钙离子对突触体组分中γ-氨基丁酸释放的影响。
Effect of calcium ion on the release of gamma-aminobutyric acid from synaptosomal fraction.
作者信息
Asakura T, Hoshino M, Kobayashi T
出版信息
J Biochem. 1982 Dec;92(6):1919-23. doi: 10.1093/oxfordjournals.jbchem.a134122.
Abstract
Brain synaptosomes released endogenous gamma-aminobutyric acid (GABA) in response to Ca2+. The release of GABA in response to 2.5 mM Ca2+ increased linearly with log[K+]0, showing that a membrane potential-dependent Ca2+ channel limits the GABA release. In the presence of Ca2+ ionophore, A23187, GABA release increased linearly with log[Ca2+]0 without altering the membrane potential of synaptosomes.
摘要
脑突触体在钙离子作用下释放内源性γ-氨基丁酸（GABA）。在2.5 mM钙离子存在时，GABA的释放量随细胞外液钾离子浓度的对数线性增加，表明膜电位依赖性钙通道限制了GABA的释放。在钙离子载体A23187存在的情况下，GABA的释放量随细胞外液钙离子浓度的对数线性增加，而不改变突触体的膜电位。
Zotero 插件