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Activation of Nuclear Factor κB by Nitric Oxide in Rat Striatal Neurones : Differential Inhibition of the p50 and p65 Subunits by Dexamethasone by C. S. Simpson; B. J. Morris is a Neuroscience article available to read on EtoBox.

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Abstract: Nitric oxide (NO), an intercellular messenger in the brain, has been implicated in both neuronal plasticity and neurotoxicity. It has been suggested that NO can activate the DNA binding activity of nuclear factor κB (NF‐κB) family proteins in some cell types while having an inhibitory effect in others. In this study we have investigated the effect of acute NO in primary neuronal cultures of rat striatum using immunohistochemistry. Exposure of neurones to the NO‐mimetic __S__‐nitroso‐__n__‐acetylpenicillamine (SNAP; 200 μ__M__) and to bacterial lipopolysaccharide (LPS; 10 μg/ml) for 30 min increased nuclear protein expression of the p50 subunit of NF‐κB. SNAP also enhanced nuclear protein expression of the p65 subunit of NF‐κB. Simultaneously, the cytoplasmic expression of phosphorylated inhibitory protein IκBα was dramatically increased by SNAP (200 μ__M__), LPS (10 μg/ml), and kainate (50 μ__M__) treatment. In the adult rat, stimulation with NOR‐3 (2 mg/kg), a NO donor, increased NF‐κB DNA binding activity in the striatum after 45 min. Because glucocorticoids inhibit NF‐κB activity, primary cultures were pretreated with dexamethasone (50 μ__M__) before SNAP, LPS, and kai

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Author

C. S. Simpson; B. J. Morris

Publisher

John Wiley and Sons; Wiley (Blackwell Publishing); Blackwell Publishing Inc.; Wiley (ISSN 0022-3042)

Published

1999

Language

EN

Field

Neuroscience (Life Sciences)