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

Neuroreport. 1999 Jan 18;10(1):37-40. doi: 10.1097/00001756-199901180-00007.

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 1-Methyl-3-isobutylxanthine / pharmacology
  • Adenylyl Cyclases / drug effects
  • Amyloid beta-Peptides / pharmacology*
  • Animals
  • Bucladesine / pharmacology
  • Cells, Cultured
  • Colforsin / pharmacology
  • Cyclic AMP / pharmacology*
  • Drug Synergism
  • Enzyme Activation
  • Microglia / metabolism*
  • Nitric Oxide / metabolism*
  • Nitric Oxide Synthase / biosynthesis
  • Nitric Oxide Synthase Type II
  • Rats
  • Rats, Sprague-Dawley

Substances

  • Amyloid beta-Peptides
  • Colforsin
  • Nitric Oxide
  • Bucladesine
  • Cyclic AMP
  • Nitric Oxide Synthase
  • Nitric Oxide Synthase Type II
  • Nos2 protein, rat
  • Adenylyl Cyclases
  • 1-Methyl-3-isobutylxanthine