INHIBITORY EFFECTS OF BETA-AMYLOID PEPTIDES ON NICOTINE-INDUCED CA2+ INFLUX IN PC12H CELLS IN CULTURE

Synthetic beta-amyloid peptides and the neuropeptide substance P (SP) were examined for their ability to modulate nicotinic response in PC12 h cells, a subclone of PC12 cells. SP, beta A1-40 and its peptide frag ment beta A25-35-NH2 significantly inhibited an increase in cytoplasmi c calcium concentrations ([Ca2+](i)) induced by nicotine in a dose-dep endent manner. Furthermore, beta A1-40 was found to inhibit the [Ca2+] (i) increase induced by depolarization with a high concentration of po tassium. These findings show that both beta A1-4O and beta A25-35-NH2 may mimic the function of SP on inhibition of nicotinic response throu gh different mechanisms.