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Amyloid β peptides mediate hypoxic augmentation of Ca 2+ channels
Author(s) -
Green Kim N.,
Peers Chris
Publication year - 2001
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.2001.00338.x
Subject(s) - long term potentiation , neurodegeneration , chemistry , hypoxia (environmental) , peptide , amyloid (mycology) , neuroscience , endocrinology , biophysics , microbiology and biotechnology , medicine , biochemistry , biology , receptor , disease , organic chemistry , oxygen , inorganic chemistry
Clinical studies indicate that neurodegeneration caused by Alzheimer's amyloid β peptide (AβP) formation can be triggered or induced by prolonged (chronic) hypoxia. Here, we demonstrate that 24‐h culture of PC12 cells in 10% O 2 leads to induction of a Cd 2+ ‐resistant Ca 2+ influx pathway and selective potentiation of l ‐type Ca 2+ current. Both effects were suppressed or prevented by a monoclonal antibody raised against the N′‐terminus of AβP, and were fully mimicked by AβP 1−40 and AβP 1−42 , but not by AβP 40−1 . Potentiation of l ‐type currents was also induced by exposure to AβP 25−35 . Our results indicate that hypoxia induces enhancement of Ca 2+ channels, which is mediated by increased AβP formation.