Change in membrane permeability induced by amyloid beta-protein fragment 25-35 in brain neurons dissociated from rats

Jpn J Pharmacol. 1995 May;68(1):77-83. doi: 10.1254/jjp.68.77.

Abstract

Effects of amyloid beta-protein fragment 25-35, A beta P(25-35), on the membrane permeability of organic molecules were examined in the brain neurons dissociated from rats by using an argon laser (equipped in flow cytometer and laser microscope) and a combination of two fluorescent dyes, fluo-3-AM and ethidium bromide. A beta P(25-35) at concentrations of 1 microM or greater induced both leakage of fluo-3 from the neurons and permeation of ethidium across the membrane in a dose-dependent manner, although both dyes are highly impermeant to the intact plasma membrane. Thus, A beta P(25-35) seems to increase not only membrane permeability of inorganic ions such as Ca2+, Na+ and K+, as previously suggested, but also that of organic molecules. Therefore, the brain neuron membrane is suggested to lose its integrity in the presence of A beta P(25-35) that leads to neuronal death.

MeSH terms

  • Amyloid beta-Peptides / pharmacology*
  • Aniline Compounds
  • Animals
  • Brain / cytology
  • Calcium / metabolism
  • Cell Membrane Permeability / drug effects*
  • Cell Survival
  • Digitoxin / pharmacology
  • Ethidium
  • Flow Cytometry
  • Fluorescent Dyes
  • In Vitro Techniques
  • Ionomycin / pharmacology
  • Lasers
  • Neurons / drug effects*
  • Neurons / metabolism
  • Peptide Fragments / pharmacology*
  • Potassium / metabolism
  • Rats
  • Rats, Wistar
  • Sodium / metabolism
  • Time Factors
  • Xanthenes

Substances

  • Amyloid beta-Peptides
  • Aniline Compounds
  • Fluorescent Dyes
  • Peptide Fragments
  • Xanthenes
  • amyloid beta-protein (25-35)
  • Fluo-3
  • Ionomycin
  • Sodium
  • Digitoxin
  • Ethidium
  • Potassium
  • Calcium