Neuroscience bulletin最新文献_第10页

Histopathological Insights into Demyelination and Remyelination After Spinal Cord Injury in Non-human Primates. 非人灵长类动物脊髓损伤后脱髓鞘和再髓鞘的组织病理学观察。

IF 5.9 2区医学

Neuroscience bulletin Pub Date : 2025-04-05 DOI: 10.1007/s12264-025-01388-2

Junhao Liu, Zucheng Huang, Kinon Chen, Rong Li, Zhiping Huang, Junyu Lin, Hui Jiang, Jie Liu, Qingan Zhu

{"title":"Histopathological Insights into Demyelination and Remyelination After Spinal Cord Injury in Non-human Primates.","authors":"Junhao Liu, Zucheng Huang, Kinon Chen, Rong Li, Zhiping Huang, Junyu Lin, Hui Jiang, Jie Liu, Qingan Zhu","doi":"10.1007/s12264-025-01388-2","DOIUrl":"https://doi.org/10.1007/s12264-025-01388-2","url":null,"abstract":"Demyelination and remyelination play key roles in spinal cord injury (SCI), affecting the recovery of motor and sensory functions. Research in rodent models is extensive, but the study of these processes in non-human primates is limited. Therefore, our goal was to thoroughly study the histological features of demyelination and remyelination after contusion injury of the cervical spinal cord in Macaca fascicularis. In a previous study, we created an SCI model in M. fascicularis by controlling the contusion displacement. We used Eriochrome Cyanine staining, immunohistochemical analysis, and toluidine blue staining to evaluate demyelination and remyelination. The results showed demyelination ipsilateral to the injury epicenter both rostrally and caudally, the former mainly impacting sensory pathways, while the latter primarily affected motor pathways. Toluidine blue staining showed myelin loss and axonal distension at the injury site. Schwann cell-derived myelin sheaths were only found at the center, while thinner myelin sheaths from oligodendrocytes were seen at the center and surrounding areas. Our study showed that long-lasting demyelination occurs in the spinal cord of M. fascicularis after SCI, with oligodendrocytes and Schwann cells playing a significant role in myelin sheath formation at the injury site.","PeriodicalId":19314,"journal":{"name":"Neuroscience bulletin","volume":" ","pages":""},"PeriodicalIF":5.9,"publicationDate":"2025-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143788581","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

Deciphering the Role of Shank3 in Dendritic Morphology and Synaptic Function Across Postnatal Developmental Stages in the Shank3B KO Mouse. 揭示Shank3B KO小鼠出生后发育阶段树突形态和突触功能中Shank3的作用。

IF 5.9 2区医学

Neuroscience bulletin Pub Date : 2025-04-01 Epub Date: 2024-12-18 DOI: 10.1007/s12264-024-01330-y

Jing Yang, Guaiguai Ma, Xiaohui Du, Jinyi Xie, Mengmeng Wang, Wenting Wang, Baolin Guo, Shengxi Wu

{"title":"Deciphering the Role of Shank3 in Dendritic Morphology and Synaptic Function Across Postnatal Developmental Stages in the Shank3B KO Mouse.","authors":"Jing Yang, Guaiguai Ma, Xiaohui Du, Jinyi Xie, Mengmeng Wang, Wenting Wang, Baolin Guo, Shengxi Wu","doi":"10.1007/s12264-024-01330-y","DOIUrl":"10.1007/s12264-024-01330-y","url":null,"abstract":"Autism Spectrum Disorder (ASD) is marked by early-onset neurodevelopmental anomalies, yet the temporal dynamics of genetic contributions to these processes remain insufficiently understood. This study aimed to elucidate the role of the Shank3 gene, known to be associated with monogenic causes of autism, in early developmental processes to inform the timing and mechanisms for potential interventions for ASD. Utilizing the Shank3B knockout (KO) mouse model, we examined Shank3 expression and its impact on neuronal maturation through Golgi staining for dendritic morphology and electrophysiological recordings to measure synaptic function in the anterior cingulate cortex (ACC) across different postnatal stages. Our longitudinal analysis revealed that, while Shank3B KO mice displayed normal neuronal morphology at one week postnatal, significant impairments in dendritic growth and synaptic activity emerged by two to three weeks. These findings highlight the critical developmental window during which Shank3 is essential for neuronal and synaptic maturation in the ACC.","PeriodicalId":19314,"journal":{"name":"Neuroscience bulletin","volume":" ","pages":"583-599"},"PeriodicalIF":5.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11978597/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142847146","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

Dysregulation of Iron Homeostasis Mediated by FTH Increases Ferroptosis Sensitivity in TP53-Mutant Glioblastoma. FTH介导的铁稳态失调增加tp53突变型胶质母细胞瘤的铁凋亡敏感性。

IF 5.9 2区医学

Neuroscience bulletin Pub Date : 2025-04-01 Epub Date: 2024-12-12 DOI: 10.1007/s12264-024-01322-y

Xuejie Huan, Jiangang Li, Zhaobin Chu, Hongliang Zhang, Lei Cheng, Peng Lun, Xixun Du, Xi Chen, Qian Jiao, Hong Jiang

{"title":"Dysregulation of Iron Homeostasis Mediated by FTH Increases Ferroptosis Sensitivity in TP53-Mutant Glioblastoma.","authors":"Xuejie Huan, Jiangang Li, Zhaobin Chu, Hongliang Zhang, Lei Cheng, Peng Lun, Xixun Du, Xi Chen, Qian Jiao, Hong Jiang","doi":"10.1007/s12264-024-01322-y","DOIUrl":"10.1007/s12264-024-01322-y","url":null,"abstract":"Iron metabolism is a critical factor in tumorigenesis and development. Although TP53 mutations are prevalent in glioblastoma (GBM), the mechanisms by which TP53 regulates iron metabolism remain elusive. We reveal an imbalance iron homeostasis in GBM via TCGA database analysis. TP53 mutations disrupted iron homeostasis in GBM, characterized by elevated total iron levels and reduced ferritin (FTH). The gain-of-function effect triggered by TP53 mutations upregulates itchy E3 ubiquitin-protein ligase (ITCH) protein expression in astrocytes, leading to FTH degradation and an increase in free iron levels. TP53-mut astrocytes were more tolerant to the high iron environment induced by exogenous ferric ammonium citrate (FAC), but the increase in intracellular free iron made them more sensitive to Erastin-induced ferroptosis. Interestingly, we found that Erastin combined with FAC treatment significantly increased ferroptosis. These findings provide new insights for drug development and therapeutic modalities for GBM patients with TP53 mutations from iron metabolism perspectives.","PeriodicalId":19314,"journal":{"name":"Neuroscience bulletin","volume":" ","pages":"569-582"},"PeriodicalIF":5.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11978602/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142813749","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

Bridge RNA-Guided Genetic Recombination Tools for Treating Neurodegenerative Nucleotide Repeat Disorders. 桥rna引导的基因重组工具治疗神经退行性核苷酸重复疾病。

IF 5.9 2区医学

Neuroscience bulletin Pub Date : 2025-04-01 Epub Date: 2025-02-18 DOI: 10.1007/s12264-025-01358-8

Fengshi Li, Jingyu Yu, Peng Wang, Tianwen Li, Qisheng Tang, Jianhong Zhu

引用次数: 0

Dynamic Routing of Theta-Frequency Synchrony in the Amygdalo-Hippocampal-Entorhinal Circuit Coordinates Retrieval of Competing Memories. 竞争记忆在杏仁核-海马体-内嗅回路坐标检索中的动态频率同步路径。

IF 5.9 2区医学

Neuroscience bulletin Pub Date : 2025-04-01 Epub Date: 2025-02-01 DOI: 10.1007/s12264-025-01356-w

Jiahua Zheng, Yiqi Sun, Fuhai Wang, Zhongyu Xie, Qianyun Wang, Jian-Ya Peng, Jianguang Ni

引用次数: 0

Histaminergic Innervation of the Ventral Anterior Thalamic Nucleus Alleviates Motor Deficits in a 6-OHDA-Induced Rat Model of Parkinson's Disease. 丘脑腹侧前核的组胺能神经支配减轻6-羟多巴胺诱导的帕金森病大鼠模型的运动缺陷。

IF 5.9 2区医学

Neuroscience bulletin Pub Date : 2025-04-01 Epub Date: 2024-12-02 DOI: 10.1007/s12264-024-01320-0

Han-Ting Xu, Xiao-Ya Xi, Shuang Zhou, Yun-Yong Xie, Zhi-San Cui, Bei-Bei Zhang, Shu-Tao Xie, Hong-Zhao Li, Qi-Peng Zhang, Yang Pan, Xiao-Yang Zhang, Jing-Ning Zhu

{"title":"Histaminergic Innervation of the Ventral Anterior Thalamic Nucleus Alleviates Motor Deficits in a 6-OHDA-Induced Rat Model of Parkinson's Disease.","authors":"Han-Ting Xu, Xiao-Ya Xi, Shuang Zhou, Yun-Yong Xie, Zhi-San Cui, Bei-Bei Zhang, Shu-Tao Xie, Hong-Zhao Li, Qi-Peng Zhang, Yang Pan, Xiao-Yang Zhang, Jing-Ning Zhu","doi":"10.1007/s12264-024-01320-0","DOIUrl":"10.1007/s12264-024-01320-0","url":null,"abstract":"The ventral anterior (VA) nucleus of the thalamus is a major target of the basal ganglia and is closely associated with the pathogenesis of Parkinson's disease (PD). Notably, the VA receives direct innervation from the hypothalamic histaminergic system. However, its role in PD remains unknown. Here, we assessed the contribution of histamine to VA neuronal activity and PD motor deficits. Functional magnetic resonance imaging showed reduced VA activity in PD patients. Optogenetic activation of VA neurons or histaminergic afferents significantly alleviated motor deficits in 6-OHDA-induced PD rats. Furthermore, histamine excited VA neurons via H1 and H2 receptors and their coupled hyperpolarization-activated cyclic nucleotide-gated channels, inward-rectifier K+ channels, or Ca2+-activated K+ channels. These results demonstrate that histaminergic afferents actively compensate for Parkinsonian motor deficits by biasing VA activity. These findings suggest that targeting VA histamine receptors and downstream ion channels may be a potential therapeutic strategy for PD motor dysfunction.","PeriodicalId":19314,"journal":{"name":"Neuroscience bulletin","volume":" ","pages":"551-568"},"PeriodicalIF":5.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11978569/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142770549","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

Pseudogene Lamr1-ps1 Aggravates Early Spatial Learning Memory Deficits in Alzheimer's Disease Model Mice. 假基因Lamr1-ps1加重阿尔茨海默病模型小鼠早期空间学习记忆缺陷

IF 5.9 2区医学

Neuroscience bulletin Pub Date : 2025-04-01 Epub Date: 2025-01-02 DOI: 10.1007/s12264-024-01336-6

Zhuoze Wu, Xiaojie Liu, Yuntai Wang, Zimeng Zeng, Wei Chen, Hao Li

{"title":"Pseudogene Lamr1-ps1 Aggravates Early Spatial Learning Memory Deficits in Alzheimer's Disease Model Mice.","authors":"Zhuoze Wu, Xiaojie Liu, Yuntai Wang, Zimeng Zeng, Wei Chen, Hao Li","doi":"10.1007/s12264-024-01336-6","DOIUrl":"10.1007/s12264-024-01336-6","url":null,"abstract":"Alzheimer's disease (AD), a neurodegenerative disorder with complex etiologies, manifests through a cascade of pathological changes before clinical symptoms become apparent. Among these early changes, alterations in the expression of non-coding RNAs (ncRNAs) have emerged as pivotal events. In this study, we focused on the aberrant expression of ncRNAs and revealed that Lamr1-ps1, a pseudogene of the laminin receptor, significantly exacerbates early spatial learning and memory deficits in APP/PS1 mice. Through a combination of bioinformatics prediction and experimental validation, we identified the miR-29c/Bace1 pathway as a potential regulatory mechanism by which Lamr1-ps1 influences AD pathology. Importantly, augmenting the miR-29c-3p levels in mice ameliorated memory deficits, underscoring the therapeutic potential of targeting miR-29c-3p in early AD intervention. This study not only provides new insights into the role of pseudogenes in AD but also consolidates a foundational basis for considering miR-29c as a viable therapeutic target, offering a novel avenue for AD research and treatment strategies.","PeriodicalId":19314,"journal":{"name":"Neuroscience bulletin","volume":" ","pages":"600-614"},"PeriodicalIF":5.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11979086/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142922322","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

Associative Learning-Induced Synaptic Potentiation at the Two Major Hippocampal CA1 Inputs for Cued Memory Acquisition. 联想学习诱导海马 CA1 两大输入端突触电位增强，促进诱导记忆的获得

IF 5.9 2区医学

Neuroscience bulletin Pub Date : 2025-04-01 Epub Date: 2024-11-27 DOI: 10.1007/s12264-024-01327-7

Bing-Ying Wang, Bo Wang, Bo Cao, Ling-Ling Gu, Jiayu Chen, Hua He, Zheng Zhao, Fujun Chen, Zhiru Wang

{"title":"Associative Learning-Induced Synaptic Potentiation at the Two Major Hippocampal CA1 Inputs for Cued Memory Acquisition.","authors":"Bing-Ying Wang, Bo Wang, Bo Cao, Ling-Ling Gu, Jiayu Chen, Hua He, Zheng Zhao, Fujun Chen, Zhiru Wang","doi":"10.1007/s12264-024-01327-7","DOIUrl":"10.1007/s12264-024-01327-7","url":null,"abstract":"Learning-associated functional plasticity at hippocampal synapses remains largely unexplored. Here, in a single session of reward-based trace conditioning, we examine learning-induced synaptic plasticity in the dorsal CA1 hippocampus (dCA1). Local field-potential recording combined with selective optogenetic inhibition first revealed an increase of dCA1 synaptic responses to the conditioned stimulus (CS) induced during conditioning at both Schaffer collaterals to the stratum radiatum (Rad) and temporoammonic input to the lacunosum moleculare (LMol). At these dCA1 inputs, synaptic potentiation of CS-responding excitatory synapses was further demonstrated by locally blocking NMDA receptors during conditioning and whole-cell recording sensory-evoked synaptic responses in dCA1 neurons from naive animals. An overall similar time course of the induction of synaptic potentiation was found in the Rad and LMol by multiple-site recording; this emerged later and saturated earlier than conditioned behavioral responses. Our experiments demonstrate a cued memory-associated dCA1 synaptic plasticity induced at both Schaffer collaterals and temporoammonic pathways.","PeriodicalId":19314,"journal":{"name":"Neuroscience bulletin","volume":" ","pages":"649-664"},"PeriodicalIF":5.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11979062/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142739970","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

Neuronal Regulation of Feeding and Energy Metabolism: A Focus on the Hypothalamus and Brainstem. 神经元摄食和能量代谢的调控：以下丘脑和脑干为中心。

IF 5.9 2区医学

Neuroscience bulletin Pub Date : 2025-04-01 Epub Date: 2024-12-20 DOI: 10.1007/s12264-024-01335-7

Jing Chen, Meiting Cai, Cheng Zhan

引用次数: 0

The Role and Mechanisms of Ubiquitin-Proteasome System-Mediated Ferroptosis in Neurological Disorders. 泛素-蛋白酶体系统介导的铁下垂在神经系统疾病中的作用和机制。

IF 5.9 2区医学

Neuroscience bulletin Pub Date : 2025-04-01 Epub Date: 2025-01-07 DOI: 10.1007/s12264-024-01343-7

Xin Liu, Wei Wang, Qiucheng Nie, Xinjing Liu, Lili Sun, Qiang Ma, Jie Zhang, Yiju Wei

引用次数: 0