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An amyloid peptide, beta A4 25-35, mimics the function of substance P on modulation of nicotine-evoked secretion and desensitization in cultured bovine adrenal chromaffin cells

journal contribution
posted on 1993-03-01, 00:00 authored by Steve Cheung, D H Small, B G Livett
The amyloid protein (beta A4) is found in the CNS of patients with Alzheimer's disease; however, the pathogenic role of this protein is not known. In the present study, a peptide fragment of beta A4 (beta A4 25-35; Gly-Ser-Asn-Lys-Gly-Ala-Ile-Ile-Gly-Leu-Met-NH2), which contains the conserved C-terminal sequence of substance P (X-Gly-Leu-Met-NH2), and the neuropeptide substance P (SP) were examined for their ability to modulate nicotine-evoked secretion from cultured bovine adrenal chromaffin cells. Secretion of the released endogenous catecholamines was monitored by electrochemical detection after separation by HPLC. Secretion induced by 10(-5) M nicotine was inhibited by SP and beta A4 25-35. The IC50 of SP and beta A4 25-35 was 3 x 10(-6) and 3 x 10(-5) M, respectively. SP and beta A4 25-35 both protected against nicotine receptor desensitization. However, beta A4 25-35 was approximately 10-fold less effective than SP in its protective effect. The present work shows that beta A4 25-35 can mimic the modulatory actions of SP on the nicotinic response of cultured bovine chromaffin cells, i.e., inhibition of the nicotinic response and protection against nicotinic desensitization. These modulatory actions may be associated with changes in nicotinic receptor levels reported to occur in Alzheimer's disease.

History

Journal

Journal of neurochemistry

Volume

60

Issue

3

Pagination

1163 - 1166

Publisher

John Wiley & Sons

Location

Chichester, Eng.

ISSN

0022-3042

Language

eng

Publication classification

CN.1 Other journal article

Copyright notice

[1993, John Wiley & Sons]

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