A beta-induced TNF-alpha expression and acetylcholine action in mouse glial cells

Life Sci. 2003 Mar 28;72(18-19):2117-20. doi: 10.1016/s0024-3205(03)00070-5.

Abstract

The brains in patients with Alzheimer's disease show chronic inflammatory responses characterized by activated glial cells and increased expression of cytokines. It is of interest to determine whether acetylcholine (ACh) affects Abeta-induced cytokine expression in the glial cells. Since it has been shown that alpha7 subunits of nicotinic ACh receptors are expressed in glial cells and that Abeta(1-42) binds to alpha7, we examined the effects of cholinergic agonists, carbachol, nicotine and oxotremorine-M, on Abeta-induced TNF-alpha expression in mouse glial cells. We did not observe any regulatory effects of ACh on Abeta-induced TNF-alpha transcription in the glial cells. We discuss the pathophysiological roles of ACh in glial cells in the brains of patients with Alzheimer's disease.

MeSH terms

  • Acetylcholine / pharmacology*
  • Amyloid beta-Peptides / pharmacology*
  • Animals
  • Carbachol / pharmacology
  • Cells, Cultured
  • Glyceraldehyde-3-Phosphate Dehydrogenases / metabolism
  • Inflammation / pathology
  • Mice
  • Muscarinic Agonists / pharmacology
  • Neuroglia / drug effects
  • Neuroglia / metabolism*
  • Nicotine / pharmacology
  • Nicotinic Agonists / pharmacology
  • Oxotremorine / pharmacology
  • Peptide Fragments / pharmacology*
  • Reverse Transcriptase Polymerase Chain Reaction
  • Tumor Necrosis Factor-alpha / biosynthesis*

Substances

  • Amyloid beta-Peptides
  • Muscarinic Agonists
  • Nicotinic Agonists
  • Peptide Fragments
  • Tumor Necrosis Factor-alpha
  • amyloid beta-protein (1-42)
  • Oxotremorine
  • Nicotine
  • Carbachol
  • Glyceraldehyde-3-Phosphate Dehydrogenases
  • Acetylcholine