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

Hye Young Yun, V. L. Dawson, T. M. Dawson

Research output: Contribution to journalArticlepeer-review

Abstract

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.

Original languageEnglish (US)
Pages (from-to)113-115
Number of pages3
JournalDiabetes Research and Clinical Practice
Volume45
Issue number2-3
DOIs
StatePublished - Sep 1999

Keywords

  • Calcium
  • NMDA
  • Nitric oxide
  • Ras

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism
  • Endocrinology

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