Rho GTPases, dendritic structure, and mental retardation

被引:285
作者
Newey, SE [1 ]
Velamoor, V [1 ]
Govek, EE [1 ]
Van Aelst, L [1 ]
机构
[1] Cold Spring Harbor Lab, Cold Spring Harbor, NY 11724 USA
来源
JOURNAL OF NEUROBIOLOGY | 2005年 / 64卷 / 01期
基金
英国惠康基金;
关键词
dendrites; spines; mental retardation; Rho GTPases; actin; cytoskeleton;
D O I
10.1002/neu.20153
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
A consistent feature of neurons in patients with mental retardation is abnormal dendritic structure and/or alterations in dendritic spine morphology. Deficits in the regulation of the dendritic cytoskeleton affect both the structure and function of dendrites and synapses and are believed to underlie mental retardation in some instances. In support of this, there is good evidence that alterations in signaling pathways involving the Rho family of small GTPases, key regulators of the actin and microtubule cytoskeletons, contribute to both syndromic and nonsyndromic mental retardation disorders. Because the Rho GTPases have been shown to play increasingly well-defined roles in determining dendrite and dendritic spine development and morphology, Rho signaling has been suggested to be important for normal cognition. The purpose of this review is to summarize recent data on the Rho GTPases pertaining to dendrite and dendritic spine morphogenesis, as well as to highlight their involvement in mental retardation resulting from a variety of genetic mutations within regulators and effectors of these molecules. (c) 2005 Wiley periodicals, Inc.
引用
收藏
页码:58 / 74
页数:17
相关论文
共 191 条
[51]   DENDRITIC SPINE ANOMALIES IN FETAL ALCOHOL SYNDROME [J].
FERRER, I ;
GALOFRE, E .
NEUROPEDIATRICS, 1987, 18 (03) :161-163
[52]   Dendritic spine pathology: Cause or consequence of neurological disorders? [J].
Fiala, JC ;
Spacek, J ;
Harris, KM .
BRAIN RESEARCH REVIEWS, 2002, 39 (01) :29-54
[53]   ACTIN IN THE NERVOUS-SYSTEM [J].
FIFKOVA, E .
BRAIN RESEARCH REVIEWS, 1985, 9 (02) :187-215
[54]   Rapid actin-based plasticity in dendritic spines [J].
Fischer, M ;
Kaech, S ;
Knutti, D ;
Matus, A .
NEURON, 1998, 20 (05) :847-854
[55]   LIM-kinase1 hemizygosity implicated in impaired visuospatial constructive cognition [J].
Frangiskakis, JM ;
Ewart, AK ;
Morris, CA ;
Mervis, CB ;
Bertrand, J ;
Robinson, BF ;
Klein, BP ;
Ensing, GJ ;
Everett, LA ;
Green, ED ;
Proschel, C ;
Gutowski, NJ ;
Noble, M ;
Atkinson, DL ;
Odelberg, SJ ;
Keating, MT .
CELL, 1996, 86 (01) :59-69
[56]   X-linked mental retardation: vanishing boundaries between non-specific (MRX) and syndromic (MRXS) forms [J].
Frints, SGM ;
Froyen, G ;
Marynen, P ;
Fryns, JP .
CLINICAL GENETICS, 2002, 62 (06) :423-432
[57]  
Fryns JP, 2000, AM J MED GENET, V94, P345, DOI 10.1002/1096-8628(20001023)94:5<345::AID-AJMG1>3.0.CO
[58]  
2-Z
[59]   Hippocampal LTP is accompanied by enhanced F-actin content within the dendritic spine that is essential for late LTP maintenance in vivo [J].
Fukazawa', Y ;
Saitoh, Y ;
Ozawa, F ;
Ohta, Y ;
Mizuno, K ;
Inokuchi, K .
NEURON, 2003, 38 (03) :447-460
[60]   Understanding mental retardation in Down's syndrome using trisomy 16 mouse models [J].
Galdzicki, Z ;
Siarey, RJ .
GENES BRAIN AND BEHAVIOR, 2003, 2 (03) :167-178