University of Occupational and Environmental Health School of Medicine, Kitakyushu 807-8555, Japan.
Cell Calcium. 2010 Dec;48(6):324-32. doi: 10.1016/j.ceca.2010.10.002. Epub 2010 Nov 2.
Multiple mechanisms that maintain Ca(2+) homeostasis and provide for Ca(2+) signalling operate in the somatas and neurohypophysial nerve terminals of supraoptic nucleus (SON) neurones. Here, we examined the Ca(2+) clearance mechanisms of SON neurones from adult rats by monitoring the effects of the selective inhibition of different Ca(2+) homeostatic molecules on cytosolic Ca(2+) (Ca(2+)) transients in isolated SON neurones. In addition, we measured somatodendritic vasopressin (AVP) release from intact SON tissue in an attempt to correlate it with Ca(2+) dynamics. When bathing the cells in a Na(+)-free extracellular solution, thapsigargin, cyclopiazonic acid (CPA), carbonyl cyanide 3-chlorophenylhydrazone (CCCP), and the inhibitor of plasma membrane Ca(2+)-ATPase (PMCA), La(3+), all significantly slowed down the recovery of depolarisation (50 mM KCl)-induced Ca(2+) transients. The release of AVP was stimulated by 50 mM KCl, and the decline in the peptide release was slowed by Ca(2+) transport inhibitors. In contrast to previous reports, our results show that in the fully mature adult rats: (i) all four Ca(2+) homeostatic pathways, the Na(+)/Ca(2+) exchanger, the endoplasmic reticulum Ca(2+) pump, the plasmalemmal Ca(2+) pump and mitochondria, are complementary in actively clearing Ca(2+) from SON neurones; (ii) somatodendritic AVP release closely correlates with intracellular Ca(2+) dynamics; (iii) there is (are) Ca(2+) clearance mechanism(s) distinct from the four outlined above; and (iv) Ca(2+) homeostatic systems in the somatas of SON neurones differ from those expressed in their terminals.
多种维持 Ca(2+) 稳态和提供 Ca(2+) 信号的机制在视上核 (SON) 神经元的体和神经垂体神经末梢中发挥作用。在这里,我们通过监测选择性抑制不同 Ca(2+) 稳态分子对分离的 SON 神经元胞质 Ca(2+) (Ca(2+)) 瞬变的影响,研究了成年大鼠 SON 神经元的 Ca(2+) 清除机制。此外,我们测量了完整 SON 组织中的体树突血管加压素 (AVP) 释放,试图将其与 Ca(2+) 动力学相关联。当将细胞置于无 Na(+) 的细胞外液中时,他莫昔芬、环匹阿尼酸 (CPA)、羰基氰化物 3-氯苯腙 (CCCP) 和质膜 Ca(2+) -ATP 酶 (PMCA) 的抑制剂 La(3+) 均显著减缓去极化 (50 mM KCl) 诱导的 Ca(2+) 瞬变的恢复。AVP 的释放被 50 mM KCl 刺激,肽释放的减少被 Ca(2+) 转运抑制剂减缓。与之前的报告相反,我们的结果表明,在完全成熟的成年大鼠中:(i) 四种 Ca(2+) 稳态途径、Na(+) / Ca(2+) 交换体、内质网 Ca(2+) 泵、质膜 Ca(2+) 泵和线粒体,在从 SON 神经元中主动清除 Ca(2+) 方面是互补的;(ii) 体树突 AVP 释放与细胞内 Ca(2+) 动力学密切相关;(iii) 存在不同于上述四种的 Ca(2+) 清除机制;(iv) SON 神经元体中的 Ca(2+) 稳态系统与它们的末梢中表达的系统不同。