Okamoto M, Matsumoto M, Ohtsuki T, Taguchi A, Mikoshiba K, Yanagihara T, Kamada T
First Department of Internal Medicine, Osaka University School of Medicine, Japan.
Biochem Biophys Res Commun. 1993 Nov 15;196(3):1356-62. doi: 10.1006/bbrc.1993.2402.
Pyramidal neurons of the hippocampal CA1 are known to be particularly vulnerable to transient ischemia resulting in "delayed neuronal death". Recent studies using aurintricarboxylic acid suggested that ischemia- or excitotoxin-induced neuronal death should share intracellular mechanisms in common with apoptosis. It is, however, unclear about involvement of endonucleases. Here using a transient (5 min) forebrain ischemia model in gerbils, we found that internucleosomal DNA fragmentation developed between 48 and 54 hr recirculations, accompanied with simultaneous or slightly preceding destruction of microtubule-associated protein 2. These results suggest that endonucleases, maybe activated by elevated intracellular Ca2+, play an important role in delayed neuronal death as well as in apoptosis.
已知海马CA1区的锥体神经元对短暂性缺血特别敏感，会导致“延迟性神经元死亡”。最近使用金精三羧酸的研究表明，缺血或兴奋性毒素诱导的神经元死亡在细胞内机制上应与凋亡有共同之处。然而，关于核酸内切酶的参与情况尚不清楚。在此，我们利用沙鼠短暂性（5分钟）全脑缺血模型发现，在再灌注48至54小时之间出现了核小体间DNA片段化，同时或略先于微管相关蛋白2的破坏。这些结果表明，核酸内切酶可能被细胞内Ca2+升高激活，在延迟性神经元死亡以及凋亡中起重要作用。
