SODIUM-DEPENDENT SECRETION AND RETENTION OF NE IN ADRENERGIC TERMINALS

以下报告代表了对功能、 生理神经分泌系统。钠可以调节一种延迟的， 钙诱导、出口介导的去甲肾上腺素([~3H]NE)分泌 大鼠心脏切片的肾上腺素能终末。分泌物是 被解释为钙通过特定途径渗透的指示 轴膜中的通道。通过其他渠道的渗透没有 必然会引起分泌物。分泌发生在一种培养液(CH-Ca)中 哪种胆碱(不是Li、K或蔗糖)取代了 Krebs-碳酸氢盐介质。胆碱以一种有限的方式发挥作用 作为细胞外保留物的钠的替代品。就像那 (Bogdanski和Brodie，1969)胆碱(25和50 mM)在蔗糖介质中 抑制非钙依赖性去甲肾上腺素的耗竭。胆碱 在CH-Ca中，延迟60-80分钟后，允许Ca被唤醒 分泌物。它的开始与时间段的长度有关， 这些终端暴露在胆碱中，而不是钙。因为分泌物是 用Mn，1 mm预防，得出的结论是电压调节的情况 频道可能终于开通了。分泌停止得更快。 在CH-Ca中加入Na之后，比末端转移之后 是一种缺钙的介质。因此，NA似乎在细胞内起作用。K (66 MM)增加CH-Ca诱发的最大分泌率 不加钠。显然，CH-Ca的轴膜已经极化。 钾去极化可打开新的钙通道。结论：NA为两 或更多的位置在轴膜或靠近轴膜可能部分调节 生理分泌物。首先，胆碱代表生理性钠 暂时阻止自发性钙通过特定于 分泌物。这不涉及钠-钙交换。第二，娜娜在 Axosol抑制分泌。任何一种功能的故障都可能导致 生理上过度的，自发释放的递质。

The following report represents continued research on a functional, physiologic neurosecretory system. Sodium can regulate a delayed, Ca-evoked, export-mediated secretion of [3H]norepinephrine ([3H]NE) in the adrenergic terminals in slices of rat heart. The secretion was interpreted to be an indication of Ca permeation through specific channels in the axolemma. Permeation through other channels did not necessarily evoke secretion. Secretion occurred in a medium (Ch-Ca) in which choline (not Li, K or sucrose) replaced the Na in a Krebs-bicarbonate medium. Choline in a limited way functioned a surrogate for Na as an extracellular requirement for retention. Like Na (Bogdanski and Brodie, 1969) choline (25 and 50 mM) in a sucrose medium inhibited the non-Ca dependent depletion of the [3H]NE. The choline (13OmM) in Ch-Ca, after a delay of 60 to 80 min, permitted Ca to evoke secretion. Its start was related to the length of the time period that the terminals had been exposed to choline, not Ca. Because secretion was prevented by Mn, lmM, it was concluded that a voltage regulated Ca channel might finally have opened. Secretion was stopped more rapidly after Na was added to the Ch-Ca than after the terminals were transferred to a Ca-deprived medium. Na thus appeared to act intracellularly. K (66mM) augmented maximal rates of secretion evoked by Ch-Ca with or without added Na. Apparently, the axolemma in Ch-Ca had been polarized and depolarization by K opened new Ca channels. Conclusions: Na at two or more sites in or proximate to the axolemma may partially regulate physiological secretion. First, choline representing physiological Na temporarily prevented spontaneous Ca entry through channels specific for secretion. This did not involve Na-Ca exchange. Second, Na in the axosol inhibited secretion. Malfunctions of either function could induce physiologically excessive, spontaneous release of transmitters.