Programmed neuronal necrosis and status epilepticus
Programmed neuronal necrosis and status epilepticus
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DOI：
10.1111/j.1528-1167.2005.01025.x
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发表时间：
2005-01-01
期刊：
影响因子：
5.6
通讯作者：
Wasterlain, TG
中科院分区：
文献类型：
--
作者：
Niquet, J;Liu, TT;Wasterlain, TG
我们研究了缺氧诱导的神经元坏死的机制在齿状回培养或癫痫持续状态（SE）在成年小鼠。我们的观察结果表明，缺氧性坏死可以是一个积极的过程开始与早期线粒体肿胀和线粒体膜电位的损失，随后细胞色素c的释放和caspase-9依赖的caspase-3的激活。这一系列的事件（或程序）是独立的蛋白质合成，可能是由能量衰竭和/或钙超载的线粒体。我们称这种坏死为程序性坏死。“成年小鼠SE后，CA 1和CA 3锥体神经元显示出坏死形态，与caspase-3免疫反应性和双链DNA断裂有关，表明程序性坏死”可能与SE诱导的神经元丢失有关。关键词：癫痫持续状态-程序性坏死-神经元丢失
We examined the mechanism of neuronal necrosis induced by hypoxia in dentate gyrus cultures or by status epilepticus (SE) in adult mice. Our observations showed that hypoxic necrosis can be an active process starting with early mitochondrial swelling and loss of the mitochondrial membrane potential, followed by cytochrome c release and caspase-9-dependent activation of caspase-3. This sequence of events (or program) was independent of protein synthesis and may be induced by energy failure and/or calcium overloading of mitochondria. We called this form of necrosis "programmed necrosis." After SE in adult mice, CA1 and CA3 pyramidal neurons displayed a necrotic morphology, associated with caspase-3 immuncireactivity and with double-stranded DNA breaks, suggesting that 11 programmed necrosis" may be involved in SE-induced neuronal loss. Key Words: Status epilepticus-Programmed necrosis-Neuronal loss.