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Single‑Neuron Reconstruction of the Macaque Primary Motor Cortex Reveals the Diversity of Neuronal Morphology

Neuroscience Bulletin 2025年第3期41卷 525-530页

作者： Siyu Li Yan Shen Yefei Chen Zexuan Hong Lewei Zhang Lufeng Ding Chao‑Yu Yang Xiaoyang Qi Quqing Shen Yanyang Xiao Pak‑Ming Lau Zhonghua Lu Fang Xu Guo‑Qiang Bi CAS Key Laboratory of Brain Function and Disease Division of Life Sciences and MedicineUniversity of Science and Technology of ChinaHefei 230026China Interdisciplinary Center for Brain Information Shenzhen-Hong Kong Institute of Brain ScienceShenzhen Institutes of Advanced TechnologyChinese Academy of SciencesShenzhen 518055China Shenzhen Technological Research Center for Primate Translational Medicine Shenzhen Key Laboratory for Molecular Biology of Neural DevelopmentShenzhen Institutes of Advanced TechnologyChinese Academy of SciencesShenzhen 518055China The Key Laboratory of Biomedical Imaging Science and System Chinese Academy of SciencesShenzhen 518055China CAS Key Laboratory of Brain Connectome and Manipulation the Brain Cognition and Brain Disease InstituteShenzhen Institutes of Advanced TechnologyChinese Academy of SciencesShenzhen 518055China Faculty of Life and Health Sciences Shenzhen University of Advanced TechnologyShenzhen 518107China

Dear Editor,The primary motor cortex,also known as MOp in rodents,F1,or M1 in primates[1],plays a crucial role in autonomous motor *** is interconnected with other motor control structures such as the basal ganglia,thalamus,and *** these connections,the corticostriatal system plays a significant role in functions including action selection,motor control,sequence learning,and habit formation[2].

关键词： habit formation autonomous motor controlit morphology action selectionmotor corticostriatal system neuron basal gangliathalamusand primary motor cortexalso

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IsoVISoR: Towards 3D Mesoscale brain Mapping of Large Mammals at Isotropic Sub-micron Resolution

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Neuroscience Bulletin 2025年第2期41卷 344-348页

作者： Chao-Yu Yang Yan Shen Xiaoyang Qi Lufeng Ding Yanyang Xiao Qingyuan Zhu Hao Wang Cheng Xu Pak-Ming Lau Pengcheng Zhou Fang Xu Guo-Qiang Bi Division of Life Sciences and Medicine CAS Key Laboratory of Brain Function and DiseaseUniversity of Science and Technology of ChinaHefei230026China Interdisciplinary Center for Brain Information Shenzhen-Hong Kong Institute of Brain ScienceShenzhen Institute of Advanced TechnologyChinese Academy of SciencesShenzhen518055China Center for Integrative Imaging Hefei National Research Center for Physical Sciences at the MicroscaleUniversity of Science and Technology of ChinaHefei230027China National Engineering Laboratory for Brain-Inspired Intelligence Technology and Application MoE Key Laboratory of Brain-Inspired Intelligent Perception and CognitionSchool of Information Science and TechnologyUniversity of Science and Technology of ChinaHefei230026China Anhui Province Key Laboratory of Biomedical Imaging and Intelligent Processing Institute of Artificial IntelligenceHefei Comprehensive National Science CenterHefei230088China Faculty of Life and Health Sciences Shenzhen University of Advanced TechnologyShenzhen518107China CAS Key Laboratory of Brain Connectome and Manipulation The Brain Cognition and Brain Disease InstituteShenzhen Institute of Advanced TechnologyChinese Academy of SciencesShenzhen518055China

Dear Editor,The mammalian brain exhibits cross-scale complexity in neuronal morphology and connectivity,the study of which demands high-resolution morphological reconstruction of individual neurons across the entire brain[1-4].Current commonly used approaches for such mesoscale brain mapping include two main types of three-dimensional fluorescence microscopy:the block-face methods,and the lightsheet-based methods[5,6].In general,the high imaging speed and light efficiency of light-sheet microscopy make it a suitable tool for high-throughput volumetric imaging,especially when combined with tissue-clearing ***,large brain samples pose major challenges to this approach.

关键词： brain mapping three dimensional fluorescence microscopy mesoscale brain mapping lightsheet based methods block face methods high throughput volumetric imaging tissue clearing techniques

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Vascular Ossification in the Developing brain:A case Study of Pediatric Sturge Weber Syndrome

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Neuroscience Bulletin 2025年第3期41卷 520-524页

作者： Ranxi Chen Shuhui Xie Jin Gao Shuli Zhang Xiaobin Zhang Yi Yao Gengxiu Zheng Fengpeng Wang Zili Liu Xuefeng Shen School of Chemistry and Chemical Engineering University of JinanJinan 250022China CAS Key Laboratory of Brain Connectome and Manipulation Shenzhen-Hong Kong Institute of Brain ScienceShenzhen Institute of Advanced Technology(SIAT)Chinese Academy of Sciences(CAS)Shenzhen 518055China The Brain Cognition and Brain Disease Institute SIATCASShenzhen 518055China Sino-Danish College University of CASBeijing 100190China HH-SIAT Joint Center for Epilepsy Research Xiamen Humanity Hospital(XHH)Xiamen 361003China Department of Pathology XHHXiamen 361003China State Key Laboratory of Brain and Cognitive Sciences CAS Center for Excellence in BiomacromoleculesInstitute of BiophysicsCASBeijing 100101China University of CAS Beijing 100049China Epilepsy Center XHHXiamen 361003China

Dear Editor,Sturge-Weber Syndrome(SWS)is a rare congenital neurocutaneous syndrome[1,2],with an estimated prevalence of 0.19 in 100,000 annually[3].It is a non-hereditary disease linked to a somatic mutation in the GNAQ,GNA11,or GNB2 gene[1],leading to vascular malformations in the cutaneous forehead,cerebral cortex,and eye[1,2].Notably,~70%of pediatric patients diagnosed with SWS exhibit brain calcification(BC)[4],though the prevalence of BC ranges from only 1%in young individuals to>20%in the senior population(>60 years old)[5].Similar to the elderly,BC in pediatric SWS patients is identified as vascular calcification[6,7],whereas BC in pediatric patients with tuberous sclerosis and tumors has been previously described as dystrophic calcification[6].

关键词： vascular calcification vascular malformations brain calcification bc brain calcification congenital neurocutaneous syndrome somatic mutation vascular ossification Sturge Weber syndrome

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Increased excitatory amino acid transporter 2 levels in basolateral amygdala astrocytes mediate chronic stress–induced anxiety-like behavior

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Neural Regeneration Research 2025年第6期20卷 1721-1734页

作者： Xirong Xu Shoumin Xuan Shuai Chen Dan Liu Qian Xiao Jie Tu Shenzhen Key Laboratory of Neuroimmunomodulation for Neurological Diseases Shenzhen-Hong Kong Institute of Brain ScienceShenzhen Institute of Advanced TechnologyChinese Academy of SciencesShenzhenGuangdong ProvinceChina CAS Key Laboratory of Brain Connectome and Manipulation Brain Cognition and Brain Disease Institute(BCBDI)Shenzhen Institute of Advanced TechnologyChinese Academy of SciencesShenzhenGuangdong ProvinceChina Guangdong Provincial Key Laboratory of Brain Connectome and Behavior the Brain Cognition and Brain Disease Institute(BCBDI)Shenzhen Institute of Advanced TechnologyChinese Academy of SciencesShenzhenGuangdong ProvinceChina University of Chinese of Academy of Sciences BeijingChina Faculty of Life and Health Sciences Shenzhen Institute of Advanced TechnologyChinese Academy of SciencesShenzhenGuangdong ProvinceChina

The conventional perception of astrocytes as mere supportive cells within the brain has recently been called into question by empirical evidence, which has revealed their active involvement in regulating brain function and encoding behaviors associated with ***, astrocytes in the basolateral amygdala have been found to play a role in the modulation of anxiety-like behaviors triggered by chronic stress. Nevertheless, the precise molecular mechanisms by which basolateral amygdala astrocytes regulate chronic stress–induced anxiety-like behaviors remain to be fully elucidated. In this study, we found that in a mouse model of anxiety triggered by unpredictable chronic mild stress, the expression of excitatory amino acid transporter 2 was upregulated in the basolateral amygdala. Interestingly, our findings indicate that the targeted knockdown of excitatory amino acid transporter 2 specifically within the basolateral amygdala astrocytes was able to rescue the anxiety-like behavior in mice subjected to stress. Furthermore, we found that the overexpression of excitatory amino acid transporter 2 in the basolateral amygdala, whether achieved through intracranial administration of excitatory amino acid transporter 2agonists or through injection of excitatory amino acid transporter 2-overexpressing viruses with GfaABC1D promoters, evoked anxiety-like behavior in mice. Our single-nucleus RNA sequencing analysis further confirmed that chronic stress induced an upregulation of excitatory amino acid transporter 2 specifically in astrocytes in the basolateral amygdala. Moreover, through in vivo calcium signal recordings, we found that the frequency of calcium activity in the basolateral amygdala of mice subjected to chronic stress was higher compared with normal *** knocking down the expression of excitatory amino acid transporter 2 in the basolateral amygdala, the frequency of calcium activity was not significantly increased, and anxiety-like behavior was ob

关键词： anxiety astrocytes basolateral amygdala behavior dihydrokainic acid excitatory amino acid transporter 2 fiber photometry glutamate LDN-212320 transporter

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Time-Dependent Transcriptional Dynamics of Contextual Fear Memory Retrieval Reveals the function of Dipeptidyl Peptidase 9 in Reconsolidation

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Neuroscience Bulletin 2025年第1期41卷 16-32页

作者： Wen-Ting Guo Wen-Xing Li Yu-Chen Liu Ya-Bo Zhao Lin Xu Qi-Xin Zhou Key Laboratory of Animal Models and Human Disease Mechanisms Laboratory of Learning and MemoryKunming Institute of ZoologyThe Chinese Academy of SciencesKunming 650223China Kunming College of Life Science University of Chinese Academy of SciencesKunming 650204China CAS Centre for Excellence in Brain Science and Intelligent Technology Shanghai 200031China Jiangsu Key Laboratory of Neuropsychiatric Diseases College of Pharmaceutical SciencesSoochow UniversitySuzhou 215123China

Numerous studies on the formation and consolidation of memory have shown that memory processes are characterized by phase-dependent and dynamic *** retrieval,as the only representation of memory content and an active form of memory processing that induces memory reconsolidation,has attracted increasing attention in recent *** the molecular mechanisms specifc to memory retrievalinduced reconsolidation have been gradually revealed,an understanding of the time-dependent regulatory mechanisms of this process is still *** this study,we applied a transcriptome analysis of memory retrieval at diferent time points in the recent memory *** expression analysis and Short Time-series Expression Miner(STEM)depicting temporal gene expression patterns indicated that most diferential gene expression occurred at 48 h,and the STEM cluster showing the greatest transcriptional upregulation at 48 h demonstrated the most significant *** then screened the diferentially-expressed genes associated with that met the expression patterns of those cluster-identifed genes that have been reported to be involved in learning and memory processes in addition to dipeptidyl peptidase 9(DPP9).Further quantitative polymerase chain reaction verifcation and pharmacological intervention suggested that DPP9 is involved in 48-h fear memory retrieval and viral vector-mediated overexpression of DPP9 countered the 48-h retrieval-induced attenuation of fear *** together,our fndings suggest that temporal gene expression patterns are induced by recent memory retrieval and provide hitherto undocumented evidence of the role of DPP9 in the retrieval-induced reconsolidation of fear memory.

关键词： Transcriptome analysis Temporal gene expression Fear memory retrieval Reconsolidation DPP9

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The interaction between KIF21A and KANK1 regulates dendritic morphology and synapse plasticity in neurons

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Neural Regeneration Research 2025年第1期20卷 209-223页

作者： Shi-Yan Sun Lingyun Nie Jing Zhang Xue Fang Hongmei Luo Chuanhai Fu Zhiyi Wei Ai-Hui Tang Hefei National Research Center for Physical Sciences at the Microscale CAS Key Laboratory of Brain Function and DiseaseMinistry of Education Key Laboratory for Membrane-less Organelles and Cellular DynamicsDivision of Life Sciences and MedicineUniversity of Science and Technology of ChinaHefeiAnhui ProvinceChina Institute of Artificial Intelligence Hefei Comprehensive National Science CenterHefeiAnhui ProvinceChina CAS Center for Excellence in Molecular Cell Sciences Division of Life Sciences and MedicineUniversity of Science and Technology of ChinaHefeiAnhui ProvinceChina Department of Neurobiology School of Life SciencesSouthern University of Science and TechnologyShenzhenGuangdong ProvinceChina Brain Research Center Southern University of Science and TechnologyShenzhenGuangdong ProvinceChina

Morphological alterations in dendritic spines have been linked to changes in functional communication between neurons that affect learning and ***-4 KIF21A helps organize the microtubule-actin network at the cell cortex by interacting with KANK1;however,whether KIF21A modulates dendritic structure and function in neurons remains *** this study,we found that KIF21A was distributed in a subset of dendritic spines,and that these KIF21A-positive spines were larger and more structurally plastic than KIF21A-negative ***,the interaction between KIF21A and KANK1 was found to be critical for dendritic spine morphogenesis and synaptic *** of either KIF21A or KANK1 inhibited dendritic spine morphogenesis and dendritic branching,and these deficits were fully rescued by coexpressing full-length KIF21A or KANK1,but not by proteins with mutations disrupting direct binding between KIF21A and KANK1 or binding between KANK1 and *** down KIF21A in the hippocampus of rats inhibited the amplitudes of long-term potentiation induced by high-frequency stimulation and negatively impacted the animals’cognitive *** together,our findings demonstrate the function of KIF21A in modulating spine morphology and provide insight into its role in synaptic function.

关键词： actin cytoskeleton dendrite KANK1 KIF21A microtubule spine morphology spine synaptic plasticity talin1

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The Current State and Future Outlook of PET Tracers for AMPA Receptors

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Neuroscience Bulletin 2025年第3期41卷 531-535页

作者： Ling Li Shenglin Wen Ji Dai Department of Psychology The Fifth Affiliated HospitalSun Yat-sen UniversityZhuhai 519000China Shenzhen Technological Research Center for Primate Translational Medicine Shenzhen-Hong Kong Institute of Brain ScienceShenzhen Institute of Advanced TechnologyChinese Academy of SciencesShenzhen 518055China CAS Key Laboratory of Brain Connectome and Manipulation The Brain Cognition and Brain Disease InstituteShenzhen Institute of Advanced TechnologyChinese Academy of SciencesShenzhen 518055China Guangdong Provincial Key Laboratory of Brain Connectome and Behavior Shenzhen Institute of Advanced TechnologyChinese Academy of SciencesShenzhen 518055China University of Chinese Academy of Sciences Beijing 100049China

AMPA Receptor and PET Tracer *** alpha-amino-3-hydroxy-5-methyl-4-isoxazolpropionic acid receptor(AMPAR)is a subtype of ionotropic glutamate *** functions as a ligand-gated ion channel and is primarily responsible for rapidly transmitting the signal from glutamate in the central nervous system[1].This receptor plays a crucial role in various cognitive functions including learning,memory,cognition,synaptic plasticity,and *** are typically composed of four subunits,namely GluA1,GluA2,GluA3,and GluA4,which can form homo-or *** subunits bind directly or indirectly to various scaffolding proteins such as transmembrane AMPA receptor regulatory proteins(TARPs).

关键词： pet tracer limitationthe synaptic plasticity cognitive functions pet tracers ampa receptors ampa receptor central nervous system ionotropic glutamate receptorit

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Inhibition of KDM6B prevents osteoarthritis by blocking growth plate-like H3K27me3 loss in bivalent genes

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Science China Life Sciences 2025年第5期68卷 1423-1436页

作者： Hao Du Yao Zhang Xi Yu Xuanhe You Diwei Wu Ze Du Yongrui Cai Zhenyu Luo Hanpeng Lu Zhixin Liao Bi-Sen Ding Ya Zhao Yan Wang Ke Xiao Fan Yang Fangji Gan Ning Ning Jiancheng Zeng Peiliang Shi Zongke Zhou Shishu Huang Department of Orthopedic Surgery and Orthopedic Research Institute West China HospitalSichuan University Rehabilitation Medicine Center West China HospitalSichuan University Key Laboratory of Birth Defects and Related Diseases of Women and Children of MOE State Key Laboratory of BiotherapyWest China Second University HospitalSichuan University Institute of Translational Medicine Medical CollegeYangzhou University Jiangsu Key Laboratory of Experimental & Translational Non-coding RNA Research College of Animal Science and Technology Sichuan Agricultural University Farm Animal Genetic Resources Exploration and Innovation Key Laboratory of Sichuan Province Sichuan Agricultural University Department of Lower Limb Surgery of Sichuan Province Orthopedic Hospital Central Laboratory of Sichuan Province Orthopedic Hospital Brain Cognition and Brain Disease Institute (BCBDI) Shenzhen Institute of Advanced TechnologyChinese Academy of Sciences (CAS)Shenzhen-Hong Kong Institute of Brain Science-Shenzhen Fundamental Research Institutions School of Mechanical Engineering Sichuan University Gem Pharmatech (Chengdu) Co. Ltd.

Osteoarthritis(OA) is the most prevalent joint disorder occurring with articular cartilage degradation. It includes a switch from an articular to a growth plate chondrocyte phenotype. Here, we investigated the histone modification profiles and found significant H3K27me3 loss in OA, which led to disease-associated gene expression. Surprisingly, these genes were occupied by both H3K27me3 and H3K4me3 in normal chondrocytes, showing a poised bivalent state. Furthermore, we observed the derepression of similar bivalent genes in growth plate chondrocytes. Finally, a KDM6B inhibitor GSK-J4 prevented the H3K27me3 loss and cartilage damage in the rat OA model. Our results reveal an inherited bivalent epigenetic signature on developmental genes that makes articular chondrocytes prone to hypertrophy and contributes to a promising epigenetic therapy for OA.

关键词： osteoarthritis histone modifications H3K27me3 bivalency growth plate

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Shaping sight: Novel thalamic plasticity channels dLGN feature preference during visual critical period

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Neuron 2025年第9期113卷 1294-1296页

作者： Chuying Zhou Xiang Gao Liming Tan Shenzhen Key Laboratory of Neuropsychiatric Modulation Shenzhen-Hong Kong Institute of Brain Science Shenzhen Institutes of Advanced Technology Chinese Academy of Sciences Shenzhen 518055 China CAS Key Laboratory of Brain Connectome and Manipulation the Brain Cognition and Brain Disease Institute Shenzhen Institutes of Advanced Technology Chinese Academy of Sciences Shenzhen 518055 China Guangdong Provincial Key Laboratory of Brain Connectome and Behavior the Brain Cognition and Brain Disease Institute Shenzhen Institutes of Advanced Technology Chinese Academy of Sciences Shenzhen 518055 China. Guangdong Provincial Key Laboratory of Brain Connectome and Behavior the Brain Cognition and Brain Disease Institute Shenzhen Institutes of Advanced Technology Chinese Academy of Sciences Shenzhen 518055 China University of Chinese Academy of Sciences Beijing 100049 China. Electronic address: lm.tan@***.

Sonoda et al. showed that dLGN neurons exhibit long-lasting shifts of tuning preference toward selective features experienced during the classical critical period. They demonstrated that this plasticity results from feedforward-input refinement, revealing a different form of experience-dependent plasticity compared to V1.

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GLP-1 receptor agonist exendin-4 suppresses food intake by inhibiting hindbrain orexigenic NPY neurons

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American Journal of Physiology - Endocrinology and Metabolism 2025年第5期328卷 E661-E674页

作者： Shen, Jiayi Wang, Mengtian Pang, Guodong Zhang, Yan Zhang, Jian Shi, Yuyan Liu, Ji Zhan, Cheng Department of Hematology The First Affiliated Hospital of USTC Hefei National Research Center for Physical Sciences at the Microscale Division of Life Science and Medicine University of Science and Technology of China Hefei China Department of Endocrinology The First Affiliated Hospital of USTC Hefei National Research Center for Physical Sciences at the Microscale Division of Life Science and Medicine University of Science and Technology of China Hefei China National Key Laboratory of Immune Response and Immunotherapy Center for Advanced Interdisciplinary Science and Biomedicine of IHM CAS Key Laboratory of Brain Function and Disease University of Science and Technology of China Hefei China School of Biomedical Engineering School of Information Science and Technology University of Science and Technology of China Hefei China

Peripherally delivered glucagon-like peptide-1 (GLP-1)-based drugs suppress eating through their action in the brain. However, the specific neuronal mechanisms, especially their impacts on the orexigenic circuit, remain largely elusive. Neuropeptide Y (NPY) neurons in the nucleus tractus solitarius (NTS) are newly identified as orexigenic neurons with a potent eating-stimulating effect, but their responses to GLP-1 drugs are unknown. Through ex vivo electrophysiological recordings, we study the impacts of GLP-1 receptor (GLP-1R) agonist exendin-4 on NTS^NPY neurons. We discovered that the GLP-1R agonist exendin-4 inhibits NTS^NPY neuronal activity via GABA_b receptors by augmenting presynaptic GABA release. We also explored the contribution of NTS^NPY neurons to exendin-4-mediated eating suppression. Interestingly, chemogenetic activation of NTS^NPY neurons effectively counteracted exendin-4-induced anorexigenic effect. Moreover, chemogenetic inhibition of NTS^NPY neurons mimicked the eating-suppressing effect of exendin-4. Collectively, our findings highlight a population of orexigenic NTS^NPY neurons that may be targeted by a GLP-1R agonist to suppress food intake, suggesting that this neuronal population has translational importance as a potential therapeutic target for obesity treatment. Copyright © 2025 The Authors.

关键词： food intake GABAb receptors GLP-1 receptor neuropeptide Y neurons the nucleus tractus solitarius

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