刺激来自脉冲标记的小鼠垂体中间叶组织的标记蛋白的钙依赖性释放。

Stimulation of calcium-dependent release of labelled protein from pulse-labelled mouse pituitary intermediate lobe tissue.

作者信息

Thornton V F

出版信息

J Physiol. 1982 Aug;329:425-37. doi: 10.1113/jphysiol.1982.sp014311.

DOI:10.1113/jphysiol.1982.sp014311

PMID:7143255

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1224788/

Abstract

The effect of K depolarization on the release of labelled protein from pulse-labelled intermediate lobe tissue of mouse pituitaries has been studied.2. Depolarization briefly stimulated Ca-dependent release of labelled protein. Co (2.5 mM) and verapamil (0.08 mM) reversibly blocked stimulation. Efflux of (45)Ca was also briefly stimulated by depolarization, but not in the presence of Co or verapamil, nor in the absence of Ca.3. The response to maintained depolarization quickly inactivated. Inactivation probably resulted from Ca-channel inactivation rather than exhaustion of available labelled protein, since responses different in magnitude but of constant time course could be obtained by depolarization in different concentrations of Ca. In addition, much more labelled protein could be released by exposure to Ba.4. Depolarization did not cause a response if the Ca concentration was 0.4 mM or less; neither did inactivation occur in these conditions, and a response occurred as soon as the Ca concentration was raised. Two separate responses could be generated by a stepwise increase in the Ca concentration during maintained depolarization. The magnitude of the two responses together was similar to the magnitude of one response at the higher Ca concentration.5. Recovery from inactivation was complete after about 20 min in normal K. However, recovery also occurred during maintained depolarization provided the Ca concentration was reduced sufficiently. Recovery was complete at 0.4 mM-Ca or less, and at higher concentrations the extent of recovery depended on the Ca concentration selected.6. It is concluded that depolarization opened potential-dependent Ca channels permitting Ca entry and causing the release of labelled products. The response was brief probably because the Ca channels were inactivated. Since the channels were not inactivated by depolarization in low Ca, inactivation may result from Ca entry.

摘要

研究了钾离子去极化对脉冲标记的小鼠垂体中间叶组织中标记蛋白释放的影响。
去极化短暂刺激了标记蛋白的钙依赖性释放。钴（2.5 mM）和维拉帕米（0.08 mM）可逆转性阻断这种刺激。去极化也短暂刺激了（45）钙的外流，但在有钴或维拉帕米存在时以及无钙时则不发生。
对持续去极化的反应很快失活。失活可能是由于钙通道失活而非可用标记蛋白的耗尽，因为通过在不同钙浓度下去极化可获得幅度不同但时间进程恒定的反应。此外，暴露于钡可释放更多的标记蛋白。
如果钙浓度为0.4 mM或更低，去极化不会引起反应；在这些条件下也不会发生失活，并且一旦钙浓度升高就会出现反应。在持续去极化期间逐步增加钙浓度可产生两个单独的反应。两个反应的幅度之和与较高钙浓度下一个反应的幅度相似。
在正常钾浓度下约20分钟后失活恢复完全。然而，只要钙浓度充分降低，在持续去极化期间也会发生恢复。在0.4 mM - 钙或更低时恢复完全，在较高浓度下恢复程度取决于所选的钙浓度。
结论是去极化打开了电压依赖性钙通道，允许钙进入并导致标记产物的释放。反应短暂可能是因为钙通道失活。由于在低钙条件下去极化不会使通道失活，失活可能是由于钙进入所致。