Expression of inducible nitric oxide synthase by neurones following exposure to endotoxin and cytokine.
In the CNS, nitric oxide (NO) has been implicated as both a mediator of neurotoxicity and a neuromodulator. The inducible NO synthase (iNOS), thought to mediate toxic effects of NO, has been attributed to glial cells in the CNS. We now report that cerebellar granule cell neurones can be stimulated by lipopolysaccharide and interferon-gamma to express iNOS in vitro, as demonstrated by reverse transcription-polymerase chain reaction and fluorescent in situ hybridisation. The expression of both constitutive NO synthase (cNOS) and iNOS by neurones suggests that NO has diverse functions in the brain, and supports the possibility that iNOS plays a role in neuronal damage and inflammation following activation of brain microglia and production of cytokines.
Minc-Golomb
D
D
Clinical Neuroscience Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland.
Tsarfaty
I
I
Schwartz
J P
JP
D000594:Amino Acid Oxidoreductases / Q000096:biosynthesis*; D000818:Animals; D002531:Cerebellum / Q000166:cytology / Q000187:drug effects / Q000201:enzymology; D016207:Cytokines / Q000494:pharmacology*; D004731:Endotoxins / Q000494:pharmacology*; D004790:Enzyme Induction / Q000187:drug effects; D017403:In Situ Hybridization; D009457:Neuroglia / Q000201:enzymology; D009474:Neurons / Q000187:drug effects / Q000201:enzymology*; D019001:Nitric Oxide Synthase; D016133:Polymerase Chain Reaction; D012313:RNA / Q000096:biosynthesis; D051381:Rats
D016207:Cytokines; D004731:Endotoxins; D012313:RNA; D019001:Nitric Oxide Synthase; D000594:Amino Acid Oxidoreductases