通过N型Ca2+通道的突触蛋白相互作用位点介导的神经递质释放的电压依赖性增强的证据。
Evidence for a voltage-dependent enhancement of neurotransmitter release mediated via the synaptic protein interaction site of N-type Ca2+ channels.
作者信息
Mochida S, Yokoyama C T, Kim D K, Itoh K, Catterall W A
机构信息
Department of Physiology, Tokyo Medical College, Tokyo 160, Japan.
出版信息
Proc Natl Acad Sci U S A. 1998 Nov 24;95(24):14523-8. doi: 10.1073/pnas.95.24.14523.
Abstract
Secretion of neurotransmitters is initiated by voltage-gated calcium influx through presynaptic, voltage-gated N-type calcium channels. These channels interact with the SNARE proteins, which are core components of the exocytosis process, via the synaptic protein interaction (synprint) site in the intracellular loop connecting domains II and III of their alpha1B subunit. Interruption of this interaction by competing synprint peptides inhibits fast, synchronous transmitter release. Here we identify a voltage-dependent, but calcium-independent, enhancement of transmitter release that is elicited by trains of action potentials in the presence of a hyperosmotic extracellular concentration of sucrose. This enhancement of transmitter release requires interaction of SNARE proteins with the synprint site. Our results provide evidence for a voltage-dependent signal that is transmitted by protein-protein interactions from the N-type calcium channel to the SNARE proteins and enhances neurotransmitter release by altering SNARE protein function.
摘要
神经递质的分泌是由电压门控钙通过突触前电压门控N型钙通道内流引发的。这些通道通过其α1B亚基连接结构域II和III的细胞内环中的突触蛋白相互作用（synprint）位点，与作为胞吐过程核心成分的SNARE蛋白相互作用。通过竞争性synprint肽中断这种相互作用会抑制快速、同步的递质释放。在这里，我们发现了一种在高渗细胞外蔗糖浓度存在时由动作电位串引发的递质释放的电压依赖性但钙非依赖性增强。这种递质释放的增强需要SNARE蛋白与synprint位点相互作用。我们的结果为一种电压依赖性信号提供了证据，该信号通过蛋白质-蛋白质相互作用从N型钙通道传递到SNARE蛋白，并通过改变SNARE蛋白功能来增强神经递质释放。
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Evidence for a voltage-dependent enhancement of neurotransmitter release mediated via the synaptic protein interaction site of N-type Ca2+ channels.通过N型Ca2+通道的突触蛋白相互作用位点介导的神经递质释放的电压依赖性增强的证据。
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