Regulation of Voltage-Gated Calcium Channels by Synaptic Proteins

被引:20
作者
Weiss, Norbert [1 ]
Zamponi, Gerald W. [1 ]
机构
[1] Univ Calgary, Dept Physiol & Pharmacol, Hotchkiss Brain Inst, Calgary, AB T2N 4N1, Canada
来源
CALCIUM SIGNALING | 2012年 / 740卷
基金
加拿大健康研究院;
关键词
Calcium channel; Cav2.1; channel; Cav2.2; Cav2.3; SNARE; Syntaxin; SNAP25; Neuron; Exocytosis; Neurotransmitter; Synaptic transmission; CYSTEINE-STRING PROTEINS; G-BETA-GAMMA; I-II-LOOP; N-TYPE; CA2+ CHANNELS; NEUROTRANSMITTER RELEASE; SYNTAXIN; 1A; TRANSMITTER RELEASE; PRESYNAPTIC CALCIUM; SUBCELLULAR-DISTRIBUTION;
D O I
10.1007/978-94-007-2888-2_33
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Calcium entry through neuronal voltage-gated calcium channels into presynaptic nerve terminal is a key step in synaptic exocytosis. In order to receive the calcium signal and trigger fast, efficient and spatially delimited neurotransmitter release, the vesicle-docking/release machinery must be located near the calcium source. In many cases, this close localization is achieved by a direct interaction of several members of the vesicle release machinery with the calcium channels. In turn, the binding of synaptic proteins to presynaptic calcium channels modulates channel activity to provide fine control over calcium entry, and thus modulates synaptic strength. In this chapter we summarize our present knowledge of the molecular mechanisms by which synaptic proteins regulate presynaptic calcium channel activity.
引用
收藏
页码:759 / 775
页数:17
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