Expression and function of inducible nitric oxide synthase in neurons.
Enzymatically derived nitric oxide (NO) has been implicated in numerous physiological and pathological processes in the brain. Whereas during development NO participates in developmental and maturation processes, excess NO production in the adult in response to inflammation, injury, or trauma participates in both cell death and repair. The expression and activity of the inducible isoform of NO synthase (iNOS) play a pivotal role in sustained and elevated NO release. Recent evidence suggests that neurons can respond to proinflammatory stimuli and take part in brain inflammation. Neuronal iNOS expression has been described in different experimental settings, including cytokine stimulation of neuronal cell lines and primary neurons in vitro as well as in animal models of stroke and neurodegeneration. This article outlines different conditions leading to iNOS gene transcription and expression in neurons and neuronal cells and highlights the potential impact on human brain inflammation and neurodegeneration.
Heneka
M T
MT
Department of Neurology, University of Bonn, Bonn, Germany
Feinstein
D L
DL
D000544:Alzheimer Disease / Q000378:metabolism; D000818:Animals; D006801:Humans; D009474:Neurons / Q000201:enzymology*; D019001:Nitric Oxide Synthase / Q000235:genetics* / Q000378:metabolism*; D052247:Nitric Oxide Synthase Type II
C496319:NOS2 protein, human; D019001:Nitric Oxide Synthase; D052247:Nitric Oxide Synthase Type II