SPINE MORPHOLOGY IN AN ANIMAL MODEL OF FRAGILE X SYNDROME

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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.