Enzymatically derived nitric oxide (NO) has been implicated in numerous phy
siological and pathological processes in the brain. Whereas during developm
ent NO participates in developmental and maturation processes, excess NO pr
oduction in the adult in response to inflammation, injury, qr trauma partic
ipates in both cell death and repair. The expression and activity of the in
ducible isoform of NO synthase (iNOS) play a pivotal role in sustained and
elevated NO release. Recent evidence suggests that neurons can respond to p
roinflammatory stimuli and take part in brain inflammation. Neuronal iNOS e
xpression 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 out
lines different conditions leading to iNOS gene transcription and expressio
n in neurons and neuronal cells and highlights the potential impact on huma
n brain inflammation and neurodegeneration. (C) 2001 Elsevier Science B.V.
All rights reserved.