Journal
JOURNAL OF NEUROCHEMISTRY
Volume 78, Issue 4, Pages 807-814Publisher
BLACKWELL SCIENCE LTD
DOI: 10.1046/j.1471-4159.2001.00478.x
Keywords
Alzheimer's disease; BAPTA AM; glutamate; hydrogen peroxide; neuronal death; nifedipine
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We examined the function of presenilin-1 (PSI) on neuronal resistance to oxidative stress. CNS neurons cultured from PS1-deficient mice exhibited increased vulnerability to H2O2 treatment compared with those from wild-type mice. Antioxidants protected the cultured neurons against the oxidative stress. An intracellular calcium chelator, BAPTA AM, as well as an L-type voltage-dependent calcium channel blocker, nifedipine, rescued the neurons from H2O2-induced death, while an N-type voltage-dependent calcium channel blocker, omega -conotoxin, or calcium release blockers from ER stores, dantrolene and xestospongin C, failed to rescue them. Wild-type and PS1-deficient neurons showed comparable increases of cytoplasmic free calcium levels after exposure to H2O2. Taken together with the data that PS1-deficient neurons exhibited increased vulnerability to glutamate, these findings imply that PS1 confers resistance to oxidative stress on neurons in calcium-dependent manners.
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