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在受到兴奋性氨基酸刺激的小脑颗粒细胞培养物中,多胺酰胺具有神经保护作用。

Polyamine amides are neuroprotective in cerebellar granule cell cultures challenged with excitatory amino acids.

作者信息

Green A C, Nakanishi K, Usherwood P N

机构信息

Department of Life Science, University of Nottingham, University Park, UK.

出版信息

Brain Res. 1996 Apr 22;717(1-2):135-46. doi: 10.1016/0006-8993(96)00042-x.

Abstract

Primary cultures of rat cerebellar granule cells have been used to assess the potential neuroprotective effects of philanthotoxins and argiotoxin-636 (ArgTX-636). These polyamine amides are potent antagonists of ionotropic L-glutamate (L-Glu) receptors. In granule cells loaded with fluo-3, ArgTX-636 and philanthotoxin-343 (PhTX-343) antagonised increases of intracellular free calcium concentration ([Ca2+]i) that were stimulated by N-methyl-D-aspartate (NMDA). The antagonism was use-dependent. Antagonism by PhTX-343 was fully reversible, but recovery following antagonism by ArgTX-636 was slow and only partial during the time-course of an experiment. Neither compound inhibited K(+)-induced increases in [Ca2+]i. In excitotoxicity studies with cerebellar granule cells, the release of lactate dehydrogenase (LDH) and morphological observations were used to assess cell death. A 20-30 min exposure to 500 microM NMDA, 100 microM L-Glu or 500 microM kainate was sufficient to kill > 90% of the cells after 18-20 h. When added 5 min prior to, and during agonist exposure, PhTX-343 and ArgTX-636 provided total neuroprotection. ArgTX-636 was about 20-30 fold more potent than PhTX-343 against NMDA, but was approximately equipotent with PhTX-343 against a kainate challenge. Neither of the toxins showed any inherent toxicity even at 400 microM and 100 microM respectively. Some analogues of PhTX-343 are more potent, both in terms of antagonism of NMDA-stimulated increases of [Ca2+]i and neuroprotection, than PhTX-343 and ArgTX-636.

摘要

大鼠小脑颗粒细胞的原代培养物已被用于评估 philanthotoxins 和银环蛇毒素 -636(ArgTX - 636)的潜在神经保护作用。这些多胺酰胺是离子型 L - 谷氨酸(L - Glu)受体的强效拮抗剂。在加载了 fluo - 3 的颗粒细胞中,ArgTX - 636 和 philanthotoxin - 343(PhTX - 343)拮抗了由 N - 甲基 - D - 天冬氨酸(NMDA)刺激引起的细胞内游离钙浓度([Ca2 + ]i)升高。这种拮抗作用具有使用依赖性。PhTX - 343 的拮抗作用是完全可逆的,但 ArgTX - 636 拮抗后的恢复缓慢,且在实验时间进程中仅部分恢复。两种化合物均未抑制钾离子诱导的 [Ca2 + ]i 升高。在小脑颗粒细胞的兴奋性毒性研究中,乳酸脱氢酶(LDH)的释放和形态学观察被用于评估细胞死亡。在 18 - 20 小时后,暴露于 500 microM NMDA、100 microM L - Glu 或 500 microM 海人藻酸 20 - 30 分钟足以杀死超过 90%的细胞。当在激动剂暴露前 5 分钟和暴露期间添加时,PhTX - 343 和 ArgTX - 636 提供了完全的神经保护作用。ArgTX - 636 对 NMDA 的效力比 PhTX - 343 强约 20 - 30 倍,但对海人藻酸刺激的效力与 PhTX - 343 大致相当。即使分别在 400 microM 和 100 microM 的浓度下,两种毒素均未显示出任何内在毒性。PhTX - 343 的一些类似物在拮抗 NMDA 刺激的 [Ca2 + ]i 升高和神经保护方面比 PhTX - 343 和 ArgTX - 636 更有效。

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