Glutamate-stimulated calcium activation of Ras/Erk pathway mediated by nitric oxide

被引：29

作者：

Yun, HY

Dawson, VL

Dawson, TM

机构：

[1] Chung Ang Univ, Coll Med, Dept Biochem, Seoul 156756, South Korea

[2] Johns Hopkins Univ, Sch Med, Dept Neurol, Baltimore, MD 21287 USA

[3] Johns Hopkins Univ, Sch Med, Dept Neurosci, Baltimore, MD 21287 USA

[4] Johns Hopkins Univ, Sch Med, Dept Physiol, Baltimore, MD 21287 USA

来源：

DIABETES RESEARCH AND CLINICAL PRACTICE | 1999年 / 45卷 / 2-3期

关键词：

nitric oxide; Ras; NMDA; calcium;

D O I：

10.1016/S0168-8227(99)00039-X

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

NMDA-type glutamate receptor-mediated increases in intracellular calcium play a critical role in synaptic plasticity involved in learning and memory. Calcium-dependent activation of Ras and extracellular signal-regulated kineses (Erks) may transmit the glutamate signal to the nucleus which is ultimately important for long-lasting neuronal responses. The mechanism by which changes in cytoplasmic calcium mediate NMDA-induced activation of Ras and Erk is not known. In cerebral cortical neurons, this calcium influx through NMDA receptors activates Ras and its downstream effector, Erk, via nitric oxide (NO) generation by calcium-dependent neuronal NO synthase. We propose that NO is a key link between NMDA-mediated increases in cytoplasmic calcium and activity-dependent long-term changes such as differentiation, survival and synaptic plasticity. (C) 1999 Elsevier Science Ireland Ltd. All rights reserved.

引用

页码：113 / 115

页数：3

共 18 条

[1] STIMULATION OF PROTEIN TYROSINE PHOSPHORYLATION BY NMDA RECEPTOR ACTIVATION [J].