甘氨酸对非氨酯缺氧保护作用的逆转

Glycine reversal of felbamate hypoxic protection.

作者信息

Wallis R A, Panizzon K L

机构信息

Sepulveda VAMC (111N-1), CA.

出版信息

Neuroreport. 1993 Jul;4(7):951-4. doi: 10.1097/00001756-199307000-00029.

DOI:10.1097/00001756-199307000-00029

PMID:8103685

Abstract

We investigated the role of glycine in felbamate hypoxic neuroprotection using the rat hippocampal slice. Following hypoxic exposure, CA1 orthodromic PS recovered a mean 26 +/- 3% of original amplitude; treatment with 1.3 mM felbamate, a recently developed anticonvulsant, increased this recovery to 95 +/- 3%. However, the addition of 10 microM glycine with felbamate during hypoxia, reduced this recovery to 16 +/- 12%. The glycine EC50 for reversal of felbamate hypoxic protection was found to be 4.4 microM. Glycine 10 microM given during hypoxia without felbamate, slightly exacerbated subsequent injury, with 13 +/- 3% recovery seen. Glycine 100 microM given alone under normoxic conditions showed no effect. Reversal of felbamate hypoxic protection was specific for glycine, and was not seen with 50 microM glutamate. These results suggest that felbamate neuroprotection from hypoxia occurs through a glycine interaction.

摘要

我们使用大鼠海马切片研究了甘氨酸在非氨酯缺氧神经保护中的作用。缺氧暴露后，CA1 区的顺向兴奋性突触后电位（PS）恢复到原始幅度的平均 26±3%；用 1.3 mM 非氨酯（一种最近开发的抗惊厥药）处理后，该恢复率增加到 95±3%。然而，在缺氧期间将 10 μM 甘氨酸与非氨酯一起添加，使该恢复率降低到 16±12%。发现用于逆转非氨酯缺氧保护作用的甘氨酸半数有效浓度（EC50）为 4.4 μM。在无非氨酯的缺氧期间给予 10 μM 甘氨酸，会使随后的损伤略有加重，观察到的恢复率为 13±3%。在常氧条件下单独给予 100 μM 甘氨酸未显示出作用。非氨酯缺氧保护作用的逆转对甘氨酸具有特异性，50 μM 谷氨酸不会出现这种情况。这些结果表明，非氨酯对缺氧的神经保护作用是通过与甘氨酸相互作用实现的。