期刊
MOLECULES AND CELLS
卷 28, 期 6, 页码 501-507出版社
KOREAN SOC MOLECULAR & CELLULAR BIOLOGY
DOI: 10.1007/s10059-009-0193-x
关键词
anterior cingulate cortex; dopamine; fragile X mental retardation; long-term potentiation; memory; prefrontal cortex
资金
- Canada Research Chair
- CIHR [CIHR66975, CIHR84256]
- Fragile X Research Foundation of Canada
- World Class University (WCU)
- National Research Foundation of Korea [R31-2008-000-10089-0] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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.
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