Neuroscience bulletin最新文献

Preoptic Neural Circuitry for Dramatic and Gentle Thermoregulation. 戏剧性和温和体温调节的视前神经回路。

IF 5.9 2区医学

Neuroscience bulletin Pub Date : 2025-06-20 DOI: 10.1007/s12264-025-01434-z

Ruiqi Pang, Haipeng Yu, Jincheng Wang, Zhiyue Shi, Huizhong Wen, Guangyan Wu, Xuan Zhang, Yueting Zhang, Qiaoqian Wei, Bo Li, Xueqing Yi, Kai Liu, Shaowen Qian, Yi Zhou

{"title":"Preoptic Neural Circuitry for Dramatic and Gentle Thermoregulation.","authors":"Ruiqi Pang, Haipeng Yu, Jincheng Wang, Zhiyue Shi, Huizhong Wen, Guangyan Wu, Xuan Zhang, Yueting Zhang, Qiaoqian Wei, Bo Li, Xueqing Yi, Kai Liu, Shaowen Qian, Yi Zhou","doi":"10.1007/s12264-025-01434-z","DOIUrl":"https://doi.org/10.1007/s12264-025-01434-z","url":null,"abstract":"Maintaining a stable body temperature is essential for survival. Multiple brain regions contribute to thermoregulation, but their specific characteristics and underlying neural mechanisms in the coordination of thermoregulation are not fully clarified. Here, we reveal the distinct roles of two preoptic subregions in warm defense in mice: the anterior ventromedial preoptic area (VMPO) and the ventral part of the lateral preoptic nucleus (vLPO). VMPO vesicular glutamate transporter 2 (Vglut2) neurons exhibited dramatic responses to rising temperatures, producing a marked decrease in core temperature by warm defense responses. In contrast, excitatory and inhibitory vLPO neurons responded gently to warm stimuli, exerting moderate effects on warm defense. Further postsynaptic tracing and caspase ablation identified distinct cell type-specific downstream targets in the dorsomedial hypothalamus (DMH) mediating these different warm defense responses. Taken together, our findings reveal distinct yet complementary pathways in the preoptic DMH network that enable both rapid and fine-tuned regulation of body temperature under elevated thermal conditions.","PeriodicalId":19314,"journal":{"name":"Neuroscience bulletin","volume":" ","pages":""},"PeriodicalIF":5.9,"publicationDate":"2025-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144333624","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

AQMFB-DWT: A Preprocessing Technique for Removing Blink Artifacts Before Extracting Pain-evoked Potential EEG. AQMFB-DWT：在提取痛诱发电位脑电图前去除眨眼伪影的预处理技术。

IF 5.9 2区医学

Neuroscience bulletin Pub Date : 2025-06-20 DOI: 10.1007/s12264-025-01425-0

Wenjia Gao, Dan Liu, Qisong Wang, Yongping Zhao, Jinwei Sun

{"title":"AQMFB-DWT: A Preprocessing Technique for Removing Blink Artifacts Before Extracting Pain-evoked Potential EEG.","authors":"Wenjia Gao, Dan Liu, Qisong Wang, Yongping Zhao, Jinwei Sun","doi":"10.1007/s12264-025-01425-0","DOIUrl":"https://doi.org/10.1007/s12264-025-01425-0","url":null,"abstract":"The pain-evoked potential electroencephalogram (EEG) is an effective electrophysiological indicator for pain assessment, yet its extraction is challenging due to interference from background activity and involuntary blinks. Although existing blink artifact-removal methods show efficacy, they face limitations such as the need for reference signals, neglect of individual differences, and reliance on user input, hindering their practical application in clinical pain assessments. In this paper, we propose a novel framework applying adaptive quadrature mirror filter banks (AQMFB) with discrete wavelet transform (DWT) to remove blink artifacts in pain EEG. Unlike traditional DWT methods that apply fixed wavelets across subjects, our method adapts wavelet construction based on the characteristics of EEG. Experimental results demonstrate that AQMFB-DWT outperforms four leading methods in removing blink artifacts with minimal distortion of pain information, all within an acceptable processing time. This technique is a valuable preprocessing step for enhancing the extraction of pain-evoked potentials.","PeriodicalId":19314,"journal":{"name":"Neuroscience bulletin","volume":" ","pages":""},"PeriodicalIF":5.9,"publicationDate":"2025-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144333622","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

Human Cortical Organoids with a Novel SCN2A Variant Exhibit Hyperexcitability and Differential Responses to Anti-Seizure Compounds. 具有新型SCN2A变体的人类皮质类器官表现出高兴奋性和对抗癫痫化合物的不同反应。

IF 5.9 2区医学

Neuroscience bulletin Pub Date : 2025-06-20 DOI: 10.1007/s12264-025-01429-w

Yuling Yang, Yang Cai, Shuyang Wang, Xiaoling Wu, Zhicheng Shao, Xin Wang, Jing Ding

{"title":"Human Cortical Organoids with a Novel SCN2A Variant Exhibit Hyperexcitability and Differential Responses to Anti-Seizure Compounds.","authors":"Yuling Yang, Yang Cai, Shuyang Wang, Xiaoling Wu, Zhicheng Shao, Xin Wang, Jing Ding","doi":"10.1007/s12264-025-01429-w","DOIUrl":"https://doi.org/10.1007/s12264-025-01429-w","url":null,"abstract":"Mutations in ion channel genes have long been implicated in a spectrum of epilepsy syndromes. However, therapeutic decision-making is relatively complex for epilepsies associated with channelopathy. Therefore, in the present study, we used a patient-derived organoid model with a novel SCN2A mutation (p.E512K) to investigate the potential of utilizing such a model as a platform for preclinical testing of anti-seizure compounds. The electrophysiological properties of the variant Nav1.2 exhibited gain-of-function effects with increased current amplitude and premature activation. Immunofluorescence staining of patient-derived cortical organoids (COs) displayed normal neurodevelopment. Multielectrode array (MEA) recordings of patient-derived COs showed hyperexcitability with increased spiking and remarkable network bursts. Moreover, the application of patient-derived COs for preclinical drug testing using the MEA showed that they exhibit differential responses to various anti-seizure drugs and respond well to carbamazepine. Our results demonstrate that the individualized organoids have the potential to serve as a platform for preclinical pharmacological assessment.","PeriodicalId":19314,"journal":{"name":"Neuroscience bulletin","volume":" ","pages":""},"PeriodicalIF":5.9,"publicationDate":"2025-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144333623","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

Interoceptive Dysfunction in Psychiatric Disorders and Non-invasive Neuromodulation for Improving Interoception. 精神疾病的内感受功能障碍和改善内感受的非侵入性神经调节。

IF 5.9 2区医学

Neuroscience bulletin Pub Date : 2025-06-19 DOI: 10.1007/s12264-025-01432-1

Huiru Cui, Jijun Wang, Chunbo Li

引用次数: 0

BIN1 Interacts with Tau Fragments to Inhibit TrkB Signaling Endosome Recycling in a Mouse Model of Alzheimer's Disease. 在阿尔茨海默病小鼠模型中，BIN1与Tau片段相互作用抑制TrkB信号内体循环

IF 5.9 2区医学

Neuroscience bulletin Pub Date : 2025-06-18 DOI: 10.1007/s12264-025-01435-y

Yanuo Wei, Ye Xi, Hui Li, Xingxing Zhang, Yu Wang, Yunpeng Li, Ronghao Fang, Jie Xiang, Shengxi Wu

{"title":"BIN1 Interacts with Tau Fragments to Inhibit TrkB Signaling Endosome Recycling in a Mouse Model of Alzheimer's Disease.","authors":"Yanuo Wei, Ye Xi, Hui Li, Xingxing Zhang, Yu Wang, Yunpeng Li, Ronghao Fang, Jie Xiang, Shengxi Wu","doi":"10.1007/s12264-025-01435-y","DOIUrl":"https://doi.org/10.1007/s12264-025-01435-y","url":null,"abstract":"Deficits in BDNF/TrkB receptor signaling lead to increased asparagine endopeptidase activity, which cleaves Tau at the N368 residue to promote Tau hyperphosphorylation and aggregation, thereby contributing to neuronal dysfunction in Alzheimer's disease (AD). However, whether Tau N368 inhibits the BDNF/TrkB signaling pathway remains poorly understood. Previous studies have shown that the internalization of the BDNF/TrkB complex, which leads to signaling endosomes, is necessary for coordinating neuronal survival and synaptic plasticity. Here, we demonstrate that Bridging Integrator 1 (BIN1) interacts with the Tau fragment N368 in P301S and Tau N368-Tg mouse brains, inhibiting BDNF/TrkB signaling by obstructing their early-endosome recycling. Overexpression of BIN1 in the hippocampus of Tau N368-Tg mice partially rescues BDNF/TrkB endosome transport and alleviates pathological and behavioral defects. Our findings suggest that dysfunction of the early-endosome pathway mediated by the Tau N368-BIN1 interaction impairs BDNF signaling, contributing to AD-associated pathological and behavioral dysfunction.","PeriodicalId":19314,"journal":{"name":"Neuroscience bulletin","volume":" ","pages":""},"PeriodicalIF":5.9,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144326365","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

The Dance Between Schwann Cells and Macrophages During the Repair of Peripheral Nerve Injury. 周围神经损伤修复过程中雪旺细胞与巨噬细胞之间的舞蹈。

IF 5.9 2区医学

Neuroscience bulletin Pub Date : 2025-06-07 DOI: 10.1007/s12264-025-01427-y

Wei Li, Guixian Liu, Jie Liang, Xiao Wang, Meiying Song, Xiaoli Liu, Luoyang Wang, Zijie Yang, Bei Zhang

引用次数: 0

HOCPCA Exerts Neuroprotection on Retinal Ganglion Cells by Binding to CaMKIIα and Modulating Oxidative Stress and Neuroinflammation in Experimental Glaucoma. HOCPCA通过与CaMKIIα结合，调节实验性青光眼的氧化应激和神经炎症，对视网膜神经节细胞具有神经保护作用。

IF 5.9 2区医学

Neuroscience bulletin Pub Date : 2025-06-02 DOI: 10.1007/s12264-025-01417-0

Panpan Li, Xin Shi, Hanhan Liu, Yuan Feng, Xiaosha Wang, Marc Herb, Haichao Ji, Stefan Wagner, Johannes Vogt, Verena Prokosch

引用次数: 0

Propofol Promotes Anesthesia Through the Activation of Centrally-Projecting Edinger-Westphal Nucleus Urocortin 1-Positive Neurons. 异丙酚通过激活Edinger-Westphal核尿皮质素1阳性神经元促进麻醉。

IF 5.9 2区医学

Neuroscience bulletin Pub Date : 2025-06-01 Epub Date: 2025-04-24 DOI: 10.1007/s12264-025-01401-8

Jing Huang, Yiwen Hu, Sheng Jing, Fuhai Bai, Zonghong Long, Zhuoxi Wu, Liang Fang, Lei Cao, Youliang Deng, Xiaohang Bao, Hong Li

引用次数: 0

How Fear Memory is Updated: From Reconsolidation to Extinction? 恐惧记忆是如何更新的：从重新巩固到消失？

IF 5.9 2区医学

Neuroscience bulletin Pub Date : 2025-06-01 Epub Date: 2025-04-09 DOI: 10.1007/s12264-025-01367-7

Jiahui Chen, Zhuowen Fang, Xiaolan Zhang, Yanrong Zheng, Zhong Chen

{"title":"How Fear Memory is Updated: From Reconsolidation to Extinction?","authors":"Jiahui Chen, Zhuowen Fang, Xiaolan Zhang, Yanrong Zheng, Zhong Chen","doi":"10.1007/s12264-025-01367-7","DOIUrl":"10.1007/s12264-025-01367-7","url":null,"abstract":"Post-traumatic stress disorder (PTSD) is a psychiatric disorder caused by traumatic past experiences, rooted in the neurocircuits of fear memory formation. Memory processes include encoding, storing, and recalling to forgetting, suggesting the potential to erase fear memories through timely interventions. Conventional strategies such as medications or electroconvulsive therapy often fail to provide permanent relief and come with significant side-effects. This review explores how fear memory may be erased, particularly focusing on the mnemonic phases of reconsolidation and extinction. Reconsolidation strengthens memory, while extinction weakens it. Interfering with memory reconsolidation could diminish the fear response. Alternatively, the extinction of acquired memory could reduce the fear memory response. This review summarizes experimental animal models of PTSD, examines the nature and epidemiology of reconsolidation to extinction, and discusses current behavioral therapy aimed at transforming fear memories to treat PTSD. In sum, understanding how fear memory updates holds significant promise for PTSD treatment.","PeriodicalId":19314,"journal":{"name":"Neuroscience bulletin","volume":" ","pages":"1054-1084"},"PeriodicalIF":5.9,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12158906/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144020687","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Genetic Etiology Link to Brain Function Underlying ADHD Symptoms and its Interaction with Sleep Disturbance: An ABCD Study. ADHD症状与脑功能相关的遗传病因及其与睡眠障碍的相互作用：一项ABCD研究。

IF 5.9 2区医学

Neuroscience bulletin Pub Date : 2025-06-01 Epub Date: 2025-01-19 DOI: 10.1007/s12264-025-01349-9

Aichen Feng, Dongmei Zhi, Zening Fu, Shan Yu, Na Luo, Vince Calhoun, Jing Sui

{"title":"Genetic Etiology Link to Brain Function Underlying ADHD Symptoms and its Interaction with Sleep Disturbance: An ABCD Study.","authors":"Aichen Feng, Dongmei Zhi, Zening Fu, Shan Yu, Na Luo, Vince Calhoun, Jing Sui","doi":"10.1007/s12264-025-01349-9","DOIUrl":"10.1007/s12264-025-01349-9","url":null,"abstract":"Attention deficit hyperactivity disorder (ADHD), a prevalent neurodevelopmental disorder influenced by both genetic and environmental factors, remains poorly understood regarding how its polygenic risk score (PRS) impacts functional networks and symptomology. This study capitalized on data from 11,430 children in the Adolescent Brain Cognitive Development study to explore the interplay between PRSADHD, brain function, and behavioral problems, along with their interactive effects. The results showed that children with a higher PRSADHD exhibited more severe attention deficits and rule-breaking problems, and experienced sleep disturbances, particularly in initiating and maintaining sleep. We also identified the central executive network, default mode network, and sensory-motor network as the functional networks most associated with PRS and symptoms in ADHD cases, with potential mediating roles. Particularly, the impact of PRSADHD was enhanced in children experiencing heightened sleep disturbances, emphasizing the need for early intervention in sleep issues to potentially mitigate subsequent ADHD symptoms.","PeriodicalId":19314,"journal":{"name":"Neuroscience bulletin","volume":" ","pages":"1041-1053"},"PeriodicalIF":5.9,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12158910/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143009082","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0