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 PC12h cells, a subclone of PC12 cells, SP, beta A1-40 and its peptide fragment beta A25-35-NH2 significantly inhibited an increase in cytoplasmic calcium concentrations ([Ca2+]i) induced by nicotine in a dose-dependent manner. Furthermore, beta A1-40 was found to inhibit the [Ca2+]i increase induced by depolarization with a high concentration of potassium. These findings show that both beta A1-40 and beta A25-35-NH2 may mimic the function of SP on inhibition of nicotinic response through different mechanisms.
Takenouchi
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Institute of Applied Biochemistry, University of Tsukuba, Japan.
Munekata
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D000595:Amino Acid Sequence; D016229:Amyloid beta-Peptides / Q000494:pharmacology*; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002478:Cells, Cultured; D003593:Cytoplasm / Q000187:drug effects / Q000378:metabolism; D008969:Molecular Sequence Data; D009538:Nicotine / Q000037:antagonists & inhibitors* / Q000494:pharmacology; D009543:Nifedipine / Q000494:pharmacology; D016716:PC12 Cells; D010446:Peptide Fragments / Q000494:pharmacology*; D011188:Potassium / Q000494:pharmacology; D051381:Rats; D011978:Receptors, Nicotinic / Q000187:drug effects; D013373:Substance P / Q000494:pharmacology
D016229:Amyloid beta-Peptides; D010446:Peptide Fragments; D011978:Receptors, Nicotinic; C078592:amyloid beta-protein (1-40); C074636:amyloid beta-protein (25-35); D013373:Substance P; D009538:Nicotine; D009543:Nifedipine; D011188:Potassium; D002118:Calcium