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Neuronal Regulation of Feeding and Energy Metabolism: A Focus on the Hypothalamus and Brainstem.
IF 5.9 2区 医学
Neuroscience bulletin Pub 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":"https://doi.org/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":""},"PeriodicalIF":5.9,"publicationDate":"2024-12-20","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
Deciphering the Role of Shank3 in Dendritic Morphology and Synaptic Function Across Postnatal Developmental Stages in the Shank3B KO Mouse.
IF 5.9 2区 医学
Neuroscience bulletin Pub 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":"https://doi.org/10.1007/s12264-024-01330-y","url":null,"abstract":"<p><p>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.</p>","PeriodicalId":19314,"journal":{"name":"Neuroscience bulletin","volume":" ","pages":""},"PeriodicalIF":5.9,"publicationDate":"2024-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","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":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Conditional Tnfaip6-Knockout in Inner Ear Hair Cells Does not Alter Auditory Function.
IF 5.9 2区 医学
Neuroscience bulletin Pub Date : 2024-12-17 DOI: 10.1007/s12264-024-01326-8
Yue Qiu, Song Gao, Xiaoqiong Ding, Jie Lu, Xinya Ji, Wenli Hao, Siqi Cheng, Haolinag Du, Yajun Gu, Chenjie Yu, Cheng Cheng, Xia Gao
{"title":"Conditional Tnfaip6-Knockout in Inner Ear Hair Cells Does not Alter Auditory Function.","authors":"Yue Qiu, Song Gao, Xiaoqiong Ding, Jie Lu, Xinya Ji, Wenli Hao, Siqi Cheng, Haolinag Du, Yajun Gu, Chenjie Yu, Cheng Cheng, Xia Gao","doi":"10.1007/s12264-024-01326-8","DOIUrl":"https://doi.org/10.1007/s12264-024-01326-8","url":null,"abstract":"<p><p>Noise-induced hearing loss is a worldwide public health issue that is characterized by temporary or permanent changes in hearing sensitivity. This condition is closely linked to inflammatory responses, and interventions targeting the inflammatory gene tumor necrosis factor-alpha (TNFα) are known to mitigate cochlear noise damage. TNFα-induced proteins (TNFAIPs) are a family of translucent acidic proteins, and TNFAIP6 has a notable association with inflammatory responses. To date, there have been few reports on TNFAIP6 levels in the inner ear. To elucidate the precise mechanism, we generated transgenic mouse models with conditional knockout of Tnfaip6 (Tnfaip6 cKO). Evaluation of hair cell morphology and function revealed no significant differences in hair cell numbers or ribbon synapses between Tnfaip6 cKO and wild-type mice. Moreover, there were no notable variations in hair cell numbers or hearing function in noisy environments. Our results indicate that Tnfaip6 does not have a substantial impact on the auditory system.</p>","PeriodicalId":19314,"journal":{"name":"Neuroscience bulletin","volume":" ","pages":""},"PeriodicalIF":5.9,"publicationDate":"2024-12-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142838594","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
Inhibition of the cGAS‑STING Pathway Reduces Cisplatin-Induced Inner Ear Hair Cell Damage. 抑制 cGAS-STING 通路可减轻顺铂诱导的内耳毛细胞损伤
IF 5.9 2区 医学
Neuroscience bulletin Pub Date : 2024-12-16 DOI: 10.1007/s12264-024-01334-8
Ying Sun, Shengyu Zou, Xiaoxiang Xu, Shan Xu, Haiying Sun, Mingliang Tang, Weijia Kong, Xiong Chen, Zuhong He
{"title":"Inhibition of the cGAS‑STING Pathway Reduces Cisplatin-Induced Inner Ear Hair Cell Damage.","authors":"Ying Sun, Shengyu Zou, Xiaoxiang Xu, Shan Xu, Haiying Sun, Mingliang Tang, Weijia Kong, Xiong Chen, Zuhong He","doi":"10.1007/s12264-024-01334-8","DOIUrl":"https://doi.org/10.1007/s12264-024-01334-8","url":null,"abstract":"<p><p>Although cisplatin is a widely used chemotherapeutic agent, it is severely toxic and causes irreversible hearing loss, restricting its application in clinical settings. This study aimed to determine the molecular mechanism underlying cisplatin-induced ototoxicity. Here, we established in vitro and in vivo ototoxicity models of cisplatin-induced hair cell loss, and our results showed that reducing STING levels decreased inflammatory factor expression and hair cell death. In addition, we found that cisplatin-induced mitochondrial dysfunction was accompanied by cytosolic DNA, which may act as a critical linker between the cyclic GMP-AMP synthesis-stimulator of interferon genes (cGAS-STING) pathway and the pathogenesis of cisplatin-induced hearing loss. H-151, a specific inhibitor of STING, reduced hair cell damage and ameliorated the hearing loss caused by cisplatin in vivo. This study underscores the role of cGAS-STING in cisplatin ototoxicity and presents H-151 as a promising therapeutic for hearing loss.</p>","PeriodicalId":19314,"journal":{"name":"Neuroscience bulletin","volume":" ","pages":""},"PeriodicalIF":5.9,"publicationDate":"2024-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142829534","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
A New Pathway Mediating Pain Sensitization after Active Sleep Deprivation.
IF 5.9 2区 医学
Neuroscience bulletin Pub Date : 2024-12-14 DOI: 10.1007/s12264-024-01337-5
Xinyue Zhao, Yanrong Zheng, Zhong Chen
{"title":"A New Pathway Mediating Pain Sensitization after Active Sleep Deprivation.","authors":"Xinyue Zhao, Yanrong Zheng, Zhong Chen","doi":"10.1007/s12264-024-01337-5","DOIUrl":"https://doi.org/10.1007/s12264-024-01337-5","url":null,"abstract":"","PeriodicalId":19314,"journal":{"name":"Neuroscience bulletin","volume":" ","pages":""},"PeriodicalIF":5.9,"publicationDate":"2024-12-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142822374","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
Dysregulation of Iron Homeostasis Mediated by FTH Increases Ferroptosis Sensitivity in TP53-Mutant Glioblastoma.
IF 5.9 2区 医学
Neuroscience bulletin Pub 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":"https://doi.org/10.1007/s12264-024-01322-y","url":null,"abstract":"<p><p>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.</p>","PeriodicalId":19314,"journal":{"name":"Neuroscience bulletin","volume":" ","pages":""},"PeriodicalIF":5.9,"publicationDate":"2024-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","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":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
The Current State and Future Outlook of PET Tracers for AMPA Receptors.
IF 5.9 2区 医学
Neuroscience bulletin Pub Date : 2024-12-11 DOI: 10.1007/s12264-024-01332-w
Ling Li, Shenglin Wen, Ji Dai
{"title":"The Current State and Future Outlook of PET Tracers for AMPA Receptors.","authors":"Ling Li, Shenglin Wen, Ji Dai","doi":"10.1007/s12264-024-01332-w","DOIUrl":"https://doi.org/10.1007/s12264-024-01332-w","url":null,"abstract":"","PeriodicalId":19314,"journal":{"name":"Neuroscience bulletin","volume":" ","pages":""},"PeriodicalIF":5.9,"publicationDate":"2024-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142807524","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
A Novel Astrocyte-Neuron Interaction to Control Complex Animal Behavior.
IF 5.9 2区 医学
Neuroscience bulletin Pub Date : 2024-12-09 DOI: 10.1007/s12264-024-01328-6
Helmut Kettenmann
{"title":"A Novel Astrocyte-Neuron Interaction to Control Complex Animal Behavior.","authors":"Helmut Kettenmann","doi":"10.1007/s12264-024-01328-6","DOIUrl":"https://doi.org/10.1007/s12264-024-01328-6","url":null,"abstract":"","PeriodicalId":19314,"journal":{"name":"Neuroscience bulletin","volume":" ","pages":""},"PeriodicalIF":5.9,"publicationDate":"2024-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142801811","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.
IF 5.9 2区 医学
Neuroscience bulletin Pub 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":"https://doi.org/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":""},"PeriodicalIF":5.9,"publicationDate":"2024-12-08","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
Role of the Thalamic Reticular Nucleus in Social Memory.
IF 5.9 2区 医学
Neuroscience bulletin Pub Date : 2024-12-07 DOI: 10.1007/s12264-024-01331-x
Xue Liu, Jianing Zhu, Junqiang Zheng, Han Xu
{"title":"Role of the Thalamic Reticular Nucleus in Social Memory.","authors":"Xue Liu, Jianing Zhu, Junqiang Zheng, Han Xu","doi":"10.1007/s12264-024-01331-x","DOIUrl":"https://doi.org/10.1007/s12264-024-01331-x","url":null,"abstract":"","PeriodicalId":19314,"journal":{"name":"Neuroscience bulletin","volume":" ","pages":""},"PeriodicalIF":5.9,"publicationDate":"2024-12-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142791776","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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