Characterization of transmitter release as a response of vertebrate neural tissue to erythrosin B.
Characterization of transmitter release as a response of vertebrate neural tissue to erythrosin B.
复制标题
脊椎动物神经组织对赤藓红 B 的反应，递质释放的表征。
DOI：
10.1016/0006-8993(84)90432-3
复制
发表时间：
1984
期刊：
影响因子：
2.9
通讯作者：
Siekevitz,P
中科院分区：
文献类型：
--
作者：
Wade,PD;Marder,E;Siekevitz,P
大鼠大脑皮层切片制备用于研究发射的响应释放的食品染料，赤藓红B，荧光素的四碘化衍生物的应用。赤藓红B（100 μM）刺激先前摄取的[3 H]去甲肾上腺素和[3 H]γ-氨基丁酸（GABA）的净释放。赤藓红诱导释放的GABA（唯一的递质研究）发生在没有添加的Ca 2+，并在河豚毒素（TTX）的存在下。用赤藓红B处理的蛙神经肌肉接头的囊泡内容物的超微结构分析显示，神经末梢中存在的突触囊泡的数量减少。通过使用荧光素和包括赤藓红B的一些卤素取代的衍生物，发现与未卤化的化合物孵育不引起净释放，而与碘、氯或溴取代的化合物孵育确实引起释放。结果发现，在光照条件下，赤藓红B（100 μM）诱导的释放量略高于黑暗条件。在该制剂中证实了赤藓红B抑制Na+、K+、Mg 2 +-ATP酶;在光照和黑暗下都是如此。在黑暗中的释放和Na+，K+，Mg 2 +-ATP酶阻断之间的差异表明，释放发生的一些其他机制，而不是通过Na+，K+，Mg 2 +-ATP酶阻断，或一个额外的光依赖性过程有助于释放。我们的结论是，赤藓红B可以推测诱导净释放的递质一般，释放不发生通过TTX敏感的Na+通道，通过囊泡释放确实发生，光有点增强释放。
A rat cerebral cortical slice preparation was used to study the response of transmitter release to the application of the food dye, Erythrosin B, a tetraiodinated derivative of fluorescein. Erythrosin B (100 μM) stimulated net release of previously taken up [3H]norepinephrine and [3H]γ-aminobutyric acid (GABA). The Erythrosin-induced release of GABA (the only transmitter studied) occured in the absence of added Ca2+, and in the presence of tetrodotoxin (TTX). Ultrastructural analysis of the vesicle content of frog neuromuscular junctions treated with Erythrosin B revealed a diminution in the number of synaptic vesicles present in the nerve terminal. By using fluorescein and some halogen-substituted derivatives including Erythrosin B, it was found that incubation with the unhalogenated compound caused no net release, whereas incubation with the iodine-, chlorine- or bromine-substituted compound did cause release. It was found that somewhat greater release induced by Erythrosin B (at 100 μM) occurred in the light than in the dark. That Erythrosin B inhibits the Na+, K+, Mg2+-ATPase was confirmed in this preparation; it did so in both light and dark. The discrepancy between release and Na+, K+, Mg2+-ATPase blockade in the dark suggests that release either occurs by some other mechanism than by Na+, K+, Mg2+-ATPase blockade, or that an additional light-dependent process contributes to the release. We conclude that Erythrosin B can presumably induce net release of transmitters generally, that release does not occur via the TTX-sensitive Na+channel, that release via vesicles does occur, and that light somewhat enhances the release.