Deficiency in parvalbumin, but not in calbindin D-28K upregulates mitochondrial volume and decreases smooth endoplasmic reticulum surface selectively in a peripheral, subplasmalemmal region in the soma of Purkinje cells
Deficiency in parvalbumin, but not in calbindin D-28K upregulates mitochondrial volume and decreases smooth endoplasmic reticulum surface selectively in a peripheral, subplasmalemmal region in the soma of Purkinje cells
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DOI：
10.1016/j.neuroscience.2006.06.008
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发表时间：
2006-09-29
期刊：
影响因子：
3.3
通讯作者：
Schwaller, B.
中科院分区：
文献类型：
--
作者：
Chen, G.;Racay, P.;Schwaller, B.
Ca2+ 结合蛋白小清蛋白 (PV) 和钙结合蛋白 D-28k (CB) 是包括神经元在内的特定细胞中细胞内 Ca2+ 缓冲的关键参与者，并对 Ca2+ 瞬变的时空方面具有深远影响。先前观察到的 PV-/- 小鼠快肌中线粒体体积密度的增加被视为维持 Ca2+ 稳态的特定补偿机制。由于小脑浦肯野细胞 (PC) 的特点是 Ca2+ 缓冲液 PV 和 CB 的高表达水平，因此提出了一个问题：在缺乏这些缓冲液的 PC 中是否会诱导稳态机制。 PV-/- PC 体细胞中的线粒体体积密度，即相对线粒体质量增加了 40%。线粒体体积密度的上调在整个体细胞中并不均匀，而是选择性地限制在质膜下方1.5μm宽度的外围区域。伴随而来的是质膜下 0.5 μm 厚的壳中质膜下光滑内质网 (sPL-sER) 表面的减少。这些改变是由于缺乏“缓慢发生”缓冲液PV而特异的，因为在CB-/-小鼠中，没有观察到外周线粒体和sPL-sER的变化。这意味着形态改变的目的是专门替代慢速缓冲 PV 的功能。我们提出了一个新概念，即参与 Ca2+ 稳态的成分的稳态机制并不总是发生在相似或密切相关的分子水平上。相反，细胞试图通过巧妙地微调参与 Ca2+ 通量调节的现有组件来恢复未受干扰（野生型）情况下盛行的 Ca2+ 信号的时空方面。 (c) 2006 年国际广播组织。由爱思唯尔有限公司出版。保留所有权利。
The Ca2+-binding proteins parvalbumin (PV) and calbindin D-28k (CB) are key players in the intracellular Ca2+-buffering in specific cells including neurons and have profound effects on spatiotemporal aspects of Ca2+ transients. The previously observed increase in mitochondrial volume density in fast-twitch muscle of PV-/- mice is viewed as a specific compensation mechanism to maintain Ca2+ homeostasis. Since cerebellar Purkinje cells (PC) are characterized by high expression levels of the Ca2+ buffers PV and CB, the question was raised, whether homeostatic mechanisms are induced in PC lacking these buffers. Mitochondrial volume density, i.e. relative mitochondrial mass was increased by 40% in the soma of PV-/- PC. Upregulation of mitochondrial volume density was not homogenous throughout the soma, but was selectively restricted to a peripheral region of 1.5 mu m width underneath the plasma membrane. Accompanied was a decreased surface of subplasmalemmal smooth endoplasmic reticulum (sPL-sER) in a shell of 0.5 mu m thickness underneath the plasma membrane. These alterations were specific for the absence of the "slow-onset" buffer PV, since in CB-/- mice neither changes in peripheral mitochondria nor in sPL-sER were observed. This implicates that the morphological alterations are aimed to specifically substitute the function of the slow buffer PV. We propose a novel concept that homeostatic mechanisms of components involved in Ca2+ homeostasis do not always occur at the level of similar or closely related molecules. Rather the cell attempts to restore spatiotemporal aspects of Ca2+ signals prevailing in the undisturbed (wildtype) situation by subtly fine tuning existing components involved in the regulation of Ca2+ fluxes. (c) 2006 IBRO. Published by Elsevier Ltd. All rights reserved.