Inhibitory effects of β-amyloid peptides on nicotine-induced Ca 2+ influx in PC12h cells in culture

Abstract

Synthetic β-amyloid peptides and the neuropeptide substance P (SP) were examined for their ability to modulate nicotinic response in PC12h cells, a subclone of PC12 cells. SP, βA1–40 and its peptide fragment βA25–35-NH 2 significantly inhibited an increase in cytoplasmic calcium concentrations ([Ca 2+] i) induced by nicotine in a dose-dependent manner. Furthermore, βA1–40 was found to inhibit the [Ca 2+] i increase induced by depolarization with a high concentration of potassium. These findings show that both βA1–40 and βA25–35-NH 2 may mimic the function of SP on inhibition of nicotinic response through different mechanisms.