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1
Inositol 1,4,5-trisphosphate-gated calcium transport through plasma membranes in nerve terminals.神经末梢中通过质膜的肌醇1,4,5 -三磷酸门控钙转运。
J Neurosci. 1996 May 1;16(9):2891-900. doi: 10.1523/JNEUROSCI.16-09-02891.1996.
2
Inositol 1,4,5-trisphosphate activates Ca2+ channels in the plasma membranes of rat brain nerve terminals.
Adv Exp Med Biol. 1991;287:97-110. doi: 10.1007/978-1-4684-5907-4_9.
3
Quantal calcium release by purified reconstituted inositol 1,4,5-trisphosphate receptors.纯化重组的肌醇1,4,5-三磷酸受体引发的量子钙释放
Nature. 1992 Mar 26;356(6367):350-2. doi: 10.1038/356350a0.
4
Flash photolysis of caged inositol 1,4,5-trisphosphate activates plasma membrane calcium current in human T cells.笼化肌醇1,4,5-三磷酸的闪光光解激活人T细胞中的质膜钙电流。
J Biol Chem. 1993 Feb 25;268(6):3889-96.
5
Fast activation and inactivation of inositol trisphosphate-evoked Ca2+ release in rat cerebellar Purkinje neurones.大鼠小脑浦肯野神经元中肌醇三磷酸诱发的Ca2+释放的快速激活和失活
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Rapid filtration studies of the effect of cytosolic Ca2+ on inositol 1,4,5-trisphosphate-induced 45Ca2+ release from cerebellar microsomes.关于胞质Ca2+对小脑微粒体中肌醇1,4,5-三磷酸诱导的45Ca2+释放影响的快速过滤研究。
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7
Caffeine-induced inhibition of inositol(1,4,5)-trisphosphate-gated calcium channels from cerebellum.咖啡因对小脑肌醇（1,4,5）-三磷酸门控钙通道的抑制作用。
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Modulation of the kinetics of inositol 1,4,5-trisphosphate-induced [Ca2+]i oscillations by calcium entry in pituitary gonadotrophs.垂体促性腺细胞中钙内流对肌醇1,4,5 -三磷酸诱导的[Ca2+]i振荡动力学的调节
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Quantal responses to inositol 1,4,5-trisphosphate are not a consequence of Ca2+ regulation of inositol 1,4,5-trisphosphate receptors.对肌醇1,4,5-三磷酸的量子反应并非由钙离子对肌醇1,4,5-三磷酸受体的调节所致。
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Receptor-activated Ca2+ influx: how many mechanisms for how many channels?受体激活的钙离子内流：多少种机制对应多少种通道？
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The separation of synaptic vesicles from nerve-ending particles ('synaptosomes').突触小泡与神经末梢颗粒（“突触体”）的分离。
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神经末梢中通过质膜的肌醇1,4,5 -三磷酸门控钙转运。

Inositol 1,4,5-trisphosphate-gated calcium transport through plasma membranes in nerve terminals.

作者信息

Ueda H, Tamura S, Fukushima N, Katada T, Ui M, Satoh M

机构信息

Department of Pharmacology, Yokohama City University School of Medicine, Japan.

出版信息

J Neurosci. 1996 May 1;16(9):2891-900. doi: 10.1523/JNEUROSCI.16-09-02891.1996.

DOI:10.1523/JNEUROSCI.16-09-02891.1996
PMID:8622120
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6579068/
Abstract

We developed new biochemical approaches to demonstrate the presence of inositol 1,4,5-triphosphate (InsP3)-gated calcium channels in presynaptic plasma membranes (SPM) and their involvement in the presynaptic receptor-mediated Ca2+ influx into nerve terminals. In perfusion experiments using SPM vesicles preloaded with 45Ca2+, InsP3 elicited the release of 45CA2+ into perfusates in a saturable manner. The InsP3- evoked 45Ca2+ release from resealed SPM vesicles was more potent than that from resealed vesicles using any other subcellular fractions. Here we also report the involvement of InsP3-gated mechanisms in the presynaptic receptor-mediated Ca2+ influx into synaptosomes (nerve terminals) by use of such resealed vesicles reconstituted with purified Gi1.

摘要

我们开发了新的生化方法，以证明突触前质膜（SPM）中存在肌醇1,4,5-三磷酸（InsP3）门控钙通道，以及它们参与突触前受体介导的Ca2+流入神经末梢的过程。在使用预加载45Ca2+的SPM囊泡进行的灌注实验中，InsP3以饱和方式促使45Ca2+释放到灌注液中。与使用任何其他亚细胞组分的重封囊泡相比，InsP3从重封的SPM囊泡诱发的45Ca2+释放更有效。在此，我们还报告了通过使用用纯化的Gi1重组的此类重封囊泡，InsP3门控机制参与突触前受体介导的Ca2+流入突触小体（神经末梢）的过程。