Protection of dentate hilar cells from prolonged stimulation by intracellular calcium chelation.
Protection of dentate hilar cells from prolonged stimulation by intracellular calcium chelation.
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通过细胞内钙螯合保护齿状门细胞免受长期刺激。
DOI：
10.1126/science.2508225
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发表时间：
1989
期刊：
影响因子：
--
通讯作者：
Schwartzkroin,PA
中科院分区：
文献类型：
--
作者：
Scharfman,HE;Schwartzkroin,PA
体内大鼠齿状回的长期传入刺激仅导致那些缺乏钙结合蛋白小白蛋白和钙结合蛋白免疫反应性的细胞变性。为了检验钙结合蛋白可以防止长时间刺激的影响的假设，在缺乏钙结合蛋白免疫反应性的细胞的海马切片中进行了细胞内记录。钙结合蛋白阴性细胞在长时间刺激下表现出电生理恶化迹象；含有钙结合蛋白的细胞则不然。当没有钙结合蛋白的神经元被含有钙螯合剂 BAPTA 的微电极刺穿，并且允许 BAPTA 扩散到细胞中时，这些细胞没有表现出恶化。这些结果表明，在中枢神经系统的复杂组织中，活动引起的细胞内钙的增加可以触发导致细胞恶化的过程，并且增加细胞的钙结合能力可以降低其对损伤的脆弱性。
Prolonged afferent stimulation of the rat dentate gyrus in vivo leads to degeneration only of those cells that lack immunoreactivity for the calcium binding proteins parvalbumin and calbindin. In order to test the hypothesis that calcium binding proteins protect against the effects of prolonged stimulation, intracellular recordings were made in hippocampal slices from cells that lack immunoreactivity for calcium binding proteins. Calcium binding protein-negative cells showed electrophysiological signs of deterioration during prolonged stimulation; cells containing calcium binding protein did not. When neurons without calcium binding proteins were impaled with microelectrodes containing the calcium chelator BAPTA, and BAPTA was allowed to diffuse into the cells, these cells showed no deterioration. These results indicate that, in a complex tissue of the central nervous system, an activity-induced increase in intracellular calcium can trigger processes leading to cell deterioration, and that increasing the calcium binding capacity of a cell decreases its vulnerability to damage.
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