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Transient glucose and amino acid deprivation induces delayed preconditioning in cultured rat cortical neurons
Author(s) -
Gáspár Tamás,
Kis Béla,
Snipes James A.,
Lenzsér Gábor,
Mayanagi Keita,
Bari Ferenc,
Busija David W.
Publication year - 2006
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 - 10.1111/j.1471-4159.2006.03899.x
Subject(s) - glutamate receptor , oxidative phosphorylation , stimulation , intracellular , endocrinology , medicine , privation , chemistry , mitochondrion , biology , biochemistry , sleep deprivation , receptor , circadian rhythm
Several studies have demonstrated that glucose deprivation, combined either with anoxia or with the inhibition of oxidative phosphorylation, leads to the development of ischemic tolerance in neurons. The aim of our experiments was to investigate whether similar effects could be achieved by transient energy deprivation without either anoxia or the inhibition of the electron transfer chain. Preconditioning was carried out by incubating primary rat cortical neuronal cultures for 3, 6 or 9 h in a glucose‐ and amino acid‐free balanced salt solution supplemented with B27 in normoxic conditions. After 24 h, neuronal cultures were exposed to oxygen–glucose deprivation, glutamate or hydrogen peroxide. Cell viability was measured 24 h after the lethal insults. Potential mechanisms that can influence free radical production were also examined. Energy deprivation protected neuronal cells against lethal stimuli (e.g. cell survival after oxygen–glucose deprivation was 33.1 ± 0.52% in the untreated group and 80.1 ± 1.27% in the 9‐h energy deprivation group), reduced mitochondrial membrane potential, decreased free radical formation, attenuated the intracellular free calcium surge upon glutamate receptor stimulation, and resulted in an elevated level of GSH. Our findings show that transient energy deprivation induces delayed preconditioning and prevents oxidative injuries and neuronal cell death.