Release of [3H]serotonin and its binding protein from enteric neurons
Release of [3H]serotonin and its binding protein from enteric neurons
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肠神经元释放[3H]血清素及其结合蛋白
DOI：
10.1016/0006-8993(79)90803-5
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发表时间：
1979
期刊：
影响因子：
2.9
通讯作者：
M. Gershon
中科院分区：
文献类型：
--
作者：
G. Jonakait;H. Tamir;A. Gintzler;M. Gershon
分析了豚鼠肠神经系统释放[3 H]5-HT及其结合蛋白SBP的情况。释放[3 H]5-HT和[3 H]NE从纵向肌条与粘附肌间神经丛预装各自的放射性胺诱发高K+和离子载体X537 A。然而，两种药物的[3 H]5-HT释放或X537 A的[3 H]NE释放均未显示Ca 2+依赖性。然而，Ca 2+依赖性（以及高Mg 2+和河豚毒素对释放的抑制）可以被证明为释放由电场刺激通过灌流[3 H]5-HT通过Serenum腔预载的外翻回肠段诱发的放射活性。光镜和电子显微镜放射自显影显示，释放的放射性的来源是轴突，特别是轴突静脉曲张含有小的透明和大的致密核心囊泡的混合物。收缩压，但不是胞质标志蛋白，乳酸脱氢酶，自发释放灌注外翻回肠。10 Hz电场刺激引起SBP（而非LDH）释放的显著增加，且这种增加的释放（而非自发释放）是Ca ~（2+）依赖性的。它的结论是SBP和5-HT可能存储在一起，至少部分在囊泡，并且都可以从去极化轴突末梢的胞吐释放。
The release of [3H]5-HT and its binding protein, SBP, from the guinea pig enteric nervous system was analyzed. Release of both [3H]5-HT and [3H]NE from strips of longitudinal muscle with adherent myenteric plexus preloaded with the respective radioactive amine was evoked by high K+and the ionophore X537A. However, Ca2+-dependence could not be shown for [3H]5-HT release by either agent or for [3H]NE release by X537A. However, Ca2+-dependence (as well as inhibition of release by high Mg2+and tetrodotoxin) could be demonstrated for the release of radio-activity evoked by electrical field stimulation of everted segments of ileum preloaded by perfusion through the serosal lumen with [3H]5-HT. Light and electron microscopic radioautography revealed that the sources of released radioactivity were axons, especially axonal varicosities containing a mixture of small clear and large dense-cored vesicles. SBP, but not the cytosol marker protein, lactic dehydrogenase, was spontaneously released from the perfused everted ileum. A marked increase in SBP (but not LDH) release was provoked by electrical field stimulation at 10 Hz, and thid increased release (but not the spontaneous release) was Ca2+-dependent. It is concluded that SBP and 5-HT are probably stored together, at least in part in vesicles, and that both can be released by exocytosis from depolarized axon terminals.