SPINE MORPHOLOGY IN AN ANIMAL MODEL OF FRAGILE X SYNDROME

点击翻译按钮获取中文摘要

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.