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: 7601659
• 负责人: WILLIAM T GREENOUGH
• 金额: $ 0.18万
• 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/7601659
• 关键词: Actins; Animal Model; Appearance; Autopsy; Computer Retrieval of Information on Scientific Projects Database; Dendrites; Dendritic Spines; Disease; F-Actin; FMRP; Fragile X Mental Retardation Protein; Fragile X Syndrome; Funding; Golgi Apparatus; Grant; Human; Institution; Link; Mental Retardation; Methodology; Morphology; Research; Research Personnel; Resources; Shapes; Source; Staining method; Stains; Synapses; Three-Dimensional Imaging; Tissues; United States National Institutes of Health; Vertebral column; mouse model; voltage

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. Fragile X mental retardation, a genetically-linked disorder, results from the inability to produce the protein FMRP. The lack of FMRP expression has been associated with altered dendritic spine morphology in human post-mortem tissue and a mouse model of the disorder. Moreover, stability of spine shape has been shown to be dependent upon the filamentous form of actin, F-actin. Golgi-impregnation studies of human autopsy tissue and of a mouse model of fragile X mental retardation syndrome suggest that dendritic spines have an underdeveloped appearance--a tendency towards elongated, tortuous spine morphology. We have tentatively hypothesized that the absence of the fragile X protein (FMRP) interferes with synaptic and dendritic maturation. With the NCMIR this we will examine dendritic segments using high voltage EM and NCMIR's recently developed actin staining methodology to provide 3-D images of dendrites and their spines to evaluate and provide more details with respect to the maturation hypothesis.

该副本是利用众多研究子项目之一 由NIH/NCRR资助的中心赠款提供的资源。子弹和 调查员（PI）可能已经从其他NIH来源获得了主要资金， 因此可以在其他清晰的条目中代表。列出的机构是 对于中心，这不一定是调查员的机构。 易碎的X智力低下是一种遗传连接的疾病，是由于无法产生蛋白质FMRP而产生的。 缺乏FMRP表达与人类后组织中的树突状脊柱形态改变有关，并且是该疾病的小鼠模型。 此外，脊柱形状的稳定性已被证明取决于肌动蛋白F-肌动蛋白的丝状形式。 人体尸检组织和脆弱X智力智能综合征小鼠模型的高尔基爆裂研究表明，树突状棘的外观欠发达 - 一种倾向，曲折的脊柱形态的趋势。 我们暂时假设缺乏脆弱的X蛋白（FMRP）会干扰突触和树突状成熟。 借助NCMIR，我们将使用高压EM和NCMIR最近开发的肌动蛋白染色方法来检查树突段，以提供树突及其刺的3-D图像，以评估和提供有关成熟假设的更多细节。