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cAMP potentiates beta-amyloid-induced nitric oxide release from microglia.

Authors
Pyo, H; Jou, I; Jung, S; Joe, E
Citation
Neuroreport, 10(1):37-40, 1999
Journal Title
Neuroreport
ISSN
0959-49651473-558X
Abstract
The beta-amyloid peptide (Abeta) has been known to activate microglia and to induce release of nitric oxide (NO). In this study, we examined the effect of cAMP on Abeta-induced microglial activation using cultured rat brain microglia. Dibutyryl-cAMP (dbcAMP) and 3-isobutyl-1-methylxanthine (IBMX) significantly potentiated Abeta(25-35)- or Abeta(1-42)-induced NO release in a dose-dependent manner. The increase in NO release was due to the increased expression of inducible nitric oxide synthase (iNOS). However, forskolin, an adenylate cyclase activator, weakly increased NO release at 10-50 microM but caused a decrease at 100 microM. These results suggest that increase in intracellular cAMP could potentiate microglial activation induced by Abeta.
MeSH terms
1-Methyl-3-isobutylxanthine/pharmacologyAdenylate Cyclase/drug effectsAmyloid beta-Peptides/pharmacology*AnimalsBucladesine/pharmacologyCells, CulturedCyclic AMP/pharmacology*Drug SynergismEnzyme ActivationForskolin/pharmacologyMicroglia/metabolism*Nitric Oxide/metabolism*Nitric Oxide Synthase/biosynthesisNitric Oxide Synthase Type IIRatsRats, Sprague-Dawley
PMID
10094129
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Pharmacology
AJOU Authors
표, 한경주, 일로조, 은혜
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