Gonadotropin-releasing hormone-induced Ca2+ transients in single identified gonadotropes require both intracellular Ca2+ mobilization and Ca2+ influx.
Gonadotropin-releasing hormone-induced Ca2+ transients in single identified gonadotropes require both intracellular Ca2+ mobilization and Ca2+ influx.
复制标题
在单一确定的促性腺激素中，促性腺激素释放激素诱导的 Ca2 瞬变需要细胞内 Ca2 动员和 Ca22 流入。
DOI：
10.1073/pnas.85.17.6566
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发表时间：
1988
影响因子：
11.1
通讯作者：
Miller,RJ
中科院分区：
文献类型：
--
作者：
Shangold,GA;Murphy,SN;Miller,RJ
我们研究了促性腺激素释放激素（GnRH）对单个大鼠垂体前叶促性腺激素细胞内游离Ca 2+浓度（[Ca 2 +]i）的影响，通过反向溶血空斑试验鉴定。浓度大于10 pM的GnRH引起的[Ca 2 +]i的增加，在确定的细胞，但不是在其他人。相反，50 mM K+诱导的去极化增加了所有细胞中的[Ca 2 +]i。GnRH诱导的Ca2+瞬变具有复杂的时程。在最初的快速上升后，[Ca2+]i下降到接近基础水平，然后是第二次延长上升和下降。快速时基上的Ca2+瞬变分析显示，响应通常由[Ca2+]i的几个快速振荡组成。去除细胞外Ca 2+或添加二氢吡啶类Ca 2+通道阻滞剂尼群地平完全阻断了[Ca 2 +]i的二次升高，但对初始尖峰没有任何影响。尼群地平也阻断50 mM K+诱导的[Ca2+]i增加，在确定的促性腺激素。促性腺激素释放激素诱导的二次上升可以增强佛波酯在尼群地平敏感的方式。只有当随后的Ca2+内流通过允许二次上升发生或通过用50 mM K+使细胞去极化产生Ca2+瞬变而被允许时，才能获得对同一细胞的GnRH刺激的多个尖峰响应。因此，对GnRH的反应似乎包括可能由三磷酸肌醇介导的Ca 2+动员的初始阶段和可能由蛋白激酶C激活的尼群地平敏感性Ca 2+通道的Ca 2+内流的后续阶段。这些阶段在控制促性腺激素分泌的相对作用进行了讨论。
We examined the effects of gonadotropin-releasing hormone (GnRH) on the intracellular free Ca2+ concentration ([Ca2+]i) in single rat anterior pituitary gonadotropes identified by a reverse hemolytic plaque assay. Concentrations of GnRH greater than 10 pM elicited increases in [Ca2+]i in identified cells but not in others. In contrast, depolarization induced by 50 mM K+ increased [Ca2+]i in all cells. Ca2+ transients induced by GnRH exhibited a complex time course. After an initial rapid rise, the [Ca2+]i fell to near basal levels only to be followed by a secondary extended rise and fall. Analysis of the Ca2+ transients on a rapid time base revealed that responses frequently consisted of several rapid oscillations in [Ca2+]i. Removal of extracellular Ca2+ or addition of the dihydropyridine Ca2+-channel blocker nitrendipine completely blocked the secondary rise in [Ca2+]i but had no effect whatsoever on the initial spike. Nitrendipine also blocked 50 mM K+-induced increases in [Ca2+]i in identified gonadotropes. The secondary rise induced by GnRH could be enhanced by a phorbol ester in a nitrendipine-sensitive fashion. Multiple spike responses to GnRH stimulation of the same cell could only be obtained if subsequent Ca2+ influx was permitted either by allowing a secondary rise to occur or by producing a Ca2+ transient by depolarizing the cells with 50 mM K+. It therefore appears that the response to GnRH consists of an initial phase of Ca2+ mobilization, probably mediated by inositol trisphosphate, and a subsequent phase of Ca2+ influx through nitrendipine-sensitive Ca2+ channels that may be activated by protein kinase C. The relative roles of these phases in the control of gonadotropin secretion are discussed.