SPINE MORPHOLOGY IN AN ANIMAL MODEL OF FRAGILE X SYNDROME

脆性 X 综合征动物模型的脊柱形态

• 批准号: 7601019
• 负责人: WILLIAM T GREENOUGH
• 金额: $ 3.69万
• 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/7601019
• 关键词: 3-Dimensional; Animal Model; Area; Brain; Chromosome Pairing; Clinical; Computer Retrieval of Information on Scientific Projects Database; Disease; Electron Microscopy; Etiology; FMR1 Gene; Fluorescence Microscopy; Fragile X Mental Retardation Protein; Fragile X Syndrome; Funding; Goals; Grant; Institution; Intention; Knockout Mice; Mental Retardation; Methods; Morphology; Neurons; Neurotransmitters; Protein Biosynthesis; Proteins; Research; Research Personnel; Resources; Source; Synapses; Techniques; United States National Institutes of Health; Vertebral column; design; insight; metabotropic glutamate receptor 2; mouse model; response

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. The primary goal of these studies has been to examine the neuronal morphology in key brain areas from a mouse model of fragile X knockout mouse, compared to that of wild-type controls. We have approached this objective using a converging-methods approach, employing techniques such as conventional serial-section electron microscopy, correlative fluorescence and light microscopy, and 3-dimensional electron microscopy. These studies were designed with the intention of providing a better insight into underlying etiology and/or consequences the clinical disorder, fragile X mental retardation. These studies have been very illuminating and the objectives are continuing to be pursued as described below. Project goals arise from our findings that 1) the fragile X mental retardation protein is synthesized at synapses, along with other proteins, in response to neurotransmitter activation of metabotropic glutamate receptors, and 2) a functioning fragile X (fmr1) gene is necessary for neurotransmitter-activated protein synthesis to occur at synapses.

这个子项目是许多研究子项目中的一个 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH来源获得了主要资金， 因此可以在其他CRISP条目中表示。所列机构为 研究中心，而研究中心不一定是研究者所在的机构。 这些研究的主要目的是检查脆性X基因敲除小鼠模型与野生型对照小鼠的关键脑区中的神经元形态。我们已经接近这个目标，使用收敛的方法的方法，采用传统的连续切片电子显微镜，相关荧光和光学显微镜，三维电子显微镜等技术。这些研究的目的是提供一个更好的了解潜在的病因和/或后果的临床障碍，脆性X智力低下。 这些研究非常有启发性，并将继续努力实现下述目标。 项目目标源于我们的发现：1）脆性X智力低下蛋白在突触处合成，沿着其他蛋白质，以响应亲代谢性谷氨酸受体的神经递质激活; 2）功能性脆性X（fmr 1）基因是神经递质激活蛋白在突触处合成所必需的。