Nitric oxide and S-nitrosylation: excitotoxic and cell signaling mechanism
Related Experiment Video
Updated: Sep 26, 2026

Application of Genetically Encoded Fluorescent Nitric Oxide (NO•) Probes, the geNOps, for Real-time Imaging of NO• Signals in Single Cells
Published on: March 16, 2017
Eric J Nelson1, Jon Connolly, Patrick McArthur
1Husson Science Research Institute, One College Circle, Bangor, ME 04401, USA.
Abstract:
This review focuses on the important physiological messenger, nitric oxide (NO), and its role in N-methyl-D-aspartate (NMDA) excitotoxicity. NO has been shown to be a key mediator of voltage-gated Ca(+2) transmembrane proteins. It remains unclear whether NO is implicated during hypoxia, or ischemic/reperfusion injuries as a neuroprotective or neurodegenerative factor. Excitotoxicity results from the excessive stimulation of excitatory glutamate receptors within the CNS. This review maintains that the feed-forward pathway precipitated by oxidative stress is the discriminating factor in the neuroprotective or neurodegenerative actions of NO.
More Related Videos
Related Concept Videos
Nitric Oxide Signaling Pathway
Paracrine Signaling
2° Amines to N-Nitrosamines: Reaction with NaNO2
Ligand-Gated Ion Channel Receptor: Gating Mechanism
Neurochemical Transmission: Sites of Drug Action
Cellular Injury IV: Necrosis

