妊娠期间给予喹啉酸对大鼠后代海马形成的影响(超微结构观察)。

M Beskid, Z Rózycka
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引用次数: 0

摘要

为了模拟胎儿组织内源性过量喹啉酸引起的先天性代谢紊乱,在妊娠期给母鼠注射喹啉酸后,对子代大鼠海马CA1区锥体细胞进行了超微结构检测。因此,在整个妊娠期间,喹啉酸以60 mmol的剂量腹腔内给予母亲,每天一次。在出生后第5天采集实验动物和对照动物的脑标本。锥体细胞内唯一观察到的变化是神经元体和树突的肿胀,以及星形胶质细胞胞质和突起的明显肿胀。除此之外,还观察到毒性作用,如水肿迹象。海马神经元被发现对喹啉酸的毒性特别敏感。高度易感神经元位于ca1区。在电生理实验中,神经元的易感性与对喹啉酸兴奋作用的反应有着显著的相关性(Perkins and Stone 1983 a,b)。该区域富含NMDA受体(Cotman et al. 1987;Greenamyre et al. 1984)。成年哺乳动物海马形成的神经元细胞体对喹啉酸毒性的敏感性已被饶有兴趣地研究(Schwarcz et al. 1984;Taraszewska et al. 1991;Kida and Matyja 1990;special et al. 1987)。然而,关于胎儿发育过程的信息却很少。因此,在我们的实验中,为了模拟胎儿组织中过量喹啉酸导致的先天性代谢紊乱,在整个妊娠期给母亲服用喹啉酸。(摘要删节250字)
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The effect of quinolinic acid administered during pregnancy on the hippocampal formation of rat's offspring (ultrastructural investigation).

The pyramidal cells of CA1 hippocampal area of rat's offspring was ultrastructurally examined after quinolinic acid administration to mothers during the gestational period, in order to mimic the congenital metabolic disturbances resulting from an endogenous excess of quinolinic acid within foetal tissues. Hence, quinolinic acid was administered to mothers intraperitoneally in a dose of 60 mmol, once daily, throughout the entire gestation period. Brain specimens were taken on Day 5 after birth, from experimental and control animals. The only observed change within the pyramidal cells was swelling of both neuronal somata and dendrites, as well as a distinct swelling of astroglia cytoplasm and processes. Besides this, toxic effects, like edema signs, were observed. Neurons of the hippocampal formation were found to be particularly susceptible to quinolinic acid toxicity. The highly vulnerable neurons were located within the CA1-area. The neuronal vulnerability correlates remarkably well with those responding to the excitatory effects of quinolinic acid in electrophysiological experiments (Perkins and Stone 1983 a,b). This region was shown to be rich in NMDA receptors (Cotman et al. 1987; Greenamyre et al. 1984). The susceptibility of neuronal cell bodies of the hippocampal formation of an adult mammalian to the quinolinic acid toxicity, has been investigated with great interest (Schwarcz et al. 1984; Taraszewska et al. 1991; Kida and Matyja 1990; Speciale et al. 1987). Yet there is little information on the course of the foetal development. Hence, in our experiments, quinolinic acid was administered to the mother throughout the gestation period in order to mimic the congenital metabolic disturbances resulting from an excess of quinolinic acid within foetal tissues.(ABSTRACT TRUNCATED AT 250 WORDS)

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