Figure 2.

Mechanisms implicated in elevated NO generation. On the right, the excitotoxicity pathway begins from excess glutamate, which through coupling with NOS enzymes via Ca²⁺ leads to an increase in NO production. On the left, the inflammatory pathway begins with any form of acute or chronic inflammation, which through the activation of inflammatory cells, including microglia, leads to the formation of de novo iNOS. In a Ca²⁺ independent manner, iNOS increases the production of NO. Both pathways culminate in the common end result of increased RNS formation. Abbreviations: iNOS, inducible nitric oxide synthase; MPTP, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine; NMDAR, N-methyl-d-aspartate receptors; nNOS, neuronal nitric oxide synthase; NO, nitric oxide; RNS, reactive nitrogen species; ↑ increase; ↓ decrease. References: [9,10,11,12,15,33,34].