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Control of depolarization-evoked presynaptic neurotransmitter release by CaV2.1 calcium channel

机译:CaV2.1钙通道控制去极化诱发的突触前神经递质的释放

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摘要

Depolarization-evoked synaptic transmission relies on the Ca2+-regulated release of quantal packets of neurotransmitters following the fusion of synaptic vesicles with the presynaptic plasma membrane. It is well known that neuronal voltage-gated Ca2+ channels (VGCC), mainly of the CaV2.1 and CaV2.2 subtypes, play a key role in the first steps of this process, by controlling extracellular Ca2+ influx into active zones of the synapse. These channels are in close association with the vesicle machinery and interact with several members of SNARE proteins (soluble NSF (N-ethylmaleimide-sensitive fusion protein) attachment protein receptor) including syntaxin 1A/1B and SNA P-25 (Q-SNARE s), and synaptotagmin 1 and synaptobrevin 2 (R-SNARE s) (reviewed in ref. ). All bind to the synprint (synaptic protein interaction) motif within the intracellular II -III linker of CaV2.1 and CaV2.2 channels and are responsible for a bidirectional coupling (i) linking the Ca2+ influx with the synaptic vesicle release machinery, which is essential for efficient, fast and spatially delimited neurotransmitter release and (ii) providing regulation of Ca2+ channel activity and thus of Ca2+ influx.
机译:去极化引起的突触传递依赖于突触小泡与突触前质膜融合后神经递质的定量包的Ca 2 + 释放。众所周知,主要是CaV2.1和CaV2.2亚型的神经元电压门控Ca 2 + 通道(VGCC)通过控制以下过程在该过程的第一步中起关键作用细胞外Ca 2 + 流入突触的活性区。这些通道与囊泡机制密切相关,并与SNARE蛋白(可溶性NSF(N-乙基马来酰亚胺敏感的融合蛋白)附着蛋白受体)的几个成员相互作用,包括语法1A / 1B和SNA P-25(Q-SNARE) ,以及synaptotagmin 1和synaptobrevin 2(R-SNARE s)(在参考文献 中进行了综述)。它们均与CaV2.1和CaV2.2通道的细胞内II -III接头内的synprint(突触蛋白相互作用)基序结合,并负责双向偶联(i)连接Ca 2 + 流入通过突触小泡释放机制,这对于有效,快速和空间分隔的神经递质释放 至关重要,并且(ii)调节Ca 2 + 通道活性,从而调节Ca < sup> 2 + 涌入。

著录项

  • 期刊名称 Channels
  • 作者

    Norbert Weiss;

  • 作者单位
  • 年(卷),期 2010(4),6
  • 年度 2010
  • 页码 431–433
  • 总页数 3
  • 原文格式 PDF
  • 正文语种
  • 中图分类 分子生物学;
  • 关键词

  • 入库时间 2022-08-17 13:08:34

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