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首页> 外文期刊>Progress in brain research >Cell death and metabolic activity during epileptiform discharges and status epilepticus in the hippocampus.
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Cell death and metabolic activity during epileptiform discharges and status epilepticus in the hippocampus.

机译:癫痫样放电过程中的细胞死亡和代谢活性以及海马的癫痫持续状态。

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摘要

Mechanisms of seizure-induced cell death were studied in organotypic hippocampal slice cultures. These develop after withdrawal of magnesium recurrent seizure-like events (SLE), which lead to intracellular and intramitochondrial calcium accumulation. The intramitochondrial Ca accumulation seems to be involved in causing increased production of NADH, measured as NAD(P)H autofluorescence. During SLEs, depolarization of mitochondria and increased production of free radicals is indicated by fluorescence measurements with appropriate dyes. During recurrent seizures, an increased failure to produce NADH is noted while at the same time free radical production seems to increase. This increase and the decline in NADH production could be involved in transition to late recurrent discharges, a phase in which status epilepticus becomes pharmacoresistant. It also coincides with increased cell death as determined with propidium iodide fluorescence. Interestingly, some of these changes can be prevented by application of alpha-tocopherol, a free radical scavenger, which also has neuroprotective effects under our experimental conditions. The results suggest that free radical-induced mitochondrial impairment is involved in seizure-induced cell death.
机译:在器官型海马切片培养物中研究了癫痫发作诱导的细胞死亡的机制。这些症状在镁复发性发作样事件(SLE)停药后发展,导致细胞内和线粒体内钙积累。以NAD(P)H自发荧光测量,线粒体内Ca积累似乎与引起NADH产生增加有关。在SLE期间,通过用适当的染料进行荧光测量可以显示线粒体的去极化和自由基产生的增加。在反复发作中,注意到产生NADH的失败增加,而自由基的产生似乎增加。 NADH产量的增加和下降可能与向晚期复发性放电的过渡有关,在该阶段癫痫持续状态成为药物耐药性。如碘化丙啶荧光法所确定的,这也与增加的细胞死亡相吻合。有趣的是,可以通过应用α-生育酚(一种自由基清除剂)来防止其中一些变化,在我们的实验条件下,α-生育酚也具有神经保护作用。结果表明自由基诱导的线粒体损伤与癫痫发作诱导的细胞死亡有关。

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