Rapid chelation of calcium entering isolated rat brain nerve terminals during stimulation inhibits neurotransmitter release.
Rapid chelation of calcium entering isolated rat brain nerve terminals during stimulation inhibits neurotransmitter release.
复制标题
在刺激过程中，钙快速螯合进入离体大鼠脑神经末梢，抑制神经递质释放。
DOI：
10.1016/0304-3940(96)12728-2
复制
发表时间：
1996
影响因子：
2.5
通讯作者：
Suplick,GR
中科院分区：
文献类型：
--
作者：
Nichols,RA;Suplick,GR
研究了钙螯合剂对离体大鼠脑神经末梢（突触体）释放神经递质谷氨酸的细胞内作用。用快速钙结合螯合剂 1,2-双(2-氨基苯氧基)乙烷-N,N,N',N'-四乙酸 (BAPTA) 预载突触体，导致 K+ 刺激的谷氨酸释放量减少至对照的近一半，而用钙螯合剂 EGTA 预载，其作用不如 BAPTA 快， 没有效果。在用二溴-BAPTA 预载突触体时也观察到了谷氨酸释放的抑制，但用二硝基-BAPTA 则没有。预加载 BAPTA 后，K+ 刺激的 Ca2+ 依赖性突触体蛋白磷酸化不受影响。结果表明，触发哺乳动物脑神经末梢分泌反应所必需的钙依赖性细胞内成分位于钙通道附近，结合；在刺激过程中钙迅速进入。
The intracellular actions of calcium chelators on the release of the neurotransmitter glutamate from isolated rat brain nerve terminals (synaptosomes) were examined. Preloading synaptosomes with the rapid calcium-binding chelator 1,2-bis(2-aminophenoxy)ethane-N,N,N′,N′- tetraacetic acid (BAPTA) resulted in a decrease in K+-stimulated glutamate release to nearly half that of controls, whereas preloading with the calcium chelator EGTA, whose action is less rapid than that of BAPTA, was without effect. Inhibition of glutamate release was also observed on preloading synaptosomes with dibromo-BAPTA, but not with dinitro-BAPTA. K+-stimulated, Ca2+-dependent synaptosomal protein phosphorylation was not affected after preloading with BAPTA. The results suggest that the calcium-dependent intracellular component essential for triggering the secretory response in mammalian brain nerve terminals resides near the calcium channels, binding; calcium rapidly on its entry during stimulation.