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短暂性窒息后培养神经元的功能变化。

Functional changes in cultured neurons following transient asphyxia.

作者信息

Daval J L, Koziel V, Nicolas F

机构信息

INSERM U.272 24-30, Nancy, France.

出版信息

Neuroreport. 1991 Feb;2(2):97-100. doi: 10.1097/00001756-199102000-00008.

Abstract

Functional responses of cultured neurons from rat cortex and hippocampus to transient hypoxia/asphyxia was studied by the measurement of [3H]2-deoxy-D-glucose (2DG) specific uptake. Hypoxic insult was induced by incubating the cells in 5% CO2/95% N2 or in 1 mM NaCN-containing culture medium for various periods of time. Cell morphology, lactate dehydrogenase efflux and protein levels were also examined. Twenty-four hours following hypoxia (6 to 8 h in an anaerobic atmosphere or 90 min in the presence of NaCN) 2DG specific transport was significantly enhanced, without morphological alteration. Cell injury was evident three days post-hypoxia, with a significantly reduced rate of cellular metabolism. The data suggest indirectly that postanoxic release of excitatory amino acids may be responsible for 'delayed neuronal death'.

摘要

通过测量[3H]2-脱氧-D-葡萄糖(2DG)的特异性摄取,研究了大鼠皮层和海马体培养神经元对短暂缺氧/窒息的功能反应。通过将细胞在5%二氧化碳/95%氮气或含1 mM氰化钠的培养基中孵育不同时间来诱导缺氧损伤。还检查了细胞形态、乳酸脱氢酶流出和蛋白质水平。缺氧后24小时(在无氧气氛中6至8小时或在氰化钠存在下90分钟),2DG特异性转运显著增强,且无形态学改变。缺氧后三天细胞损伤明显,细胞代谢率显著降低。数据间接表明,缺氧后兴奋性氨基酸的释放可能是“延迟性神经元死亡”的原因。

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