Requirement for the synaptic protein interaction site for reconstitution of synaptic transmission by P/Q-type calcium channels
Requirement for the synaptic protein interaction site for reconstitution of synaptic transmission by P/Q-type calcium channels
复制标题
DOI：
10.1073/pnas.262787699
复制
发表时间：
2003-03-04
影响因子：
11.1
通讯作者：
Catterall, WA
中科院分区：
文献类型：
--
作者：
Mochida, S;Westenbroek, RE;Catterall, WA
在细胞培养的上级颈神经节神经元中表达传导P/Q型Ca 2+电流的Ca（v）2.1通道，并测量由这些外源性表达的Ca 2+通道启动的神经传递。缺失的突触蛋白相互作用（synprint）网站之间的结构域II和III的Ca（v）2.1通道的细胞内环降低其在突触传递的有效性。令人惊讶的是，这种效果与外源表达通道的突触前定位丢失相关。传导L型Ca 2+电流的Ca（v）1.2通道在支持突触传递方面是无效的，但是将Ca（v）2.1通道的突触印记位点替换到Ca（v）1.2中足以建立由L型Ca 2+电流通过外源性Ca（v）1.2通道启动的突触传递。从传导N型Ca 2+电流的Ca（v）2.2通道中替换synprint位点甚至比Ca（v）2.1更有效。我们的研究结果表明，本地化和功能的外源性Ca 2+通道的神经末梢的上级颈神经节神经元需要一个功能的synprint网站，并建议，结合可溶性NSF附着蛋白受体（SNARE）蛋白的synprint网站是一个必要的许可事件的神经末梢本地化突触前Ca 2+通道。
Ca(v)2.1 channels, which conduct P/Q-type Ca2+ currents, were expressed in superior cervical ganglion neurons in cell culture, and neurotransmission initiated by these exogenously expressed Ca2+ channels was measured. Deletions in the synaptic protein interaction (synprint) site in the intracellular loop between domains II and III of Ca(v)2.1 channels reduced their effectiveness in synaptic transmission. Surprisingly, this effect was correlated with loss of presynaptic localization of the exogenously expressed channels. Ca(v)1.2 channels, which conduct L-type Ca2+ currents, are ineffective in supporting synaptic transmission, but substitution of the synprint site from Ca(v)2.1 channels in Ca(v)1.2 was sufficient to establish synaptic transmission initiated by L-type Ca2+ currents through the exogenous Ca(v)1.2 channels. Substitution of the synprint site from Ca(v)2.2 channels, which conduct N-type Ca2+ currents, was even more effective than Ca(v)2.1. Our results show that localization and function of exogenous Ca2+ channels in nerve terminals of superior cervical ganglion neurons require a functional synprint site and suggest that binding of soluble NSF attachment protein receptor (SNARE) proteins to the synprint site is a necessary permissive event for nerve terminal localization of presynaptic Ca2+ channels.