Structural Modulation of Dendritic Spines during Synaptic Plasticity

被引:94
作者
Fortin, Dale A. [1 ]
Srivastava, Taasin [1 ]
Soderling, Thomas R. [1 ]
机构
[1] Oregon Hlth & Sci Univ, Vollum Inst, Portland, OR 97239 USA
基金
美国国家卫生研究院;
关键词
LTP; dendrite; spine; actin; translation; microRNA; LONG-TERM POTENTIATION; GLUR2-LACKING AMPA RECEPTORS; ACTIN-DEPOLYMERIZING FACTOR; CAMKII MESSENGER-RNA; POSTSYNAPTIC DENSITY; ARP2/3; COMPLEX; PROTEIN-SYNTHESIS; F-ACTIN; MICE LACKING; PROFILIN-I;
D O I
10.1177/1073858411407206
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
The majority of excitatory synaptic input in the brain is received by small bulbous actin-rich protrusions residing on the dendrites of glutamatergic neurons. These dendritic spines are the major sites of information processing in the brain. This conclusion is reinforced by the observation that many higher cognitive disorders, such as mental retardation, Rett syndrome, and autism, are associated with aberrant spine morphology. Mechanisms that regulate the maturation and plasticity of dendritic spines are therefore fundamental to understanding higher brain functions including learning and memory. It is well known that activity-driven changes in synaptic efficacy modulate spine morphology due to alterations in the underlying actin cytoskeleton. Recent studies have elucidated numerous molecular regulators that directly alter actin dynamics within dendritic spines. This review will emphasize activity-dependent changes in spine morphology and highlight likely roles of these actin-binding proteins.
引用
收藏
页码:326 / 341
页数:16
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