Suppr超能文献

[镁缺乏致敏感小鼠听源性惊厥发作的特征]

[Characteristics of the audiogenic convulsive crisis in mice made sensitive by magnesium deficiency].

作者信息

Bac P, Tran G, Paris M, Binet P

机构信息

Laboratoire de Biologie animale, Centre Pharmaceutique, Université Paris XI, Chatenay-Malabry, France.

出版信息

C R Acad Sci III. 1993 Jul;316(7):676-81.

PMID:8019889
Abstract

Mice of the OF1, C57BL/6, AKR, C3H/He, DBA/2, BALB/C, B6D2F1 and CBA strains are susceptible to audiogenic seizures after 40 or 20 days of acute magnesium deficiency. The duration of the various phases of the audiogenic seizure response (at 100 dBA) (wild running latency period, convulsions latency period and the clonic and tonic convulsions) among these mice was measured. Using the Kruskall-Wallis test, no difference was recorded using these measurements and those obtained for genetically audio-susceptible animals. This shows that acute magnesium deficiency-induced audiogenic seizures develop in exactly the same way as in genetically audio-susceptible animals (21-days-old DBA/2 mice). Lower intensity (60 and 80 dBA) produced only audiogenic seizures in magnesium deficient mice. Repeated auditory stimulation caused an increase in the number of lethal seizures. Sound-induced seizures in magnesium deficient mice provide a sensitive screening test for anti convulsive drug, and for drugs use in magnesium depletion.

摘要

OF1、C57BL/6、AKR、C3H/He、DBA/2、BALB/C、B6D2F1和CBA品系的小鼠在急性镁缺乏40天或20天后易发生听源性惊厥。测量了这些小鼠听源性惊厥反应(在100分贝)各阶段的持续时间(狂奔潜伏期、惊厥潜伏期以及阵挛性和强直性惊厥)。使用克鲁斯卡尔-沃利斯检验,这些测量结果与从基因上对声音敏感的动物获得的测量结果相比,未发现差异。这表明急性镁缺乏诱导的听源性惊厥的发展方式与基因上对声音敏感的动物(21日龄的DBA/2小鼠)完全相同。较低强度(60和80分贝)仅在缺镁小鼠中引发听源性惊厥。重复听觉刺激导致致死性惊厥数量增加。缺镁小鼠中的声音诱发惊厥为抗惊厥药物以及用于耗镁的药物提供了一种灵敏的筛选试验。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验