Fragile X mental retardation protein in learning-related synaptic plasticity

被引:39
作者
Mercaldo, Valentina [1 ]
Descalzi, Giannina [1 ]
Zhuo, Min [1 ,2 ]
机构
[1] Univ Toronto, Fac Med, Dept Physiol, Toronto, ON M5S 1A8, Canada
[2] Seoul Natl Univ, Dept Brain & Cognit Sci, Seoul 151746, South Korea
关键词
anterior cingulate cortex; dopamine; fragile X mental retardation; long-term potentiation; memory; prefrontal cortex; LONG-TERM POTENTIATION; FMR1 KNOCKOUT MICE; MOUSE MODEL; GABA(A) RECEPTOR; MESSENGER-RNA; OUT MICE; SOMATOSENSORY CORTEX; DOPAMINE-RECEPTORS; PREFRONTAL CORTEX; DENDRITIC SPINES;
D O I
10.1007/s10059-009-0193-x
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Fragile X syndrome (FXS) is caused by a lack of the fragile X mental retardation protein (FMRP) due to silencing of the Fmr1 gene. As an RNA binding protein, FMRP is thought to contribute to synaptic plasticity by regulating plasticity-related protein synthesis and other signaling pathways. Previous studies have mostly focused on the roles of FMRP within the hippocampus - a key structure for spatial memory. However, recent studies indicate that FMRP may have a more general contribution to brain functions, including synaptic plasticity and modulation within the prefrontal cortex. In this brief review, we will focus on recent studies reported in the prefrontal cortex, including the anterior cingulate cortex (ACC). We hypothesize that alterations in ACC-related plasticity and synaptic modulation may contribute to various forms of cognitive deficits associated with FXS.
引用
收藏
页码:501 / 507
页数:7
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