Amyloid beta protein does not interact with tachykinin receptors coupled to inositol phospholipid hydrolysis in human astrocytoma cells

Brain Res. 1993 Jan 8;600(1):166-8. doi: 10.1016/0006-8993(93)90416-k.

Abstract

We have tested the interaction between amyloid beta protein (A beta P) and tachykinin receptors in cultured UC-11MG astrocytoma cells, which express high affinity substance P receptors and respond to substance P with an unusually large stimulation of polyphosphoinositide hydrolysis. Both the full-length A beta P (A beta P1-40) and the fragment 25-35 (A beta P25-35) did not affect the stimulation of [3H]inositolmonophosphate (InsP) formation by substance P. A beta P25-35 was also inactive when applied to the cultures 18 or 72 h prior to the assay. In addition, A beta P25-35 did not displace specifically bound [3H]SarMet substance P from its recognition sites in intact UC-11MG cells. These results suggest that, at least in this specific cell type, amyloid peptides do not interact with substance P receptors.

MeSH terms

  • Amyloid beta-Peptides / pharmacology*
  • Astrocytoma / metabolism*
  • Dimethyl Sulfoxide / pharmacology
  • Humans
  • Inositol Phosphates / metabolism*
  • Peptide Fragments / pharmacology
  • Phosphatidylinositol Phosphates
  • Phosphatidylinositols / metabolism*
  • Receptors, Neurotransmitter / drug effects
  • Receptors, Neurotransmitter / metabolism*
  • Receptors, Tachykinin
  • Substance P / analogs & derivatives
  • Substance P / metabolism
  • Substance P / pharmacology
  • Tumor Cells, Cultured

Substances

  • Amyloid beta-Peptides
  • Inositol Phosphates
  • Peptide Fragments
  • Phosphatidylinositol Phosphates
  • Phosphatidylinositols
  • Receptors, Neurotransmitter
  • Receptors, Tachykinin
  • substance P, Sar(9)-Met(O2)(11)-
  • Substance P
  • Dimethyl Sulfoxide