Amyloid beta-protein fragment 25-35 causes activation of cytoplasmic calcium in neurons

Biochem Biophys Res Commun. 1992 May 15;184(3):1441-7. doi: 10.1016/s0006-291x(05)80044-0.

Abstract

The cellular mechanism by which beta-amyloid has its effect on neurons is unknown. Based on observations that endogenous neurotoxins, such as glutamate and platelet activating factor (PAF), cause activation of cytoplasmic calcium, we tested if this was true with beta-amyloid. Using nerve growth factor-treated PC12 cells, we noted that the active beta-amyloid fragment, containing residues 25 to 35, caused a specific and dose-dependent increase in intracellular calcium due to an influx of extracellular calcium.

Publication types

  • Comparative Study
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Aequorin
  • Amyloid beta-Peptides / pharmacology*
  • Animals
  • Calcimycin / pharmacology
  • Calcium / metabolism*
  • Cytoplasm / metabolism
  • Dose-Response Relationship, Drug
  • Kinetics
  • Luminescent Measurements
  • Nerve Growth Factors / pharmacology*
  • Neurons / drug effects
  • Neurons / metabolism*
  • PC12 Cells
  • Peptide Fragments / pharmacology*
  • Platelet Activating Factor / pharmacology

Substances

  • Amyloid beta-Peptides
  • Nerve Growth Factors
  • Peptide Fragments
  • Platelet Activating Factor
  • amyloid beta-protein (25-35)
  • Calcimycin
  • Aequorin
  • Calcium