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12 日龄大鼠锂-匹罗卡品癫痫持续状态后海马神经元损伤的时间进程。

Time course of neuronal damage in the hippocampus following lithium-pilocarpine status epilepticus in 12-day-old rats.

机构信息

Department of Developmental Epileptology, Institute of Physiology, Academy of Sciences of the Czech Republic, Prague, Czech Republic.

出版信息

Brain Res. 2010 Oct 8;1355:174-9. doi: 10.1016/j.brainres.2010.07.072. Epub 2010 Jul 29.

Abstract

Status epilepticus (SE) leads to serious damage in hippocampus of the adult brain. Much less is known about immature brain where neuronal degeneration may have different localization and time course. Lithium-pilocarpine SE was induced in 12-day-old male Wistar rats. Six different intervals after SE (from 4 h to 1 week) were studied using Fluoro-Jade B staining. Three to four animals were used for every interval. Severity of damage in individual parts of hippocampal formation was semi-quantified. A consistent neuronal damage occurred in all hippocampal fields (CA 1, CA 3, dentate gyrus) at all survival intervals. Hippocampal fields CA 1 and CA 3 exhibited degeneration of interneurons located mainly in stratum oriens and pyramidale at shorter intervals (4-12h). Massive degeneration of pyramidal cells started at 24h in CA 1 and at 48 h in CA 3. Dentate gyrus exhibited degenerating neurons in granular layer with a peak at short intervals (4-8 h), and molecular layer was spared. The lower blade of dentate gyrus was more affected than the upper blade. Damage of hilar neurons was negligible. Our results demonstrate that SE elicited in immature rats causes acute neurodegeneration in the hippocampus. Time course of this degeneration is different for individual parts of hippocampal formation and for individual cell types.

摘要

癫痫持续状态(SE)可导致成年人大脑海马区严重损伤。对于发育中大脑(神经元退化可能具有不同的定位和时程),我们知之甚少。本研究在 12 日龄雄性 Wistar 大鼠中诱导锂-匹罗卡品 SE。使用 Fluoro-Jade B 染色,在 SE 后 6 个不同时间点(4 h 至 1 周)进行研究。每个时间点使用 3 到 4 只动物。使用半定量方法对海马结构各部分的损伤严重程度进行评估。在所有存活时间点,所有海马区(CA1、CA3、齿状回)均出现一致的神经元损伤。在较短的间隔(4-12 h)内,海马区 CA1 和 CA3 的中间神经元位于层状或锥体层,出现退行性变。CA1 中的锥体细胞在 24 h 时开始大量退化,CA3 中在 48 h 时开始退化。齿状回颗粒层的神经元出现退行性变,在短时间间隔(4-8 h)达到高峰,分子层未受影响。下齿状回比上齿状回更容易受到影响。齿状回门区神经元的损伤可以忽略不计。我们的结果表明,在幼鼠中诱导的 SE 可引起海马区急性神经退行性变。这种退行性变的时间进程对于海马结构的不同部位和不同的细胞类型是不同的。

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