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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
{"title":"Neuronal Regulation of Feeding and Energy Metabolism: A Focus on the Hypothalamus and Brainstem.","authors":"Jing Chen, Meiting Cai, Cheng Zhan","doi":"10.1007/s12264-024-01335-7","DOIUrl":"10.1007/s12264-024-01335-7","url":null,"abstract":"<p><p>In the face of constantly changing environments, the central nervous system (CNS) rapidly and accurately calculates the body's needs, regulates feeding behavior, and maintains energy homeostasis. The arcuate nucleus of the hypothalamus (ARC) plays a key role in this process, serving as a critical brain region for detecting nutrition-related hormones and regulating appetite and energy homeostasis. Agouti-related protein (AgRP)/neuropeptide Y (NPY) neurons in the ARC are core elements that interact with other brain regions through a complex appetite-regulating network to comprehensively control energy homeostasis. In this review, we explore the discovery and research progress of AgRP neurons in regulating feeding and energy metabolism. In addition, recent advances in terms of feeding behavior and energy homeostasis, along with the redundant neural mechanisms involved in energy metabolism, are discussed. Finally, the challenges and opportunities in the field of neural regulation of feeding and energy metabolism are briefly discussed.</p>","PeriodicalId":19314,"journal":{"name":"Neuroscience bulletin","volume":" ","pages":"665-675"},"PeriodicalIF":5.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142865022","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 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
{"title":"The Role and Mechanisms of Ubiquitin-Proteasome System-Mediated Ferroptosis in Neurological Disorders.","authors":"Xin Liu, Wei Wang, Qiucheng Nie, Xinjing Liu, Lili Sun, Qiang Ma, Jie Zhang, Yiju Wei","doi":"10.1007/s12264-024-01343-7","DOIUrl":"10.1007/s12264-024-01343-7","url":null,"abstract":"<p><p>Ferroptosis is a form of cell death elicited by an imbalance in intracellular iron concentrations, leading to enhanced lipid peroxidation. In neurological disorders, both oxidative stress and mitochondrial damage can contribute to ferroptosis, resulting in nerve cell dysfunction and death. The ubiquitin-proteasome system (UPS) refers to a cellular pathway in which specific proteins are tagged with ubiquitin for recognition and degradation by the proteasome. In neurological conditions, the UPS plays a significant role in regulating ferroptosis. In this review, we outline how the UPS regulates iron metabolism, ferroptosis, and their interplay in neurological diseases. In addition, we discuss the future application of small-molecule inhibitors and identify potential drug targets. Further investigation into the mechanisms of UPS-mediated ferroptosis will provide novel insights and strategies for therapeutic interventions and clinical applications in neurological diseases.</p>","PeriodicalId":19314,"journal":{"name":"Neuroscience bulletin","volume":" ","pages":"691-706"},"PeriodicalIF":5.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142952370","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
Type 2 Diabetes Mellitus Exacerbates Pathological Processes of Parkinson's Disease: Insights from Signaling Pathways Mediated by Insulin Receptors. 2型糖尿病加剧帕金森病的病理过程：胰岛素受体介导的信号通路的见解
IF 5.9 2区 医学
Neuroscience bulletin Pub Date : 2025-04-01 Epub Date: 2025-01-04 DOI: 10.1007/s12264-024-01342-8
Shufen Liu, Tingting Liu, Jingwen Li, Jun Hong, Ali A Moosavi-Movahedi, Jianshe Wei
{"title":"Type 2 Diabetes Mellitus Exacerbates Pathological Processes of Parkinson's Disease: Insights from Signaling Pathways Mediated by Insulin Receptors.","authors":"Shufen Liu, Tingting Liu, Jingwen Li, Jun Hong, Ali A Moosavi-Movahedi, Jianshe Wei","doi":"10.1007/s12264-024-01342-8","DOIUrl":"10.1007/s12264-024-01342-8","url":null,"abstract":"<p><p>Parkinson's disease (PD), a chronic and common neurodegenerative disease, is characterized by the progressive loss of dopaminergic neurons in the dense part of the substantia nigra and abnormal aggregation of alpha-synuclein. Type 2 diabetes mellitus (T2DM) is a metabolic disease characterized by chronic insulin resistance and deficiency in insulin secretion. Extensive evidence has confirmed shared pathogenic mechanisms underlying PD and T2DM, such as oxidative stress caused by insulin resistance, mitochondrial dysfunction, inflammation, and disorders of energy metabolism. Conventional drugs for treating T2DM, such as metformin and glucagon-like peptide-1 receptor agonists, affect nerve repair. Even drugs for treating PD, such as levodopa, can affect insulin secretion. This review summarizes the relationship between PD and T2DM and related therapeutic drugs from the perspective of insulin signaling pathways in the brain.</p>","PeriodicalId":19314,"journal":{"name":"Neuroscience bulletin","volume":" ","pages":"676-690"},"PeriodicalIF":5.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142927537","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
Exploring the Therapeutic Potential of Psychedelics in Chronic Pain Management: A New Frontier in Medicine. 探索致幻剂在慢性疼痛管理中的治疗潜力：医学的新前沿。
IF 5.9 2区 医学
Neuroscience bulletin Pub Date : 2025-04-01 Epub Date: 2025-01-20 DOI: 10.1007/s12264-025-01351-1
Cong Lin, Xue Wang, Xiaohui Wang
{"title":"Exploring the Therapeutic Potential of Psychedelics in Chronic Pain Management: A New Frontier in Medicine.","authors":"Cong Lin, Xue Wang, Xiaohui Wang","doi":"10.1007/s12264-025-01351-1","DOIUrl":"10.1007/s12264-025-01351-1","url":null,"abstract":"","PeriodicalId":19314,"journal":{"name":"Neuroscience bulletin","volume":" ","pages":"719-722"},"PeriodicalIF":5.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143009081","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
Histamine H1 Receptor in Medial Septum Cholinergic Circuit: New Hope for Fear-related Disorders?
IF 5.9 2区 医学
Neuroscience bulletin Pub Date : 2025-04-01 Epub Date: 2025-02-01 DOI: 10.1007/s12264-025-01357-9
Kang Liu
{"title":"Histamine H<sub>1</sub> Receptor in Medial Septum Cholinergic Circuit: New Hope for Fear-related Disorders?","authors":"Kang Liu","doi":"10.1007/s12264-025-01357-9","DOIUrl":"10.1007/s12264-025-01357-9","url":null,"abstract":"","PeriodicalId":19314,"journal":{"name":"Neuroscience bulletin","volume":" ","pages":"737-740"},"PeriodicalIF":5.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143074774","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
To Attack or Not: A Neural Circuit Coding Sexually Dimorphic Aggression. 攻击与否：编码两性二态攻击的神经回路。
IF 5.9 2区 医学
Neuroscience bulletin Pub Date : 2025-04-01 Epub Date: 2025-01-03 DOI: 10.1007/s12264-024-01345-5
Qiuhong Xin, Hailan Hu
{"title":"To Attack or Not: A Neural Circuit Coding Sexually Dimorphic Aggression.","authors":"Qiuhong Xin, Hailan Hu","doi":"10.1007/s12264-024-01345-5","DOIUrl":"10.1007/s12264-024-01345-5","url":null,"abstract":"","PeriodicalId":19314,"journal":{"name":"Neuroscience bulletin","volume":" ","pages":"728-730"},"PeriodicalIF":5.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142922323","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
Direct Hippocampal and Thalamic Inputs to Layer 3 Pyramidal Cells in the Medial Entorhinal Cortex Revealed by Monosynaptic Rabies Tracing.
IF 5.9 2区 医学
Neuroscience bulletin Pub Date : 2025-04-01 Epub Date: 2025-03-10 DOI: 10.1007/s12264-025-01363-x
Ze Chen, Dietmar Schmitz, John J Tukker
{"title":"Direct Hippocampal and Thalamic Inputs to Layer 3 Pyramidal Cells in the Medial Entorhinal Cortex Revealed by Monosynaptic Rabies Tracing.","authors":"Ze Chen, Dietmar Schmitz, John J Tukker","doi":"10.1007/s12264-025-01363-x","DOIUrl":"10.1007/s12264-025-01363-x","url":null,"abstract":"","PeriodicalId":19314,"journal":{"name":"Neuroscience bulletin","volume":" ","pages":"707-712"},"PeriodicalIF":5.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143597434","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
Halting the Progression of Alzheimer's Disease: Is the Goal in Sight? 阻止阿尔茨海默病的进展：目标在眼前吗？
IF 5.9 2区 医学
Neuroscience bulletin Pub Date : 2025-04-01 Epub Date: 2024-12-27 DOI: 10.1007/s12264-024-01339-3
Yu-Juan Jia, Xuan-Yue Wang, Jie Liu, Yan-Jiang Wang, Colin L Masters, Jun-Hong Guo
{"title":"Halting the Progression of Alzheimer's Disease: Is the Goal in Sight?","authors":"Yu-Juan Jia, Xuan-Yue Wang, Jie Liu, Yan-Jiang Wang, Colin L Masters, Jun-Hong Guo","doi":"10.1007/s12264-024-01339-3","DOIUrl":"10.1007/s12264-024-01339-3","url":null,"abstract":"","PeriodicalId":19314,"journal":{"name":"Neuroscience bulletin","volume":" ","pages":"723-727"},"PeriodicalIF":5.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142896321","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
Cation Channel TMEM63A Autonomously Facilitates Oligodendrocyte Differentiation at an Early Stage.
IF 5.9 2区 医学
Neuroscience bulletin Pub Date : 2025-04-01 Epub Date: 2025-02-21 DOI: 10.1007/s12264-024-01338-4
Yue-Ying Wang, Dan Wu, Yongkun Zhan, Fei Li, Yan-Yu Zang, Xiao-Yu Teng, Linlin Zhang, Gui-Fang Duan, He Wang, Rong Xu, Guiquan Chen, Yun Xu, Jian-Jun Yang, Yongguo Yu, Yun Stone Shi
{"title":"Cation Channel TMEM63A Autonomously Facilitates Oligodendrocyte Differentiation at an Early Stage.","authors":"Yue-Ying Wang, Dan Wu, Yongkun Zhan, Fei Li, Yan-Yu Zang, Xiao-Yu Teng, Linlin Zhang, Gui-Fang Duan, He Wang, Rong Xu, Guiquan Chen, Yun Xu, Jian-Jun Yang, Yongguo Yu, Yun Stone Shi","doi":"10.1007/s12264-024-01338-4","DOIUrl":"10.1007/s12264-024-01338-4","url":null,"abstract":"<p><p>Accurate timing of myelination is crucial for the proper functioning of the central nervous system. Here, we identified a de novo heterozygous mutation in TMEM63A (c.1894G>A; p. Ala632Thr) in a 7-year-old boy exhibiting hypomyelination. A Ca<sup>2+</sup> influx assay suggested that this is a loss-of-function mutation. To explore how TMEM63A deficiency causes hypomyelination, we generated Tmem63a knockout mice. Genetic deletion of TMEM63A resulted in hypomyelination at postnatal day 14 (P14) arising from impaired differentiation of oligodendrocyte precursor cells (OPCs). Notably, the myelin dysplasia was transient, returning to normal levels by P28. Primary cultures of Tmem63a<sup>-/-</sup> OPCs presented delayed differentiation. Lentivirus-based expression of TMEM63A but not TMEM63A_A632T rescued the differentiation of Tmem63a<sup>-/-</sup> OPCs in vitro and myelination in Tmem63a<sup>-/-</sup> mice. These data thus support the conclusion that the mutation in TMEM63A is the pathogenesis of the hypomyelination in the patient. Our study further demonstrated that TMEM63A-mediated Ca<sup>2+</sup> influx plays critical roles in the early development of myelin and oligodendrocyte differentiation.</p>","PeriodicalId":19314,"journal":{"name":"Neuroscience bulletin","volume":" ","pages":"615-632"},"PeriodicalIF":5.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143468608","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
Reprogramming miR-146b-snphb Signaling Activates Axonal Mitochondrial Transport in the Zebrafish M-cell and Facilitates Axon Regeneration After Injury. 重编程miR-146b-snphb信号激活斑马鱼m细胞轴突线粒体运输并促进损伤后轴突再生
IF 5.9 2区 医学
Neuroscience bulletin Pub Date : 2025-04-01 Epub Date: 2024-12-08 DOI: 10.1007/s12264-024-01329-5
Xin-Liang Wang, Zong-Yi Wang, Xing-Han Chen, Yuan Cai, Bing Hu
{"title":"Reprogramming miR-146b-snphb Signaling Activates Axonal Mitochondrial Transport in the Zebrafish M-cell and Facilitates Axon Regeneration After Injury.","authors":"Xin-Liang Wang, Zong-Yi Wang, Xing-Han Chen, Yuan Cai, Bing Hu","doi":"10.1007/s12264-024-01329-5","DOIUrl":"10.1007/s12264-024-01329-5","url":null,"abstract":"<p><p>Acute mitochondrial damage and the energy crisis following axonal injury highlight mitochondrial transport as an important target for axonal regeneration. Syntaphilin (Snph), known for its potent mitochondrial anchoring action, has emerged as a significant inhibitor of both mitochondrial transport and axonal regeneration. Therefore, investigating the molecular mechanisms that influence the expression levels of the snph gene can provide a viable strategy to regulate mitochondrial trafficking and enhance axonal regeneration. Here, we reveal the inhibitory effect of microRNA-146b (miR-146b) on the expression of the homologous zebrafish gene syntaphilin b (snphb). Through CRISPR/Cas9 and single-cell electroporation, we elucidated the positive regulatory effect of the miR-146b-snphb axis on Mauthner cell (M-cell) axon regeneration at the global and single-cell levels. Through escape response tests, we show that miR-146b-snphb signaling positively regulates functional recovery after M-cell axon injury. In addition, continuous dynamic imaging in vivo showed that reprogramming miR-146b significantly promotes axonal mitochondrial trafficking in the pre-injury and early stages of regeneration. Our study reveals an intrinsic axonal regeneration regulatory axis that promotes axonal regeneration by reprogramming mitochondrial transport and anchoring. This regulation involves noncoding RNA, and mitochondria-associated genes may provide a potential opportunity for the repair of central nervous system injury.</p>","PeriodicalId":19314,"journal":{"name":"Neuroscience bulletin","volume":" ","pages":"633-648"},"PeriodicalIF":5.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142791755","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
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