The role of neuronal calcium sensors in balancing synaptic plasticity and synaptic dysfunction

被引：13

作者：

Kerrigan, Talitha L. ^{[1
]}

Whitcomb, Daniel J. ^{[1
]}

Regan, Philip L. ^{[1
,2
]}

Cho, Kwangwook ^{[1
,2
]}

机构：

[1] Univ Bristol, HenryWellcome Labs Integrat Neurosci & Endocrinol, Sch Clin Sci, Fac Med & Dent, Bristol BS1 3NY, Avon, England

[2] Univ Bristol, MRC Ctr Synapt Plast, Bristol BS1 3NY, Avon, England

来源：

FRONTIERS IN MOLECULAR NEUROSCIENCE | 2012年 / 5卷

基金：

英国生物技术与生命科学研究理事会; 英国惠康基金;

关键词：

neuronal calcium sensor; long-term synaptic plasticity; Alzheimer's disease; LONG-TERM DEPRESSION; AMPA RECEPTOR TRAFFICKING; ALZHEIMERS-DISEASE; BINDING-PROTEIN; CA2+; PICK1; TRANSMISSION; HIPPOCAMPUS; ACTIVATION; CALSENILIN;

D O I：

10.3389/fnmol.2012.00057

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Neuronal calcium sensors (NCS) readily bind calcium and undergo conformational changes enabling them to interact and regulate specific target molecules. These interactions lead to dynamic alterations in protein trafficking that significantly impact upon synaptic function. Emerging evidence suggests that NCS and alterations in Ca2+ mobilization modulate glutamate receptor trafficking, subsequently determining the expression of different forms of synaptic plasticity. In this review, we aim to discuss the functional relevance of NCS in protein trafficking and their emerging role in synaptic plasticity. Their significance within the concept of "translational neuroscience" will also be highlighted, by assessing their potential as key molecules in neurodegeneration.

引用

页数：6

共 56 条

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Ames JB, 2012, FRONT MOL NEUROSCI, V5, DOI [10.3389/fnmol.2012.00010, 10.1016/j.bbagen.2011.10.003]

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