and the sympathetic nervous system.","PeriodicalId":19314,"journal":{"name":"Neuroscience bulletin","volume":" ","pages":""},"PeriodicalIF":5.8,"publicationDate":"2025-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145318610","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Modulation of Glutamate Release by Dexmedetomidine Preserves Dendritic Spines and Alleviates Cognitive Impairment in a Murine Model of Perioperative Neurocognitive Disorder. 右美托咪定调节谷氨酸释放保存树突棘并减轻围手术期神经认知障碍小鼠模型的认知障碍。

IF 5.8 2区医学

Neuroscience bulletin Pub Date : 2025-10-17 DOI: 10.1007/s12264-025-01518-w

Yan Zhang, Junzhao Li, Xueju Wang, Zhongyu Zhang, Shuai Long, Chuanyu Edward Li, Yan Liu, John Man Tak Chu, Raymond Chuen-Chung Chang, Gordon Tin-Chun Wong, Yong Zhang

{"title":"Modulation of Glutamate Release by Dexmedetomidine Preserves Dendritic Spines and Alleviates Cognitive Impairment in a Murine Model of Perioperative Neurocognitive Disorder.","authors":"Yan Zhang, Junzhao Li, Xueju Wang, Zhongyu Zhang, Shuai Long, Chuanyu Edward Li, Yan Liu, John Man Tak Chu, Raymond Chuen-Chung Chang, Gordon Tin-Chun Wong, Yong Zhang","doi":"10.1007/s12264-025-01518-w","DOIUrl":"https://doi.org/10.1007/s12264-025-01518-w","url":null,"abstract":"Perioperative neurocognitive disorders (PNDs) represent a significant challenge in the perioperative setting, while the pathophysiology of PNDs remains unclear. Utilizing a murine model of abdominal surgery, we found that abnormal glutamatergic neurotransmission in the medial prefrontal cortex (mPFC) and hippocampus contributes to postoperative cognitive impairments. Increases in the frequency of miniature excitatory postsynaptic currents in both the mPFC and CA1 neurons indicate enhanced presynaptic glutamate release while having little effect on inhibitory neurotransmission. Surgery also enhances glutamate release from presynaptic terminals in the Schaffer collateral pathway. In addition, abdominal surgery increased the activation of microglia and astrocytes, elevated central inflammatory markers, and reduced excitatory amino-acid transporter-2 expression. Dexmedetomidine significantly mitigates the postoperative cognitive deficits by reducing inflammation and preserving neuronal structural complexity and dendritic spine stability, likely through inhibiting glutamate release and enhancing its reuptake. These findings advance our understanding of the etiology of PNDs and provide hints for potential intervention.","PeriodicalId":19314,"journal":{"name":"Neuroscience bulletin","volume":" ","pages":""},"PeriodicalIF":5.8,"publicationDate":"2025-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145308724","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Unveiling Butyrate as a Parkinson's Disease Therapy. 揭示丁酸盐作为帕金森病的治疗。

IF 5.8 2区医学

Neuroscience bulletin Pub Date : 2025-10-15 DOI: 10.1007/s12264-025-01498-x

António E Abreu, Nuno Empadinhas, Sandra Morais Cardoso

引用次数: 0

Chemokine CCL2 Mediates Neuroglial Crosstalk and Drives Chronic Pain Pathogenesis. 趋化因子CCL2介导神经胶质相互作用并驱动慢性疼痛发病机制。

IF 5.8 2区医学

Neuroscience bulletin Pub Date : 2025-10-14 DOI: 10.1007/s12264-025-01519-9

Junyu Lu, Yunxin Shi, Yongkang Li, Ziyi Niu, Shengxi Wu, Ceng Luo, Rou-Gang Xie

{"title":"Chemokine CCL2 Mediates Neuroglial Crosstalk and Drives Chronic Pain Pathogenesis.","authors":"Junyu Lu, Yunxin Shi, Yongkang Li, Ziyi Niu, Shengxi Wu, Ceng Luo, Rou-Gang Xie","doi":"10.1007/s12264-025-01519-9","DOIUrl":"https://doi.org/10.1007/s12264-025-01519-9","url":null,"abstract":"Chronic pain, frequently comorbid with neuropsychiatric disorders, significantly impairs patients' quality of life and functional capacity. Accumulating evidence implicates the chemokine CCL2 and its receptor CCR2 as key players in chronic pain pathogenesis. This review examines the regulatory mechanisms of the CCL2/CCR2 axis in chronic pain processing at three hierarchical levels: (1) Peripheral Sensitization: CCL2/CCR2 modulates TRPV1, Nav1.8, and HCN2 channels to increase neuronal excitability and CGRP signaling and calcium-dependent exocytosis in peripheral nociceptors to transmit pain. (2) Spinal Cord Central Sensitization: CCL2/CCR2 contributes to NMDAR-dependent plasticity, glial activation, GABAergic disinhibition, and opioid receptor desensitization. (3) Supraspinal Central Networks: CCL2/CCR2 signaling axis mediates the comorbidity mechanisms of pain with anxiety and cognitive impairment within brain regions, including the ACC, CeA, NAc, and hippocampus, and it also increases pain sensitization through the descending facilitation system. Current CCL2/CCR2-targeted therapeutic strategies and their development status are discussed, highlighting novel avenues for chronic pain management.","PeriodicalId":19314,"journal":{"name":"Neuroscience bulletin","volume":" ","pages":""},"PeriodicalIF":5.8,"publicationDate":"2025-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145286713","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

PET Molecular Imaging of the Endocannabinoid System in Psychiatric Disorders. 精神疾病内源性大麻素系统的PET分子成像。

IF 5.8 2区医学

Neuroscience bulletin Pub Date : 2025-10-13 DOI: 10.1007/s12264-025-01515-z

Chunyi Cui, Xiaofeng Dou, Peili Cen, Chentao Jin, Jing Wang, Jiaqi Niu, Chenxi Xue, Mei Tian, Hong Zhang, Yan Zhong

{"title":"PET Molecular Imaging of the Endocannabinoid System in Psychiatric Disorders.","authors":"Chunyi Cui, Xiaofeng Dou, Peili Cen, Chentao Jin, Jing Wang, Jiaqi Niu, Chenxi Xue, Mei Tian, Hong Zhang, Yan Zhong","doi":"10.1007/s12264-025-01515-z","DOIUrl":"https://doi.org/10.1007/s12264-025-01515-z","url":null,"abstract":"Psychiatric disorders have emerged as significant contributors to the global burden of disease in recent decades. The endocannabinoid system (ECS) influences a range of physiological and pathophysiological processes, including nociception, cognition, appetite, memory, and behavior, serving as a crucial mediator in psychiatric disorders. Imaging the ECS provides valuable insights into the pathophysiological mechanisms underlying psychiatric disorders and enhances clinical management strategies. As an advanced noninvasive molecular imaging modality, positron emission tomography (PET) enables the in vivo exploration of biological processes at the cellular and molecular levels. Recent advancements have led to the development of numerous PET tracers that target various components of the ECS, offering opportunities to visualize, characterize, and quantify ECS activity in psychiatric disorders in vivo. In this review, we summarize the existing PET tracers for ECS imaging and discuss their applications in diverse psychiatric conditions, including cannabis use disorder, alcohol use disorder, post-traumatic stress disorder, schizophrenia, and eating disorders.","PeriodicalId":19314,"journal":{"name":"Neuroscience bulletin","volume":" ","pages":""},"PeriodicalIF":5.8,"publicationDate":"2025-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145286703","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Serotonergic Projection from the Dorsal Raphe Nucleus to the Basolateral Amygdala Bidirectionally Modulates Sociability in Mice. 中缝背核向基底外侧杏仁核的5 -羟色胺能双向调节小鼠的社交能力。

IF 5.8 2区医学

Neuroscience bulletin Pub Date : 2025-10-10 DOI: 10.1007/s12264-025-01520-2

Yehui Zhang, Yuxiang Zhang, Yuwei Diao, Guangyi Yang, Guangrui Yang, Xuchu Weng, Chun Hu

引用次数: 0

Complement C3a Suppresses Spinal Cord Neural Stem Cell Activation by Inhibiting UCHL1 via the NF-κB p65/Nrf2 Pathway. 补体C3a通过NF-κB p65/Nrf2通路抑制UCHL1抑制脊髓神经干细胞活化

IF 5.8 2区医学

Neuroscience bulletin Pub Date : 2025-10-03 DOI: 10.1007/s12264-025-01488-z

Lu Ding, Xinyue Li, YaQin Guo, Feng-Quan Zhou, David Y B Deng

{"title":"Complement C3a Suppresses Spinal Cord Neural Stem Cell Activation by Inhibiting UCHL1 via the NF-κB p65/Nrf2 Pathway.","authors":"Lu Ding, Xinyue Li, YaQin Guo, Feng-Quan Zhou, David Y B Deng","doi":"10.1007/s12264-025-01488-z","DOIUrl":"https://doi.org/10.1007/s12264-025-01488-z","url":null,"abstract":"Activation of spinal cord neural stem cells (NSCs) and subsequent neurogenesis holds a promising alternative for spinal cord injury (SCI) repair. Our previous study demonstrated that complement C3a, derived from reactive astrocytes, inhibits NSC proliferation by suppressing protein aggregate clearance through the deubiquitinating enzyme ubiquitin carboxy-terminal hydrolase L1 (UCHL1)-proteasome system post-SCI. However, the potential molecular mechanism by which C3a modulates NSC activation via this pathway remains unclear. Here, we revealed that C3a/C3a receptor (C3aR) signaling activated NF-κB p65, which in turn inhibited Nrf2 activity and UCHL1 expression, resulting in diminished proteasome activity and the accumulation of protein aggregates, and ultimately impaired NSC activation. Both knockdown of NF-κB p65 and Nrf2 upregulation restored UCHL1 expression and proteasome activity in vitro, promoting NSC activation by enhancing protein aggregate clearance. Mechanistically, we found that NF-κB p65 regulated Nrf2 activity through a dual mechanism: (1) promoting Keap1-dependent ubiquitination and proteasome degradation of Nrf2; (2) inhibiting protein kinase C-mediated Nrf2 phosphorylation and nuclear translocation. Using the dual-luciferase reporter assay and chromatin immunoprecipitation (ChIP) analysis, we further identified UCHL1 as a direct transcriptional target of Nrf2. Importantly, in vivo experiments using SCI mice confirmed that either C3aR blockade, NF-κB p65 knockdown, or Nrf2 overexpression could rescue SCI-induced UCHL1 downregulation. Together, this study uncovers the C3a-NF-κB p65-Nrf2-UCHL1-proteasome axis as a critical regulator of NSC activation after SCI. This may provide novel molecular targets and intervention strategies for SCI repair.","PeriodicalId":19314,"journal":{"name":"Neuroscience bulletin","volume":" ","pages":""},"PeriodicalIF":5.8,"publicationDate":"2025-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145225496","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Bridging the Gap: The Neuro-immune Axis as a Key Player in Neurodegenerative Disorders. 弥合差距：神经免疫轴在神经退行性疾病中的关键作用。

IF 5.8 2区医学

Neuroscience bulletin Pub Date : 2025-10-01 Epub Date: 2025-06-25 DOI: 10.1007/s12264-025-01439-8

Tingting Liu, Haojie Wu, Jianshe Wei

引用次数: 0

Parvalbumin and Somatostatin Neurons in the Thalamic Reticular Nucleus Modulate Visual Information Processing in V1 of Mouse. 丘脑网状核中的小白蛋白和生长抑素神经元调节小鼠V1视觉信息加工。

IF 5.8 2区医学

Neuroscience bulletin Pub Date : 2025-10-01 Epub Date: 2025-07-21 DOI: 10.1007/s12264-025-01458-5

Jiamin Bu, Guangwei Xu, Yifeng Zhou

引用次数: 0