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谷氨酸诱导的神经元死亡并非小脑培养中的程序性细胞死亡。

Glutamate-induced neuronal death is not a programmed cell death in cerebellar culture.

作者信息

Dessi F, Charriaut-Marlangue C, Khrestchatisky M, Ben-Ari Y

机构信息

INSERM U29, Paris, France.

出版信息

J Neurochem. 1993 May;60(5):1953-5. doi: 10.1111/j.1471-4159.1993.tb13427.x.

Abstract

Activation of programmed cell death has recently been suggested to be involved in the delayed neuronal death of CA1 hippocampal neurons after global ischemia based on protection offered by protein synthesis inhibitors. Here, we studied the effects of transcriptional (actinomycin D) and translational (cycloheximide and anisomycin) inhibitors on glutamate-induced neuronal death in cerebellar granule cell cultures. The effects of aurintricarboxylic acid, an endonuclease inhibitor, were studied as well. No protection against glutamate toxicity could be observed with any of these inhibitors. We also analyzed the genomic DNA of glutamate-treated cells on agarose gel electrophoresis. No DNA degradation could be observed after glutamate exposure. We conclude that glutamate-induced neuronal death does not exhibit the features of apoptosis in cultured granule cells.

摘要

基于蛋白质合成抑制剂所提供的保护作用,近来有人提出程序性细胞死亡的激活参与了全脑缺血后海马CA1区神经元的延迟性死亡。在此,我们研究了转录抑制剂(放线菌素D)及翻译抑制剂(环己酰亚胺和茴香霉素)对小脑颗粒细胞培养物中谷氨酸诱导的神经元死亡的影响。同时也研究了核酸内切酶抑制剂金精三羧酸的作用效果。使用这些抑制剂均未观察到对谷氨酸毒性的保护作用。我们还在琼脂糖凝胶电泳上分析了经谷氨酸处理的细胞的基因组DNA。谷氨酸暴露后未观察到DNA降解。我们得出结论,谷氨酸诱导的神经元死亡在培养的颗粒细胞中未表现出凋亡特征。

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