甘氨酸可增强大鼠海马CA1神经元中的NMDA反应。

Glycine potentiates NMDA responses in rat hippocampal CA1 neurons.

作者信息

Minota S, Miyazaki T, Wang M Y, Read H L, Dun N J

机构信息

Department of Pharmacology, Loyola University Stritch School of Medicine, Maywood, IL 60153.

出版信息

Neurosci Lett. 1989 May 22;100(1-3):237-42. doi: 10.1016/0304-3940(89)90691-5.

DOI:10.1016/0304-3940(89)90691-5

PMID:2569702

Abstract

When superfused onto rat hippocampal slices, glycine (0.1-0.5 mM) potentiated the depolarization induced by pressure application of NMDA in normal Krebs solution and the synaptic discharge evoked by stimulation of the Schaffer collateral-commissural inputs to the CA1 pyramidal neurons bathed in Mg2+-free media; the effects were not prevented by strychnine. In addition, glycine partially reversed the blocking effect of D-2-amino-5-phosphonovalerate (AP5) on N-methyl-D-aspartate (NMDA)-induced depolarization. These results show that glycine at relatively high concentrations potentiates the NMDA-mediated response in hippocampal slices.

摘要

当将甘氨酸（0.1 - 0.5 mM）灌注到大鼠海马切片上时，在正常的 Krebs 溶液中，它能增强由压力施加 NMDA 所诱导的去极化，以及在无镁培养基中刺激 CA1 锥体神经元的 Schaffer 侧支 - 连合输入所诱发的突触放电；士的宁不能阻止这些效应。此外，甘氨酸部分逆转了 D - 2 - 氨基 - 5 - 磷酸戊酸（AP5）对 N - 甲基 - D - 天冬氨酸（NMDA）诱导的去极化的阻断作用。这些结果表明，相对高浓度的甘氨酸能增强海马切片中 NMDA 介导的反应。