期刊
NEUROBIOLOGY OF DISEASE
卷 31, 期 1, 页码 127-132出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.nbd.2008.04.002
关键词
Fragile X Syndrome; spines; dendrite branching; MPEP; fenobam; prepulse inhibition of startle; metabotropic glutamate receptor; primary hippocampal neuron culture
资金
- NICHD NIH HHS [P30 HD024064-19, R01 HD038038-05, R01 HD038038, P30 HD024064, R01 HD38038] Funding Source: Medline
Lack of fragile X mental retardation protein (FMRP) causes Fragile X Syndrome, the most common form of inherited mental retardation. FMRP is an RNA-binding protein and is a component of messenger ribonucleoprotein complexes, associated with brain polyribosomes, including dendritic polysomes. FMRP is therefore thought to be involved in translational control of specific mRNAs at synaptic sites. In mice lacking FMRP, protein synthesis-dependent synaptic plasticity is altered and structural malformations of dendritic protrusions occur. One hypothesized cause of the disease mechanism is based on exaggerated group I mGluR receptor activation. In this study, we examined the effect of the mGluR5 antagonist MPEP on Fragile X related behavior in Fmr1 KO mice. Our results demonstrate a clear defect in prepulse inhibition of startle in Fmr1 KO mice, that could be rescued by MPEP. Moreover, we show for the first time a structural rescue of Fragile X related protrusion morphology with two independent mGluR5 antagonists. (C) 2008 Elsevier Inc. All rights reserved.
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