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神经毒剂β-N-草酰-L-α,β-二氨基丙酸是青蛙脊髓中“偏爱谷氨酸”受体的强效激动剂。

The neurolathyrogen, beta-N-oxalyl-L-alpha,beta-diaminopropionic acid, is a potent agonist at 'glutamate preferring' receptors in the frog spinal cord.

作者信息

Pearson S, Nunn P B

出版信息

Brain Res. 1981 Feb 9;206(1):178-82. doi: 10.1016/0006-8993(81)90112-8.

DOI:10.1016/0006-8993(81)90112-8
PMID:6258722
Abstract

A neurotoxic amino acid, beta-N-oxalyl-L-alpha,beta-diaminopropionate (beta-ODAP), found in seeds of Lathyrus sativus and a possible causative agent of neurolathyrism, was equipotent with kainate as a depolarizing agent of frog spinal cord ventral roots. beta-ODAP and kainate appeared to act on a common receptor, as their actions could not be differentiated pharmacologically. These results could explain some of the symptoms of neurolathyrism.

摘要

一种神经毒性氨基酸,β-N-草酰-L-α,β-二氨基丙酸(β-ODAP),存在于山黧豆种子中,是神经性山黧豆中毒的一种可能致病因子,它作为青蛙脊髓腹根的去极化剂与红藻氨酸效力相当。β-ODAP和红藻氨酸似乎作用于共同的受体,因为它们的作用在药理学上无法区分。这些结果可以解释神经性山黧豆中毒的一些症状。

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1
The neurolathyrogen, beta-N-oxalyl-L-alpha,beta-diaminopropionic acid, is a potent agonist at 'glutamate preferring' receptors in the frog spinal cord.神经毒剂β-N-草酰-L-α,β-二氨基丙酸是青蛙脊髓中“偏爱谷氨酸”受体的强效激动剂。
Brain Res. 1981 Feb 9;206(1):178-82. doi: 10.1016/0006-8993(81)90112-8.
2
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J Neurosci. 1989 Jun;9(6):2073-9. doi: 10.1523/JNEUROSCI.09-06-02073.1989.
3
Induction of astrocyte glutamine synthetase activity by the Lathyrus toxin beta-N-oxalyl-L-alpha,beta-diaminopropionic acid (beta-L-ODAP).山黧豆毒素β-N-草酰-L-α,β-二氨基丙酸(β-L-ODAP)对星形胶质细胞谷氨酰胺合成酶活性的诱导作用。
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The Lathyrus excitotoxin beta-N-oxalyl-L-alpha,beta-diaminopropionic acid is a substrate of the L-cystine/L-glutamate exchanger system xc-.山黧豆兴奋性毒素β-N-草酰-L-α,β-二氨基丙酸是L-胱氨酸/L-谷氨酸交换体系统xc-的一种底物。
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Receptor interactions of beta-N-oxalyl-L-alpha,beta-diaminopropionic acid, the Lathyrus sativus putative excitotoxin, with synaptic membranes.山黧豆潜在兴奋性毒素β-N-草酰-L-α,β-二氨基丙酸与突触膜的受体相互作用。
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Unraveling the mechanism of β-N-oxalyl-α,β-diaminopropionic acid (β-ODAP) induced excitotoxicity and oxidative stress, relevance for neurolathyrism prevention.解析 β-N-草酰基-α,β-二氨基丙酸(β-ODAP)诱导的兴奋性毒性和氧化应激的机制,与预防神经莱姆病的相关性。
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