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. 1994 May 23;173(1-2):147-50.
doi: 10.1016/0304-3940(94)90170-8.

Inhibitory effects of beta-amyloid peptides on nicotine-induced Ca2+ influx in PC12h cells in culture

T Takenouchi  1 , E Munekata
Affiliations

Inhibitory effects of beta-amyloid peptides on nicotine-induced Ca2+ influx in PC12h cells in culture

T Takenouchi et al. Neurosci Lett. .

Abstract

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.

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