MITOCHONDRIAL BIOENERGETICS IN NEURONS

神经元中的线粒体生物能量学

• 批准号: 7601078
• 负责人: NEIL R SMALHEISER
• 金额: $ 1.09万
• 依托单位: UNIVERSITY OF CALIFORNIA, SAN DIEGO
• 依托单位国家: 美国
• 财政年份: 2007
• 资助国家: 美国
• 起止时间: 2007-05-01 至 2008-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7601078
• 关键词: Bioenergetics; Chemosensitization; Computer Retrieval of Information on Scientific Projects Database; Dendritic Spines; Development; Funding; Goals; Grant; Growth; Institution; Investigation; Knowledge; Laboratories; Learning; Mitochondria; Mitochondrial Proteins; Neuronal Plasticity; Neurons; Phase; Production; Protein Biosynthesis; Regulation; Research; Research Personnel; Resources; Role; Signal Transduction; Source; Synaptic plasticity; United States National Institutes of Health

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Our goal is to identify promising gaps in current knowledge regarding the roles for mitochondria in providing energy for use in signal transduction, protein synthesis, neuronal plasticity and learning. Local regulation of protein synthesis at dendritic spines for synaptic plasticity is under intensive investigation by many laboratories. Yet, we noticed that local regulation of mitochondrial ATP production and protein synthesis was almost totally ignored in this context. Our Arrowsmith searches suggest that mitochondrial protein synthesis might be involved in regulating longterm potentiation, dendritic spine development or synaptic plasticity, particularly in late or sustained phases of consolidation and growth.

这个子项目是许多研究子项目中利用 资源由NIH/NCRR资助的中心拨款提供。子项目和 调查员(PI)可能从NIH的另一个来源获得了主要资金， 并因此可以在其他清晰的条目中表示。列出的机构是 该中心不一定是调查人员的机构。 我们的目标是找出目前关于线粒体在信号转导、蛋白质合成、神经元可塑性和学习中提供能量的作用的知识中有希望的空白。许多实验室正在深入研究树突棘蛋白质合成的局部调控对突触可塑性的影响。然而，我们注意到，在这种情况下，线粒体ATP生产和蛋白质合成的局部调节几乎完全被忽视。我们的Arrowsmith搜索表明，线粒体蛋白质合成可能参与调节长期增强、树突棘发育或突触可塑性，特别是在巩固和生长的后期或持续阶段。