Expression and function of inducible nitric oxide synthase in neurons

Citation
Mt. Heneka et Dl. Feinstein, Expression and function of inducible nitric oxide synthase in neurons, J NEUROIMM, 114(1-2), 2001, pp. 8-18
Citations number
72
Categorie Soggetti
Neurosciences & Behavoir
Journal title
JOURNAL OF NEUROIMMUNOLOGY
ISSN journal
01655728 → ACNP
Volume
114
Issue
1-2
Year of publication
2001
Pages
8 - 18
Database
ISI
SICI code
0165-5728(20010301)114:1-2<8:EAFOIN>2.0.ZU;2-5
Abstract
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.